Glomerulonephritis and Chronic Renal Failure - the Crucial Role of Chemical Exposure

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by Uffe Ravnskov, MD, PhD

Glomerulonephritis, the commonest cause of end-stage renal failure in most countries, is worsened and may even be caused by exposure to chemicals present on many work places, at home and in the public environment. 

The commonest nephrotoxic chemicals are hydrocarbons, present for instance in organic solvents, glues, fuels, paints and motor exhausts. Exposure is common among painters, printers, cabinet makers, fitters and mechanics, electricians, in much manufacturing, and in many other occupations

Also nephrotoxic are silicates, the main components in rocks and sand. Exposure is prevalent among miners, foundry and quarry workers, sandblasters, glaziers, and workers in the production and handling of asbestos, mineral wool and fiber glass. 

Other chemicals that may promote glomerulonephritis or other kidney diseases include gold, lead, mercury and various drugs, for instance non-steroidal antiinflammatory drugs and lithium 

Recent studies have found that even diabetic kidney disease may be worsened by exposure to toxic chemicals. Exposure should also be ruled out in patients with kidney parenchymal diseases of unknown origin

As seen from the following more than 60% of patients with end-stage renal failure caused by glomerulonephritis have been exposed to toxic chemicals. Most important for patients with progressive renal failure is therefore to discontinue any exposure to nephrotoxic chemicals and drugs

© Uffe Ravnskov
      Published on February 9, 2001
. Last modified November 8, 2001
This site is updated and extended regularly. Comments and critical views are most welcome



Although glomerulonephritis is a rare disease, it is the commonest cause  of end-stage renal failure in most countries. It is possible to live a normal life even with a substantial reduction of renal function, but when the function goes down below ten per cent of normal, symptoms such as muscular weakness, tiredness, itching, anemia and nausea may eventually invalidate the patient seriously. This condition is called end-stage renal disease and may soon become life-threatening.


Previously, all patients with end-stage renal disease died, but to-day it is possible to maintain life by dialysis treatment or by transplanting a kidney from another human being. However, it is still a catastrophe for the patient and the patient´s family because there is a great shortage of kidneys for transplantation, and dialysis treatment is disabling. Two to three times a week the patient is chained to a dialysis machine for many hours and despite that the patient`s health is not optimal. A tedious diet and many drugs are necessary to combat the many complications of end-stage renal failure and the mortality is high. Every year 20-30 per cent of all dialysis patients die, but new patients constantly arrive. Therefore, although glomerulonephritis is a rare disease it is costly for society. In many countries treatment of renal failure alone takes four to five per cent of the total health budget.

Glomerulonephritis is an innocent condition as long as the renal function is normal. The “patient” has no symptoms and the diagnosis may remain undetected unless his urine is examined. Here, a routine laboratory test may reveal the presence of small amounts of protein and blood in the urine (named proteinuria and hematuria, respectively), and with a microscope red blood cells and casts of the renal tubules may be seen also. If a patient with these findings is admitted to a renal department for further investigations it is likely that the doctor with a fine syringe will take out a small sample of the kidney tissue, a so-called kidney biopsy. A microscopic analysis of the kidney tissue most often, but not always, will reveal deposits of immunoglobulins and/or complement factors in the glomeruli, the minute filters of the kidney. In spite of these laboratory abnormalities the “patient” may remain healthy for the rest of his life.  

Glomerulonephritis may also appear acutely, often in association with an upper respiratory infection, but even spontaneously. Acute glomerulonephritis has usually a benign course, even in cases where the renal function is seriously affected in the acute stage, as the function recovers completely in most patients. 

But in some patients glomerulonephritis may be associated with the nephrotic syndrome, a high blood pressure and a decreased renal function. If these complications do not occur in association with an acute onset as described above, but rather appear gradually and insidiously, the disease will most often, sooner or later, proceed to end-stage renal failure. 

This is the greatest challenge for researchers in nephrology to-day, to understand why, once renal function has worsened, most cases of glomerulonephritis and other diseases of the kidney tissue progress to end-stage renal failure, irrespective of any treatment.

In the following I shall present a hypothesis, that explains the cause of progressive renal failure in many patients, a hypothesis that is based on solid scientific evidence, but is ignored or met by disbelief by most nephrologists.

The aim of the website is not only to inform colleagues, but also  patients and their relatives. Therefore I have tried to present the text in a way so that it should become understood by a layman. Certain scientific terms are explained on a separate file. These words are marked as hyperlinks - just click on it and use the back button to get back to the text. Here I have also given references to the relevant scientific literature. If you are unfamiliar with the way scientists present or search information, but are interested in deepening your knowledge, go to a university library with the references and ask the librarian for help.

What is the Cause of Glomerulonephritis? 

According to current concepts glomerulonephritis is an immunologic disease. Immune complex formation, the reaction between antibody and antigen, is said to occur in the glomeruli, the microscopic globular capillary filters of the kidney. When immune complexes are formed, various enzymes in the blood and on the surface of the cells, the so-called complement factors, are activated by the reaction, and the complement factors together with other chemical processes that are initiated by them, allegedly destroy the glomerular filtering apparatus and sooner or later the whole kidney.

In a particular type of glomerulonephritis called minimal change nephropathy it is not the formation of  immune complexes that is considered detrimental, but the white blood cells´ production of lymphokines. One of their effects is that they increase the permeability of the glomerular basement membrane. 

The above is a very simple presentation of the current view. In the following I shall give some more detailed explanations and arguments for the concept. Authoritative and comprehensive reviews can be found elsewhere (Dixon 1968, Wilson & Dixon 1981,  Cameron 1982, Couser 1993,  Couser 1998, Couser 1999). However, to follow my arguments for the new toxic-allergic hypothesis it is not necessary to understand all details of the immunological concept. 

As I shall demonstrate in the following, there are numerous experimental and clinical observations that are in serious conflict with the classical concept. The aim of this website is to question this concept and to present a new theory about the causation of glomerulonephritis, in particular to explain why the disease in some patients proceeds to renal failure and how it may be possible to stop and even reverse this process. The theory and the numerous studies that support it, have been presented in medical journals since many years. By unknown reasons the issue has gained little interest among nephrologists and little is mentioned about the subject in the textbooks.

In the present review I have concentrated on the association between hydrocarbon exposure and glomerulonephritis because this is the area that has been studied most thoroughly and this is also the most widespread type of toxic exposure. Among other chemicals that have been associated with glomerulonephritis are silicon, mercury, lithium and gold. Many drugs are known to be able to induce glomerulonephritis also; the most important ones are a type of pain-killers called non-steroidal-antiinflammatory-drugs, or NSAID, but also lithium and certain antibiotics. In the following I shall discuss the importance of silicon compounds and NSAID. Hopefully I shall be able to update the website later on with more information about other types of toxic exposure.

Arguments and Counter-Arguments for the Classical Concept

In the following I shall present the arguments for the classical concept and after each argument my counter-argument. After that I shall tell you about the new toxic-allergic hypothesis and the scientific evidence for that idea and also explain why the clinical and experimental findings fit much better with the toxic-allergic hypothesis than with the classical concept.


Although I have tried to explain the many arguments for and against the classical concept in a popular way they may appear rather complicated if you are unfamiliar with biological science. Therefore, if you are not a doctor or a researcher and if you find the arguments too complicated I will suggest that you precede directly to the toxic-allergic hypothesis. For the experienced researcher more comprehensive reviews of the arguments can be found elsewhere (Ravnskov 1985, Ravnskov 1989, Ravnskov 1998, Ravnskov 1999, Ravnskov 2000a, Ravnskov 2000b).

This website is based on the medical literature. Click on the names of the authors in the text to get the references. In a few of the more recent papers there is a link to the abstract of the article also. Reprints of the most recent of my own papers are still available.



Argument for the Classical Concept: 

The Postinfectious Occurrence

As mentioned above, glomerulonephritis often starts 1-3 weeks after an infectious disease  at a time where the body´s immune system is working hardest to combat the infection. The best studied variant is acute poststreptococcal glomerulonephritis, a particular type of glomerulonephritis that appears after an infection of the throat or the skin with certain strains of streptococci (a type of bacteria), the so-called nephritogenic strains. The start of a kidney disease shortly after the start of an infection strongly suggests that the infection, or the immune response that it has elicited, is an important causal factor.  


The close association between an infection and the onset of the disease is a good argument for the idea that the immune system is involved in some way, but it does not prove that the infection or the immunological reactions by themselves is the very cause. The large majority of infectious diseases are not associated with glomerulonephritis, and many cases of glomerulonephritis are not initiated by an infectious disease indicating that an infectious process alone is insufficient and not even necessary to produce the disease. Evidently, there must be contributing factors, either hereditary, or environmental, or both.

A strong case for a participating role of hydrocarbon exposure in poststreptococcal glomerulonephritis is the following observation.  Fifteen patients with poststreptococcal glomerulonephritis and fifteen patients who had had an infection with a nephritogenic streptococcal strain without developing glomerulonephritis were asked about possible exposure to organic solvents, fuels, glues or other hydrocarbons timely associated with the onset of the disease (Ravnskov 1978). Ten of the patients with glomerulonephritis had been exposed during the period between the streptococcal infection and the acute onset of the nephritis, whereas none of the control individuals reported exposure timely associated with their infection. In some patients the exposure was heavy, but short and confined to the mentioned period only; others had been exposed less heavily, but during long periods before the streptococcal infection. All exposed patients were ten years or older, five of them were adults, whereas four of the five unexposed patients were preschool children attending a daytime nursery and the interview of these children was performed six months to three years after recovery from the acute glomerulonephritis. Exposure may thus have occurred without the parents knowing or it may have been forgotten by them.

Another interesting observation from this study was the result of a follow-up study. Four of the patients had been exposured also after the acute onset of the disease, three of them had renal failure. The other eleven had not been exposed, nine of them had normal renal function, two had an insignificant lowering.

The logical explanation from this study is that a streptococcal infection, even with strains that are especially known to produce glomerulonephritis, does not harm the kidneys unless the patient is exposed at the same time for nephrotoxic chemicals. Either the chemicals make the kidneys susceptible to immunological harassment, or the chemicals enhance the renal damage by attacking another part of the kidneys, the tubules, and the combined effects of the immunological reactions and the toxic damage may produce the serious kidney disease. The study also points to the influence of continued exposure on renal function.   

In this connection it is worth mentioning that epidemics of acute poststreptococcal glomerulonephritis have been described from oil-producing areas such as Trinidad and Macaraibo in Venezuela (Poon-King et al 1967, Rodriques-Iturbe et al 1976) and here the disease often progressed to renal failure, whereas acute poststreptococcal glomerulonephritis usually is a benign disease, at least in children. Also, in most countries glomerulonephritis has become a rare disease, but not in Kuwait, a small country where a large proportion of the population is engaged in the oil industry (Seligson et al 1985).

Argument for the Classical Concept:

The Immunofluorescence Microscopic Findings

In most patients with glomerulonephritis a microscopic investigation of the renal tissue using immunofluorescence microscopy shows deposits of antibodies and complement factors in the glomeruli. The presence of both antibodies and complement in the glomeruli strongly suggests that a formation of immune complexes has taken place with unfortunate consequences for the glomerular filters. Plasma proteins, that normally are unable to pass the glomerular basement membrane because of their size, now leak to the urine and eventually, renal function goes down.


Immune complexes in the glomeruli may have been formed outside the kidneys and thereafter trapped in the glomeruli. Even if they have been formed in the glomeruli, their formation may not necessarily damage the kidneys, as has been demonstrated in numerous animal experiments (see later). 

That the mere presence of immune complexes in the glomeruli may be unimportant for glomerular function is obvious from numerous clinical observations. For instance, patients with cancer, various internal diseases, and even healthy individuals, often have immune complexes located to the glomeruli without having any signs or symptoms of renal disease (Sutherland et al 1974, Pascal et al 1976, Larsen 1979, Helin et al 1980, Hoorntje et al 1980, Waldherr et al 1989, Rosenberg et al 1990, Suganuma et al 1994). Glomerular immune complexes are also found in normally functioning kidney grafts (Antignac et al 1988). Very often such findings have been classified as glomerulonephritis, but to call a deposition of immune complexes for a kidney disease when the kidneys are functioning normally and the urine is normal, is misuse of medical terminology.

There are disturbing observations from the animal kingdom also. Great amounts of glomerular immune deposits have been found in a large proportion of sheep, steers, guinea pigs, horses, mice and rabbits with normal urine and normal kidney function (Lerner & Dixon 1966, Lerner et al. 1968, Steblay & Rudofsky 1971, Banks & Henson 1972, Markham et al 1973, Neale et al 1984). Again, these findings have been classified as glomerulonephritis, but if the presence of immune complexes alone is a disease you could equally well call dirty nails for a disease.


Also, if a glomerular formation of immune complexes were the direct cause of glomerulonephritis, the amount of immune complexes should correlate with the renal function and the course of the disease. Patients with many deposits should more often have renal failure than patients with little or no deposits, and many deposits should also mean that the disease has a more serious outcome, this is pure logic. But there is no association whatsoever between the amount of glomerular deposits or the degree of glomerular damage, and the renal function and the outcome; this has been documented in numerous studies (Riemenschneider et al 1980, Ramzy et al 1981, Wehrmann et al 1989, Lee & Koh 1993. More references can be found in these papers). In fact, about a fifth of all patients with serious glomerulonephritis have no glomerular deposits at all.


Another fact, that has gained little interest among nephrologists is that many patients with glomerulonephritis have deposits of immunoglobulins but not of complement. If the disease were the result of immune complex formation in the glomeruli, both immunoglobulins and complement should be present because complement is always participating in the formation of an immune complex.


These observations are difficult to understand if the classical hypothesis were true, but as seen in the following they are easily explained by the toxic-allergic hypothesis, which says that the deposits are secondary to the real cause, the toxic-allergic damage of the tubulointerstitial tissue and the glomerular basement membrane. Any macromolecule may be caught in the glomerular filters, in particular if the glomerulus is damaged by toxic or allergic reactions. In the following sections I shall tell about the many studies that in various ways have shown that the depostion of immune components in the glomeruli is a secondary phenomenon secondary to the toxic-allergic damage of the kidneys.


Argument for the Classical Concept:

Human Anti-Glomerular-Basement Nephritis

In a special type of glomerulonephritis, the so-called anti-glomerular-basement-membrane (anti-GBM) nephritis, antibodies against the glomerular basement membranes (shortened GBM) are found in the blood of the patients during active periods of the disease. By immunofluorescence microscopy such antibodies are also found lying closely to the GBM as a linear band. These findings strongly suggest that the attack of the antibodies on the GBM is the cause of the disease. 


Anti-GBM antibodies are found now and then in the blood and even in the kidneys of healthy individuals without any clinical signs of glomerulonephritis (Zimmerman et al 1979, Bailey et al 1981, Bernard et al 1986). They have also been found in the blood of transplanted patients whose own kidneys allegedly have been destroyed by anti GBM-nephritis (Couser et al 1973). But although the same antibodies still were present in the blood and even located in the transplanted kidney, the latter was completely normal. As these anti-GBM antibodies were blamed for having destroyed the patient´s own kidneys, but did not harm the transplanted kidney, an attack of such antibodies alone cannot explain the serious disease. 

An important co-factor must be necessary, a factor that was present when the patient became sick, but was absent after the transplantation. The factor may for instance have been an exposure to nephrotoxic chemicals. In accordance, a large numer of case stories have been published where anti-GBM nephritis had been preceded by heavy exposure to various kinds of toxic chemicals closely time-asociated with the acute onset of the disease.

(In fact, most of the published case histories of glomerulonephritis associated with toxic exposure concern this very rare type of glomerulonephritis. This fact has of course been used by those who are skeptic to the association in general. How come that this rare variant predominates among the case stories? Why haven't more case histories about exposed patients with the common variants of glomerulonephritis been published? The reason is simple. Anti-GBM nephritis is very often followed by lung bleedings, the so-called Goodpasture´s syndrome. A patient with glomerulonephritis and lung bleedings automatically stimulates the doctor to ask for toxic airborn exposure. Unfortunately, few doctors asks patients with glomerulonephritis alone.)

Argument for the Classical Concept:

Immunological Disturbances 

Many immunologic functions are disturbed in glomerulonephritis. The number of a special type of white blood cells, the T-cells may be lowered and their function may be imperfect. Also other kinds of white blood cells do a bad work, and the production of antibodies is decreased or abnormal (Ravnskov 1985). For instance, antibodies may be produced that are directed against the patients own tissue, in particular against components of the renal cells, a condition called auto-immunity. These findings clearly indicate that a disturbance of the immune system is an important factor in the causation of the disease.



Disturbances of the immune system are in accord with both hypotheses because almost all chemicals that have been associated with glomerulonephritis, inhibit or derange the immune system (Ravnskov 1985). Again, immunological processes may participate in the creation of glomerulonephritis, but they are not necessarily the very cause.

Argument for the Classical Concept:

Acute and Chronic Serum Sickness

Numerous experimental models have demonstrated that glomerulonephritis can be produced in animals by immunological methods. In one of the first models, acute or one-shot serum sickness, rabbits were injected with bovine serum albumin. A few days´ later, when the rabbit´s immune system has started to produce antibodies against the injected antigen, typical acute glomerulonephritis with proteinuria and haematuria develops, a strong argument that an acute infection may induce glomerulonephritis
(Germuth 1953). The injected antigen, the bovine serum albumin molecules, are caught in the glomerular filters and when the antigens are attacked by the rabbit´s anti-bovine-albumin antibodies the resulting formation of immune complexes injures the glomeruli. If several injections of bovine albumin are given (chronic serum sickness), the rabbit eventually may develop serious glomerulonephritis with impaired renal function (Dixon et al 1961).




No doubt, the acute serum sickness model is a good simulation of human, acute glomerulonephritis. However, no serious or persistent renal damage is produced after a single injection of foreign serum albumin. Just as in most human types of acute glomerulonephritis, the only symptoms are transient proteinuria and haematuria at most and the renal function remains normal. In numerous similar animal models the researchers have claimed that they have produced glomerulonephritis. The only thing that has been produced however, is a formation or deposition of immune complexes in the glomeruli followed by mild and transient urinary abnormalities, or less than that. 


Let me stress again: a deposition of immune complexes in the kidneys (or elsewhere) without any other symptoms is not a disease. In all mammals, including human beings, there is normally a steady production of immune complexes in the body. This is part of the normal defense against foreign molecules and microorganisms. Immune complexes are disposed by various ways as garbage and may be found in many parts of the body, including the glomeruli, in all healthy individuals. Glomerulonephritis is a clinical problem, or a serious disease, only if it is followed by kidney failure or the nephrotic syndrome. (You may add also: a high blood pressure, but a high blood pressure rarely appears in the absence of renal failure or the nephrotic syndrome).

The chronic serum sickness model seems to be a good argument for the classical hypothesis. However, to induce serious glomerulonephritis it is necessary to inject large amounts of the antigen several times during several weeks. In most human infections bacterial or viral antigen rarely appear during longer periods in the blood circulation because it is quickly eliminated by our immune system. But there are exceptions. Serious glomerulonephritis may be seen associated with chronic infections, such as hepatitis, malaria, schistosomiasis, and an infected atrioventricular shunt. In these diseases the steady discharge of microbial antigens into the blood may be a contributing and perhaps even the main cause of glomerulonephritis. In accordance, glomerulonephritis secondary to chronic bacterial infections are most often cured by antibiotics directed against the infectious agent, whereas antibiotics have no effect on other types of glomerulonephritis, not even on glomerulonephritis secondary to an acute infection.



Argument for the Classical Concept:

The Active Heymann Nephritis Model 
(Autologous Immune Complex Nephritis) 

If a rat is immunized with certain extracts of its own kidney a severe glomerulonephritis develops. Immune complex formation inside the glomeruli leads to severe proteinuria and eventually renal failure (Heymann et al 1959, Heymann et al 1962). This is a strong argument that an immunological reaction inside the glomeruli is the cause of glomerulonephritis.


To develop serious glomerulonephritis in this animal model it is necessary to mix the injected tissue extract with Freund´s adjuvant. This substance is a mixture of mycobacteria emulsified with mannide monooleate in hydrocarbon oils and has been used in countless animal experiments to enhance the immunological reactions. It is a striking fact, however, that in experimental glomerulonephritis no serious kidney damage is produced without the use of Freund´s adjuvant. In the section Experimental Anti-GBM Nephritis I shall show that the reason why Freund's adjuvant produces glomerulonephritis is not an enhancement of the immunological reactions but a toxic effect on the kidneys.

What also has been ignored is that an injection of Freund's adjuvant alone produces typical glomerulonephritis with deposition of immune complexes in the glomeruli (Miettinen 1982, Ravnskov 1989). This means that experimental glomerulonephritis produced with the aid of Freund's adjuvant cannot be used as support of the classical concept, because who knows if it is the immunization, or the injection of the nephrotoxic substance, Freund's adjuvant. or a combination of these measures, that are producing the disease?

The similarity with acute poststreptococcal glomerulonephritis is striking: a streptococcal infection without exposure to toxic chemicals may be harmless (Ravnskov 1978) just as an immunization of the rat without the use of Freund´s adjuvant is harmless. The similarity goes further, because just as an injection of Freund´s adjuvant can produce glomerulonephritis by itself, hydrocarbon exposure alone can do it also. This has most convincingly been demonstrated by the animal experiments.

However, even if Freund´s adjuvant alone can produce glomerulonephritis, the disease becomes more serious if the injection is combined with an immunization. Obviously the immune system is participating in the production of glomerulonephritis, but it is not causing it by itself.

Argument for the Classical Concept:

The Passive Heymann Nephritis Model 

Antibodies against the rat kidney can be produced in rabbits by immunization of the rabbit with injections of a rat kidney extract into the rabbit. If these rabbit anti-rat kidney antibodies are injected into a rat they will immediately attack the rat´s glomeruli After a number of injections the rat develops glomerulonephritis with renal failure, a strong argument for the idea that an immunological reaction in the glomeruli alone can produce serious glomerulonephritis (Barabas & Lanigan 1974, Feenstra et al 1975).




This type of experimental glomerulonephritis develops in two steps. In the first stage, the heterologous phase, the rabbit anti-rat-kidney antibodies (the foreign, or heterologous antibodies) attack the rat´s glomeruli. At this stage a granular deposition of complement factors and rabbit antibodies are seen in the glomeruli. But this reaction does not result in any kidney damage and no proteinuria is seen. The second stage, the autologous phase, begins a few days later. As the injected anti-rat kidney antibodies come from another species, they are recognized as “foreign” by the rat´s immune system. Consequently, the rat starts to produce antibodies against the foreign antibodies. At this time, both rabbit and rat antibodies are seen in the glomeruli.

A reaction between antigen and antibody is the starting signal for inflammation. Normally, an inflammatory reaction protects us against foreign intruders such as bacteria, virus and other foreign substances. In the autologous phase the antibodies attack the foreign rabbit antibodies, that are located to the glomerular basement membrane. Therefore, the inflammation may destruct not only the intruders, but also the basement membrane.


The reason why the first reaction, the heterologous phase, does not damage the kidney but the second does, may partly be that the second involves many more antibodies, and partly because the second reaction happens to a membrane that is already damaged a little, just as a flu is harmless in healthy youngsters but can kill the old and the weak. By this way the GBM of the rat is damaged both from the immune complex formation between the injected, foreign anti-kidney antibodies and certain parts of the GBM, but also from the reactions between the rat’s own antibodies, the autologous antibodies, that are attacking the injected rabbit antibodies and thus indirectly also the GBM.


That it is the second reaction, the autologous phase that is crucial has been shown in an elegant variant of the experiment. Here, the rats were made tolerant to rabbit immunoglobulin by desensibilization before the experiment. As a result no renal damage was seen; the autologous phase had been eliminated. (Zanetti & Druet 1980).

Even if it were correct that glomerulonephritis in the passive Heymann nephritis is produced by immunological means only, the mechanism is of course highly unlikely in human beings, because no one would ever have injected anti-human antibodies. To assume that the passive Heymann nephritis is a model of human glomerulonephritis should demand that the patient produces antibodies against his own GBM, but also, at the same time, produces antibodies against his own immunoglobulins, a hitherto unknown combination of events in glomerulonephritis.

It is possible to demonstrate in another way that the rat's own anti-kidney antibodies alone are unable to hurt the kidney. If anti-kidney antibodies (extracted from a rat with active Heymann nephritis) are injected into a healthy rat, these antibodies immediately locate to the glomeruli together with complement, indicating that an antigen-antibody reaction has taken place in the glomeruli.
But no kidney damage is seen, just as no damage was seen during the heterologous phase. The urine is normal as is the renal function, clearly indicating that a direct immunological attack against the glomeruli is harmless - a crucial factor is missing (Sugisaki et al 1973, Fleuren et al 1980, Abrass et al 1983, Ravnskov 1998).

  Argument for the Classical Concept:

Experimental Anti-GBM Nephritis

An immunization of experimental animals with extracts of the glomerular basement membrane (GBM) mixed with Freund´s adjuvant produces serious glomerulonephritis. In this type of glomerulonephritis the antibodies and the complement factors are seen by immunofluorescence microscopy as a fine, linear band along the GBM (Steblay 1962, Unanue & Dixon 1967). This finding clearly demonstrates that the anti-GBM antibodies are attacking the GBM. The reaction between antibodies and antigen is followed by immune complex formation and inflammation, strongly suggesting that the kidney damage is caused by this reaction.


Again, serious glomerulonephritis is produced only if Freund´s adjuvant is used; an immunization alone does produce a linear deposition of antibodies and complement but it does not produce proteinuria or renal failure. As mentioned previously Freund´s adjuvant produces glomerulonephritis alone (Miettinen 1982). Therefore, the mentioned experiment is no proof that immunological reactions alone are causing glomerulonephritis. Most probably, Freund´s adjuvant sensitises the kidneys for immunological assaults. This is suggestive from the following experiment.

At first, rats were injected with Freund´s adjuvant alone. After 2-3 weeks rabbit anti-rat-GBM antibodies were injected into these rats in 1/20-1/15 of the amount required to produce glomerulonephritis in the Masugi model (see below). Control rats, that had not been pre-treated with Freund´s adjuvant, were injected with antibodies too. The pre-treated rats developed glomerulonephritis in two steps, just as in the Masugi nephritis (see below) and in the passive Heymann model, whereas no damage was seen in the rats that were not pre-treated with Freund´s adjuvant (Watson et al 1965)

Evidently, Freund´s adjuvant is an important co-factor in this experiment. The difference was not due to a stronger immunization of the rats that had been injected with Freund´s adjuvant because the amount of antibodies extracted from their kidneys was not larger than the amount of antibodies extracted from the kidneys of the rats in the control group. Again, the most reasonable conclusion is that Freund´s adjuvant predisposes the kidneys to immunological harassment (Ravnskov 1989).

  Argument for the Classical Concept:

Passive Anti-GBM Nephritis

(Masugi Nephritis)

The experimental induction of anti-GBM nephritis is not dependent on Freund´s adjuvant because it is also seen after injection of foreign anti-GBM antibodies alone (foreign, or heterologous: from another animal species), just as passive Heymann nephritis can be produced by injecting foreign anti-kidney antibodies (Unanue & Dixon 1962).


Again, just as in passive Heymann nephritis, this type of glomerulonephritis can be separated into two steps. The first step, the heterologous phase, is followed by trace proteinuria at most and no renal damage is seen. At this stage only rabbit antibodies can be seen in the glomeruli. A few days later a serious glomerulonephritis may develop. At this stage, the autologous phase, the rabbits own antibodies can be seen in the glomeruli also, obviously attacking the foreign antibodies that are located along the glomerular basement membrane. Thus, two immunological process are taking place in the glomeruli: immune complex formation between the foreign (heterologous) anti-GBM antibodies and the GBM, which is harmless; and immune complex formation between the rat´s own (autologous) antibodies and the foreign antibody. And again, the second reaction can be abolished if the animals are made tolerant to the injected, foreign antibodies before the experiment (Hammer & Dixon 1963).


Once again it has been demonstrated that a direct attack on the kidney by one´s own antibodies does not produce glomerulonephritis. A crucial factor is missing.

The Toxic-Allergic Hypothesis

According to this hypothesis the first and causal event in glomerulonephritis is not an infection or an immunological reaction in the glomeruli, but an exposure to nephrotoxic  chemicals, either by inhalation, by skin contact or by ingestion. The precise mechanism by which the chemicals produce renal damage is still uncertain, but the primary targets are most probably the tubular cells and/or the cells of the immune system. The deposition of immunoglobulins and complement in the glomeruli is a secondary phenomenon with little importance for glomerular function or structure (Ravnskov 1985, Ravnskov 1988, Ravnskov 1989, Ravnskov 1998, Ravnskov 1999).


The tubular cells have many important functions in the body. They regulate the balance of salt and water in the blood, they maintain the body’s acid/base balance, they prevent important substances from being lost in the urine after having been filtered out through the glomerular filters, and many toxic substances are taken up from the blood and secreted into the urine by these cells. The latter function is probably crucial for the start of glomerulonephritis because if too much of a toxic chemical has come into the blood, its accumulation in the tubular cell may damage and even kill the cell. The damage of the tubular cells may lead to inflammation and scarring of the interstitium. These changes lead to shrinkage of the renal tissue, the tubules become narrow,the urine flow is retarded, and gradually renal function goes down.


Another possibility is that white blood cells react with the chemical and starts an allergic reaction. Also this reaction may lead to inflammation in the interstitium. White blood cells may become stimulated by the allergic reaction to produce lymfokines, small molecules that may damage the epithelial cells of the GBM resulting in an increased permeability to plasma proteins and facilitate the deposition of macromolecules, for instance antibodies and complement factors, in the glomeruli. Such damage may even be produced directly by the toxic chemicals. Most probably all mechanisms operate together. 




If the toxic-allergic hypothesis is correct the following predictions should be satisfied:

1. Workers exposed to nephrotoxic chemicals should more often have symptoms of glomerulonephritis than other people. 
2. Patients with glomerulonephritis should have been exposed more often to nephrotoxic chemicals than other people.

3. Patients with glomerulonephritis and a decreased renal function should have been exposed more often than patients with glomerulonephritis and normal function.

4. Discontinuation of the exposure should improve renal function and the course of the disease.

5. The renal function and the course should be closer associated with the tubulointerstitial changes than with the glomerular changes.

6. Exposure of laboratory animals to nephrotoxic chemicals should produce glomerulonephritis with renal failure.


In the following I shall show that all of these predictions have been fulfilled.



The Cross-Sectional Studies

In a cross-sectional study signs of the disease is sought in individuals exposed for the suspected causal factor and in non-exposed individuals of the same age and sex. If the factor is causal, the disease should be seen more often in the exposed than in the unexposed individuals.

A large number of cross-sectional studies of workers with occupational exposure to hydrocarbons have been published. These studies included refinery workers, dry-cleaners, floor layers , printers, road workers, paint sprayers and a variety of other workers exposed to organic solvents or fuels. In at least fourteen studies these workers had more often urinary findings typical for early glomerulonephritis than had the unexposed control individuals (Askergren et al 1981a, Askergren et al 1981b, Viau et al 1987, Hotz et al 1989, Hotz et al 1990a, Hotz et al 1990b, Hashimoto et al 1991, Hotz et al 1991, Mutti et al 1992, Yaqoob et al 1993a, Hotz et al 1993, Stevenson et al 1995, Huber et al 1998, Pai et al 1998). In three of the studies the workers even had a decreased renal function more often (Hotz et al 1990b, Yaqoob et al 1993a, Pai et al 1998).

Thus, without doubt, exposure to hydrocarbons does induce renal damage typical of glomerulonephritis. It should be stressed, however, that it was seen only in a few of the exposed workers, and that these workers were healthy by all standards and had no other symptoms or signs of disease. The blood and urinary findings were mild in most workers and may have remained undetected if the laboratory tests had not been performed. What these studies have shown is that hydrocarbon exposure affects the kidneys of a few individuals but to a small degree only. 


As hydrocarbon exposure is prevalent in most societies and as clinically significant glomerulonephritis is a rare disease,  a further factor, probably a hereditary predisposition, is necessary. If this unknown factor is present, however, hydrocarbon exposure may result in serious glomerulonephritis. This has been shown most convincingly by the case-control studies.

 Case-Control Studies

In a case-control study a number of patients with the disease in question (here glomerulonephritis) are asked whether they have been exposed to the risk factor (here toxic chemicals) more often than a similar number of control individuals without the disease and of the same age and sex. 

To-day, nineteen case-control studies of hydrocarbon exposure have been performed (Zimmerman et al 1975, Lagrue et al 1977, Ravnskov 1978, Ravnskov et al 1979, Finn et al 1980, van der Laan 1980, Franchini et al 1982, Ravnskov et al 1983, Bell et al 1985, Harrison et al 1986, Harrington et al 1989, Steenland et al 1990, Sesso et al 1990, Yaqoob et al 1992, Porro et al 1992, Stengel et al 1995, Nuyts et al 1995, Asal et al 1996, Huber et al 2000). In the large majority of these studies patients with glomerulonephritis had been exposed more often to hydrocarbons (mainly fuels, glues, paints, solvents and motor exhausts) than had the control individuals (Ravnskov 2000a). In a few studies the exposure difference was trivial, but two of them included only patients with early stages of the disease (van der Laan 1980, Harrington et al 1989), and two studies included one group of patients with normal or mildly reduced renal function and little exposure, and one group of patients with chronic renal failure and much exposure (Stengel et al 1995, Asal et al 1996). In four studies, that included patients with end-stage renal failure only, 60-80 per cent of the patients had been exposed (Zimmerman et al 1975, Finn et al 1980, Steenland et al 1990, Yaqoob et al 1992).

Thus, taking all studies together, a strong, inverse association was found between degree of exposure and renal function, and a direct association between degree of exposure and stage of the disease indicating that the most important effect of the exposure is a worsening of renal function
(Ravnskov 2000a).

Patients with glomerulonephritis and normal or only slightly depressed renal function may not necessarily have been exposed more than most of us who live in a western society, whereas patients with glomerulonephritis and more advanced renal failure have been exposed more often, in particular patients with end-stage renal failure. 

However, even if two studies that included acute glomerulonephritis did not find an increased exposure to hydrocarbons we cannot exclude that such exposure also may start glomerulonephritis because some individuals may be more sensitive to hydrocarbon exposure than others. If so, a short, but intensive exposure may suffice to start the disease, but as most people experience such exposure once or perhaps several times in their life, the total exposure of patients with early glomerulonephritis may not necessarily exceed the exposure of most people. To know if a short exposure may start the disease it is necessary to study the timely association between the exposure and the onset of the disease. One of the case-control studies had addressed this question. As mentioned in the section named The postinfectious occurrence the acute onset of the disease was closely time-associated with exposure to organic solvents in ten of the fifteen patients.

The Cohort Studies

In a cohort study a number of healthy individuals (the cohort) are followed during a period of time. Either all individuals are exposed and the frequency of the disease is compared with the frequency in the general population, or the cohort could represent a random sample of the population. In the latter case the suspected disease factor is asked for among those who have acquired the disease at follow-up and those who have not. However, the rarity of glomerulonephritis demands that a conventional cohort study should include at least 22000 exposed individuals to be able to demonstrate a statistically significant increase of the disease (Churchill et al 1983).

Instead of recording new cases among healthy individuals, renal function and degree of exposure can be recorded in patients with established disease.

In one such study fifty patients with glomerulonephritis were followed for 7-8 years. At follow-up nine of 26 patients, who were heavily exposed to hydrocarbons, had end-stage renal failure, but this was not seen in any of 24 moderately or rarely exposed patients (
Bell et al 1985).

In a more recent study 68 patients with glomerulonephritis were followed for five years. At follow-up 21 of 29 patients with progressive renal failure had been exposed to hydrocarbons, whereas exposure was noted only in five of 39 patients with stable renal function. Furthermore, it was noted that when the exposure was eliminated in these five patients, their renal function improved (Yaqoob et al 1993b).

Together with the case-control studies these two studies show that the most important effect of hydrocarbon exposure is a worsening of renal function. The logical conclusion is of course that all patients with glomerulonephritis and renal failure should be questioned in depth about possible toxic exposure and if such exposure is present, attempts should be performed to eliminate the exposure. As I shall demonstrate soon, an attempt to do that in a few patients was succesful.

Human Experiments

Evidently we cannot test the hypothesis by exposing human beings for hydrocarbons. But an unintentional "experiment" was performed some years ago i Spain. Adulterated cooking oil that contained aniline, oleoanilides and azobenzene, was sold for human consumption. 842 patients were admitted to hospital with severe symptoms of intoxication. Four of them had glomerulonephritis with renal failure. As this number is at least 150 times higher than the normal incidence of end-stage glomerulonephritis during a whole year there can be no doubt that the glomerulonephritis was caused by the chemicals (Navas-Palacios et al 1984).

Instead of exposing healthy individuals we can ask exposed patients to discontinue the exposure and see what happens. Only one such study has been published. In that study fifteen of thirty exposed patients discontinued the exposure. Initially the renal function in these patients was lower and the blood pressure higher compared with the fifteen patients who did not succeed in discontinuing the exposure. In spite of that the course of the disease was more favourable (Ravnskov 1986), just as in the follow-up studies by Bell et al 1985 and  Yaqoob et al 1993b mentioned in the section The Cohort Studies, and with the findings in the Case-Control Studies. 

Evidently, the most important influence of hydrocarbon exposure in glomerulonephritis is its effect on renal function. Exposure is prevalent in patients with renal failure and renal function may improve when the exposure is discontinued.  


Treatment with certain analgesics, named non-steroidal-antiinflammatory drugs, or NSAID, may in rare circumstances induce a renal disease. In some patients the disease develops in the course of a few days with a clinical picture similar to so-called acute tubular, acute tubulo-interstitial, or acute interstital nephritis with allergic symptoms, such as rash, fever, eosinophilia and acute renal failure. In most patients the disease develops more insidiously with heavy proteinuria, a slowly worsening of the kidney function and a rising blood pressure. A microscopic investigation of a kidney biopsy specimen may in some patients reveal almost normal glomeruli as in so-called minimal change nephropathy. Other patients may have more or less pronounced depositions of immune components in the glomeruli in a pattern similar to membranous glomerulonephritis. In a few patients other glomerulonephritis subgroups are seen. Almost all patients have tubular, interstitial or tubulointerstitial changes.

As mentioned, NSAID nephropathy may often be followed by a reduced kidney function and the disease may progress to end-stage renal failure unless NSAID treatment is discontinued. If so, almost all patients recover, most of them with normal renal function.

The various clinical and laboratory appearances of NSAID nephropathy has led to the idea that the mechanisms behind them also vary. However, in an analysis of 97 case histories published in medical journals a pattern emerged that was suggestive of a common allergic mechanism
(Ravnskov 1999). As the findings may have importance for an understanding of the mechanisms behind glomerulonephritis in general I shall shortly recapitulate them.

Three main groups of nephritis were recorded, 19 patients with acute tubular, interstitial or tubulointerstitial nephritis (to be short grouped together as "acute nephritis" in the following), 38 patients with minimal change nephropathy and 19 patients with membranous glomerulonephritis. A few other types were seen also, but they were too few to allow a systematic analysis.

It appeared that signs and symptoms of allergy were found in all the three main variants, most often in patients with acute NSAID nephropathy, least often in patients with membranous glomerulonephritis.

It was also obvious that the NSAID treatment time before the start of the disease differed substantially. Patients with acute nephritis had taken NSAID for on average 1.7 months, patients with minimal change nephropathy for on average 8.2 months, and patients with membranous glomerulonephritis for on average 39 months.

As is typical for most cases of acute nephritis due to other causes proteinuria was least pronounced in the acute NSAID nephritis, whereas heavy proteinuria was prevalent in the two other varieties, most pronounced in patients with minimal change nephropathy. In fact, the degree of proteinuria was independent on the amount of immune deposits in the glomeruli,  in accordance with what I mentioned in the section Immunofluorescence Microscopy. 

A typical finding on a kidney biopsy from patients with glomerulonephritis and heavy proteinuria is swelling and fusion of the podocytes, the glomerular epithelial cells. In accordance, such changes were found in all of the patients with minimal change nephropathy and membranous glomerulonephritis, but patients with acute NSAID nephritis had podocyte fusion also, although to a lesser degree, in support of a common mechanism behind all three types of NSAID nephropathy. 

The general finding of podocyte swelling is suggestive of an allergic reaction involving activation of lymphocytes. It is well-known that activated lymphocytes may produce chemical substances, so-called lymphokines, that increase the permeability of the glomerular filters. Little attention has been raised to the fact that fusion of the podocytes is seen in most cases of acute nephritis due to other drugs also, although to a lesser degree than in glomerulonephritis, possibly because there is a time lag before the production of lymphokines is maximal
(Ravnskov 1999).

Most important was that the renal function in NSAID nephropathy was strongly associated with the tubulointerstitial changes and strongly inversely associated with the amount of immune deposits in the glomeruli. The logical interpretation of this finding is of course that the primary damage is located to the tubulointerstitial tissue and that the glomerular changes are secondary and without importance for renal function. If the reaction against the NSAID is violent, the course is more dramatic and renal failure is prevalent, but with a short course, few if any immune components are deposited in the glomerular filters. With a milder and more protracted cause, time will allow more macromolecules to be caught in the glomeruli.

A relevant question: In most patients with acute nephritis due to an allergic reaction to a drug the kidney disease appears abruptly and the course is rapid and violent. If NSAID nephropathy is the result of an allergic reaction also, why is the course generally much more slow and why are the typical allergic symptoms absent in many patients, in particular those with a protracted course of the disease? The explanation may be that NSAIDs inhibit a variety of immunologic reactions, the very effect that has made these drugs suitable for treatment of inflammatory diseases. Most probably the milder course in NSAID nephropathy compared with acute nephritis induced by other drugs is due to a delay of the immunologic reactions induced by the offending NSAID itself causing the immune system to work ineffectively and in slow motion.

In conclusion, it is suggested that the various kidney diseases seen after NSAID treatment are not separate entities, but varying results of a common mechanism, an allergic reaction to the drug. In case the allergic reaction is strong and the effects of the offending drug on the immune system are weak, the patient will present with acute tubular, interstitial or tubulointerstitial nephritis. In case the allergic reaction is moderate, time will allow the lymphocytes that participate in the allergic reaction to produce lymphokines with unfavourable effects on the podocytes leading to heavy proteinuria. In case the allergic reaction is weak or the effects of the offending NSAID on the immune system is strong, the course will be even more protracted and as a result immune complexes, present in the blood circulation now and then, even in healthy individuals, will be caught in the glomeruli. The immune deposits are not causing the disease, they are secondary to the glomerular damage that is produced by the allergic reactions in the body.

Are allergic mechanisms participating also in glomerulonephritis associated with exposure to toxic chemicals? This is suggestive from one of the animal experiments. By exposing mice to carbon tetrachloride the researchers induced a mesangial glomerulonephritis with deposition of IgG in the glomeruli. However, if the mice were irradiated before the exposure no glomerulonephritis was seen (Ogawa et al 1992 ). As the cells of the immunological system are particularly sensitive to irradiation this finding suggests that allergic reactions may be crucial, at least in glomerulonephritis induced by carbontetrachloride. Again you may ask, why is the course in most patients with glomerulonephritis much more protracted than in acute allergic, tubulointerrstitial nephritis? The same answer is valid. Almost all chemicals that have been associated with glomerulonephritis are toxic both to the kidneys' tubules and to the body's immune system (Ravnskov 1985).

Silicon nephropathy

To-day at least 60 case histories of glomerulonephritis associated with exposure to silicon have been published. Silicon is an element the salts of which, named silicates, are the main components in rocks and sand. Exposure to silicates is prevalent among miners, foundry and quarry workers, sandblasters, tile setters, glaziers, and workers in the production and handling of asbestos, mineral wool and fiber glass. The type of renal disease seen in such individuals is most often so-called focal, segmental glomerulonephritis, and a characteristic feature is the simultaneous presence of an auto-immune disease such as Wegener granulomatosis or systemic lupus erythematosus.

Case reports are weak evidence, because the association could occur by chance. However, there is also epidemiological evidence, that silicon or silicon salts may produce serious glomerulonephritis.

Cross-sectional studies of workers with occupational exposure to silicon compounds have shown that some of them may have urinary findings typical for early glomerulonephritis (Ng et al 1992, Ng et al 1993, Boujemaa et al 1994), even after a short exposure (Hotz et al 1995). After many years the exposure may result in serious kidney damage. In a cohort study of 2412 men who had worked on average eight years  in a South Dakota gold mine between 1940 and 1965 the incidence of end-stage renal failure in 1977 was significantly higher than in the general population; in particular end-stage renal failure due to glomerulonephritis (Calvert et al 1997). In a review of 583 reported cases of silicosis (a serious lung disease caused by chronic inhalation of silicates) in Michigan between 1985 and 1995 a reduction of renal function was found in about a third of them (Rosenman et al 2000).

Case control studies are also in support. In one such study of 272 patients with chronic renal failure and 272 people with normal renal function, 52 (19%) of the patients had been exposed to silicon-containing compounds but only 24 (8.8%) of  the control individuals. Among the various diagnostic groups 16% of 38 patients with glomerulonephritis, and 26% of 39 patients with diabetic nephropathy had been exposed (Nuyts et al 1995). In another case-control study fourteen of sixteen patients with glomerulonephritis and Wegener granulomatosis had been exposed to nephrotoxic chemicals, most of them to silica and silicon-containing compounds (Nuyts et al 1995).

As is the case with almost all other chemicals associated with glomerulonephritis, chemicals derived from silicon are known for having disturbing effects on the immune system, in particular it has been found that autoimmunity is a common finding, seen both in exposed workers, and in experimental animals (Tervaert et al 1998; Parks et al 1999)

Thus, although studies of silicon-associated glomerulonephritis are much fewer, these studies suggest that exposure to silicon may also lead to end-stage glomerulonephritis.

Diabetic Kidney Disease
(Diabetic Nephropathy)

In many countries diabetic nephropathy has become the most common cause of end-stage renal failure. It is a common belief that the complications to diabetes, including renal disease, is due to maltreatment of the diabetic condition. However, many studies have shown that this is only part of the truth, because many patients develop severe diabetic complications in spite of a meticulous control of the blood glucose level, and most diabetic patients survive for many years with a normal kidney function in spite of a badly controlled diabetes.

Other factors obviousoly contribute to the development of kidney disease in diabetic patients. One factor may be exposure to toxic chemicals because what has been said about glomerulonephritis in the previous sections seems to be valid for diabetic nephropathy also. This appears from two recent case-control studies.

In one of the studies 113 patients with juvenile diabetes for at least ten years were asked for hydrocarbon exposure since the diagnosis of diabetes had been settled. The exposure was minimal in a group of 45 patients without signs of kidney disease. In a group of 37 patients with microalbuminuria, the mildest form of diabetic kidney disease, and in a group of 31 patients with established nephropathy the exposure was significantly higher than in the first group, most pronounced in the group with overt kidney disease. Those with significant exposure had mainly been exposed to petroleum products, greasing and degreasing agents, paints and glues (Yaqoob et al 1994).

Another study included 39 patients with diabetic nephropathy and chronic renal failure. Compared with healthy control individuals the diabetic patients had  been more often exposed to a variety of chemicals, including lead (28% exposed against 9.9% of the control individuals), welding fumes (18% against 7%), silicon-containing compounds (26% against 8.8%), chromium (23% against 3.7%) and hydrocarbons (39% against 25.7%) (Nuyts et al 1995).


As seen from the preceding sections all six predictions have been fulfilled. In addition, almost all clinical and experimental observations are in better accordance with the toxic-allergic hypothesis than with the classical, immunological concept. 

The Predictions

The Evidence
1st prediction Workers exposed to nephrotoxic chemicals should more often have symptoms of glomerulonephritis than other people. In 14 cross-sectional studies of workers exposed to hydrocarbons and in four studies of workers exposed to silicon compounds, the exposed workers had more often symptoms of glomerulonephritis than had the unexposed control individuals. 
2nd prediction Patients with glomerulonephritis should have been exposed more often to nephrotoxic chemicals than other people. All case-control studies that included patients with chronic or end-stage renal failure found significantly more exposure in patients compared with control individuals of the same sex and age. A strong, inverse association was found between renal function and degree of exposure. 
3rd prediction Patients with glomerulonephritis and a decreased renal function should have been exposed more often than patients with glomerulonephritis and normal function.
4th prediction Discontinuation of the exposure should improve renal function and the course of the disease. In the four studies, that had addressed this question, renal function worsened mainly or exclusively in patients who continued their exposure to hydrocarbons
5th prediction The renal function and the course should be closer associated with the tubulointerstitial changes than with the glomerular changes. Numerous studies have shown that the course and the renal function is strongly associated with the degree of tubulointerstitial damage but only weakly, if at all, by the degree of glomerular damage
6th prediction

Exposure of laboratory animals to nephrotoxic chemicals should produce glomerulonephritis with renal failure.

In 14 experimental studies most of the human glomerulonephritis subgroups have been produced by a variety of hydrocarbons. Also gold, lithium and mercury have produced glomerulonephritis in experimental animals (not yet reviewed here)


What to do?

You may probably ask why so little has been done to treat and prevent renal failure in patients who are exposed to toxic chemicals. How come that most nephrologists consider the problem of minor importance?

There are several answers. Most important is probably that patients with glomerulonephritis and other kidney diseases are not questioned professionally. Many doctors are not familiar with the working conditions of their patients, and many patients are unaware of their exposure. Therefore the doctor get the impression that heavy, toxic exposure is unusual, in particular if mainly patients with normal renal function are questioned.

However, it is a striking fact that more than 50 per cent of patients with glomeruloinephritis and end-stage renal failure have had prolonged and heavy exposure to nephrotoxic chemicals, in particular to organic solvents, fuels and motor exhausts. But to detect such exposure it is necessary to co-operate with experts in occupational medicine, as has been the case in almost all the scientific studies that I have referred to in the preceeding sections. Many times I have seen that even heavy and prolonged exposure may remain undetected unless the patient is interviewed by someone who is familiar with the working conditions in the trade and industry.

Therefore, if you suffer from glomerulonephritis, diabetic kidney disease or a kidney disease of unknown origin, in particular if your kidney function is reduced and if you think you may be exposed to toxic chemicals: 

US:            The Patient & Family Council of the National Kidney Foundation
                 American Association of Kidney Patients
                 National Organization for Renal Disease    
Canada:      The Kidney Foundation of Canada
Sweden:      Riksförbundet för njursjuka


Acute interstitial nephritis
A kidney disease characterized by acute onset, a decreased renal function and microscopic changes mainly located to the renal interstitium (edema and/or infiltration of white blood cells).
Acute tubular nephritis
A kidney disease characterized by acute onset, a decreased renal function and microscopic changes mainly located to the renal tubules. 
Acute tubulo-interstitial nephritis (ATIN) A kidney disease characterized by acute onset, a decreased renal function and microscopic changes located to the tubules and the renal interstitium 


The dominating protein in the plasma. The normal level of albumin in the plasma of healthy individuals is about 4 gram per liter.


A substance, foreign to the body, that stimulates the immune system to produce antibody or to elicit a response from white blood cells. The resulting antibodies and the reacting cells are specific for the stimulating antigen


A plasma protein (immunoglobulin) that has the ability to combine with the antigen that caused its production (see above)
Atrioventricular shunt A device for drainage of the cerebral ventricular fluid ("water on the brain"), for instance inoperated between the ventricles of the brain and the right atrium of the heart.

Auto-immune disease

A condition where the immune system reacts against the body's own constituents


Cylindric formations in the urine produced by protein that has coagulated inside the renal tubules. Casts may contain various blood cells or tubular epithelial cells.


A complex system of more than 30 various enzymes in serum and on the surface of cells. They are activated for instance by contact with immune complexes and microorganisms. Being activated they will start various types of  inflammatory reactions in the tissue and thus contribute to an elimination of  microorganisms or damaged cells.

Electron microscope

With a (transmission) electron microscope it is possible to reveal the ultrastructure of the interior of cells. An electron microscope may enlarge by almost 500,000 times. 
Eosinophilia An increased number of a certain type of white blood cells, the eosinophilic leucocytes. An abnormally high number of eosinophils is a common finding in patients with an allergic disease. 
Focal, segmental glomerulonephritis Glomerulonephritis localized to a few glomeruli only (focal) and in these glomeruli only to segments of the glomerulus (segmental). One of the many unanswered questions about glomerulonephritis is how an immunological disease can be focal and segmental. The phenomenon is easily explained by the toxic-allergic hypothesis (Ravnskov 1988).

Glomerular basement membrane (GBM)

The membrane that separate the capillary walls in the glomerulus from the urinary space. The primary urine is produced by blood filtered through the GBM

(plural: glomeruli)

A glomerulus is composed of 5-6 capillary loops that spring from the afferent arteriole (the arteriole that leds to the glomeruli) and end in the efferent arteriole (the arteriole that leads away from the glomerulus), surrounded by Bowman's capsule. The wall of a glomerular capillary is composed of three layers, the endothelial cells that line the inside of the capillary wall, the glomerular basement membrane, and the glomerular epithelial cells (also named podocytes) that are continuous with the cells lining the inside of Bowman's capsule which again are continuous with the tubular cells. Each kidney has about 1 million glomeruli. 

Goodpasture's syndrome

A rare disease characterized by anti-GBM nephritis and bleedings from the lungs


Blood in the urine


A chemical compund the core of which is composed by carbon and hydrogen atoms. In an aliphatic hydrocarbon the carbon atoms are put together  as a chain; in an aromatic hydrocarbon they are put together as a ring or as several rings (polyaromatic hydrocarbons). The most important sources of hydrocarbon exposure are mineral oil, petroleum distillates and combustion fumes. Most fuels and solvents are produced by distillation of mineral oil at different temperatures. As it is extremely difficult to isolate a pure hydrocarbon by distillation all hydrocarbon products are composed of hundreds or thousands of different hydrocarbon molecules.

Immune complex

The union of antigen, antibody and complement

Immunofluorescence microscopy

A technique used to localize specific constituents in tissue sections. Specific antibodies against the constituent in question are tagged with fluorescent chemicals. In the microscope it is thus possible to recognize the localization in the tissue of any constituent provided a specific antibody is available. In glomerulonephritis the technique is primarily used to identify various immunoglobulins and complement components in the glomeruli.


A group of plasma proteins, produced by the immune system and functioning as antibodies. There are five types of immunoglobulins, immunoglobulin G (IgG), A (IgA), M (IgM), D (IgD) and E (IgE)


An influx into the tissue of blood cells and fluid caused by reactions of the immune system against injury or foreign substances, for instance microorganisms or chemicals. 

Interstitium, renal

The connective tissue that binds together the glomeruli and the tubules


A substance produced by lymphocytes (a kind of white blood cells) when the lymphocyte is stimulated by an antigen. Lymphokines are released to the blood circulation and they can thus exert their effect far away from the cells that produced it

Membranous glomerulonephritis

A subgroup of glomerulonephritis characterized by granular deposits of immunoglobulins and complement lying on the outside of the glomerular basement membrane beneath the epithelial cells. They have a typical appearance on electron microscopy.  Membranous glomerulonephritis is thought to be caused by auto-immunity, eg. the antibodies áttack some of the body's own components located in the glomerulus.

Minimal change nephropathy

A subgroup of glomerulonephritis characterized by heavy proteinuria but with no or minimal changes seen by light microscopy and no deposits of immunoglobulins or complement factors are seen by immunofluorescence microscopy. Electron microscopy shows fusion of the podocytes. Minimal change nephropathy is the most common type of glomerulonephritis in children and there is much evidence that the increased permeability of the glomerular filter and the resulting  proteinuria and podocyte fusion is caused by lymphokines

Nephrotic syndrome 

A combination of heavy proteinuria, low plasma albumin and fluid retention in the body. 


Toxic to the kidneys


The fluid that remains when all cells of the blood (red and white blood cells and platelets) have been eliminated (by centrifugation).


Another name for the glomerular epithelial cell, see glomerulus

Primary urine

The fluid that is produced after filtration of the blood in the glomeruli. Almost 200 liter primary urine is produced by the glomeruli every 24 hour. After having passed the renal tubules this amount is reduced to 1-3 liter urine


An increased amount of plasma proteins in the urine. Normal urine has less than 25 mg protein per liter. Urine from patients with the nephrotic syndrome has 4 gram protein per liter or more
Systemic Lupus Erythematosus (SLE) A chronic, autoimmune, inflammatory disease, most commonly affecting the skin, the joints (arthritis) and the kidneys (glomerulonephritis), but many other organs may be affected as well. 
Serum The fluid that remains when blood has coagulated and the clot has been removed, eg. serum is plasma without fibrinogen.


A white blood cell produced in the thymus. T-cells have important functions in the body's defense against microorgaanisms


Microscopic channels that lead the primary urine through the kidney to the pelvis of the kidney from where it goes down to the urinary bladder. During the passage through the tubules, salt, water and other useful substances are reabsorped from the primary urine and toxic substances are excreted into it. The tubules also maintain the body's acid-base balance.

Tubulointerstitial tissue

The tissue that surrounds the glomeruli, composed of the tubules (normally by far the major part) and the interstitial tissue. In inflammatory states the interstitial tissue is increased and may be dominated by white blood cells and/or edema and/or connective or fibrous tissue, a condition called interstitial nephritis. In case the tubules are abnormal also, it is called tubulointerstitial nephritis.
Wegener Granulomatosus Wegener's granulomatosis is a rare type of autoimmune inflammation of small arteries and veins (vasculitis). Most often the disease is located to the lungs, the nasal cavities and the kidneys. If the kidneys are engaged the clinical picture is glomerulonephritis.



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  18. Cameron JS. Glomerulonephritis: current problems and understanding. J Lab Clin Med 1982;99:755-787.

  19. Carroll N, Crock GW, Funder CC, Green CR, Ham KN, Tange JD. Glomerular epithelial cell lesions induced by N,N´-diacetylbenzidine. Lab Invest 1974; 31: 239-245.

  20. Condie LW, Smallwood CL, Laurie RD. Comparative renal and hepatotoxicity of halomethanes: bromodichloromethane, bromoform, chloroform, dibromochloromethane and methylene chloride. Drug Chem Toxicol 1983; 6: 563-78.

  21. Couser WG, Wallace A, Monaco AP, Lewis EJ. Succesful renal transplantation in patients with circulating antibody to glomerular basement membrane: Report of two cases. Clin Nephrol 1973; 1: 381-388.  

  22. Couser WG, Steinmuller DR, Stilmant MM, Salant DJ, Lowenstein MM. Experimental glomerulonephritis in the isolated perfused rat kidney. J Clin Invest 1978; 62: 1275-87.

  23. Couser WG, Salant DJ. In situ immune complex formation and glomerular injury. Kidney Int 1980; 17: 1-13.  

  24. Couser WG. Pathogenesis of glomerulonephritis. Kidney Int 1993; 44(Suppl 42):S19-S26.

  25. Couser WG. Pathogenesis of glomerular damage in glomerulonephritis. Nephrol Dial Transplant 1998; 13(suppl 1): 10-15.

  26. Couser WG. Glomerulonephritis. Lancet 1999; 353: 1509-1515

  27. De Broe ME, D´Haese PC, Nuyts GD, Elseviers MM. Occupational renal diseases. Curr Opinion Nephrol Hypertens 1996; 5: 114-121.

  28. Dixon FJ, Feldhan JD, Vasquez JJ. Experimental glomerulonephritis. The pathogenesis of a laboratory model resembling the spectrum of human glomerulonephritis. J Exp Med 1961; 113: 899-920.

  29. Dixon FJ. The pathogenesis of glomerulonephritis . Am J Med 1968; 44: 493-498.

  30. Dunn TB, Morris HP, Wagner BP. Lipemia and glomerular lesions in rats fed diets containing N-N´-diacetyl- and 4, 4-4´, 4´-tetramethylbenzidine. Proc Soc Exp Biol Med 1956; 91: 105-7.

  31. Easley JR, Holland JM, Gipson LC, Whitaker MJ. Renal toxicity of middle distillates of shale oil and petroleum in mice. Toxicol Appl Pharmacol 1982; 65: 84-91.

  32. Erwin DT, Donadio JV, Holley KE. The clinical course of idiopathic membranous nephropathy. Mayo Clinic Proc 1973; 48: 697-712.

  33. Fabre R, Truhaut R, Laham S. Recherches toxicologiques sur les solvants de remplacement du benzène. IV. - Étude des xylènes (1). Arch Mal Profess 1960; 21: 301-313.

  34. Feenstra K, van der Lee R, Greben HA et al. Experimental glomerulonephritis in the rat induced by antibodies directed against tubular antigens. I. The natural history: a histologic and immunohistologic study at the light microscopeic and the ultrastructural level. Lab Invest 1975; 32: 235-242

  35. Finn R, Fennerty AG, Ahmad R. Hydrocarbon exposure and glomerulonephritis. Clin Nephrol 1980; 14: 173-5.

  36. Fleuren GJ, Grond J, Hoedemaeker PJ.The pathogenetic role of free-circulating antibody in autologous immune complex glomerulonephritis. Clin Exp Immunol 1980; 41: 205-217.

  37. Franchini I, Lucertini S, Chiesa E, Mutti A. Organic solvent exposure and chronic glomerulonephritis: a case-control study. X. Medichem 1982; 14-16: 169-75.

  38. Germuth FG. A comparative histologic and immunologic study in rabbit of induced hypersensitivity of the serum sickness type. J Exp Med 1953; 97: 257-282.

  39. Gormly AA, Smith PS, Seymour AE, Clarkson AR, Woodroffe AJ. IgA glomerular deposits in experimental cirrhosis. Am J Pathol  1981; 104: 50-54

  40. Gregorini G, Ferioli A, Donato F, Tira P, Morassi L, Tardanico R, Lancini L, Maiorca R. Association between silica exposure and necrotizing crescentic glomerulonephritis with p-ANCA and anti-MPO antibodies: a hospital-based case-control study. Adv Exp Med Biol 1993; 336: 435-40.  

  41. Hammer DK, Dixon FJ. Experimental glomerulonephritis. II. Immunologic events in the pathogenesis of nephrotoxic serum nephritis. J Exp Med 1963; 117: 1019-1034.

  42. Harman JW. Chronic glomerulonephritis and the nephrotic syndrome induced in rats with N,N´-diacetylbenzidine. J Pathol 1971; 104: 119-128

  43. Harrington JM, Whitby H, Gray CN, Reid FJ, Aw TC, Waterhouse JA. Renal disease and occupationbal exposure to organic solvents: a case referent approach. Brit J Industr Med 1989; 46: 643-50.

  44. Harrison DJ, Thomson D, MacDonald MK. Membranous glomerulonephritis. J Clin Pathol 1986; 39: 167-71.

  45. Hashimoto DM, Kelsey KT, Seitz T, Feldman HA, Yakes B, Christiani DC. The presence of urinary cellular sediment and albuminuria in newspaper pressworkers exposed to solvents. J Occupat Med 1991; 33: 517-526.

  46. Helin H, Pasternack A, Hakala T, Penttinen K, Wager O. Glomerular electron-dense deposits and circulating immune complexes in patients with mkalignant tumours. Clin Nephrol 1980; 14: 23-30.

  47. Heymann W, Hackel DB, Harwood S. et al. Production of nephrotic syndrome in rats by Freund´s adjuvant and rat kidney suspension. Proc Soc Exp Biol Med 1959; 100: 660-664.

  48. Heymann W, Hunter JLP, Hackel DB. Experimental auto-immune nephrosis in rats: III. J Immunol 1962; 88: 135-141.

  49. Hoorntje SJ, Kallenberg CGM, Weening JJ, Donker AJM, The TH, Hoedemaeker PJ. Immune-complex glomerulopathy in patients treated with captopril. Lancet 1980; 1:1212-1215

  50. Hotz P, Pilliod J, Söderström D, Rey F, Boillat MA, Savolainen H. Relation between renal function tests and a retrospective organic solvent exposure score. Brit J Industr Med 1989; 46: 815-819.

  51. Hotz P, Pilliod J, Bernard A, Rey F, Boillat MA. Erythrocytes glomérulaires, albuminurie, glycosaminoglycanes et exposition aux hydrocarbures. Schweiz Med Wschr 1990a; 120: 999-1004.

  52. Hotz P, Pilliod J, Bernard A, Berode M, Rey F, Mazzocato C, Guillemin M, Boillat M-A. Hydrocarbon exposure, hypertension and kidney function tests. Int Arch Occup Environ Health 1990b; 62: 501-508.

  53. Hotz P, Pilliod J, Berode M, Rey F, Boillat MA. Glycosaminoglycans, albuminuria and hydrocarbon exposure. Nephron 1991; 58: 184-191.

  54. Hotz P, Thielemans N, Bernard A, Gutzwiller F, Lauwerys R. Serum laminin, hydrocarbon exposure, and glomerular damage. Brit J Industr Med 1993; 50: 1104-1110.

  55. Hotz P. Occupational hydrocarbon exposure and chronic nephropathy. Toxicology 1994;90:163-283

  56. Huber W, Ritz E, Fliser D. Does occupational exposure to toxins increase albumin excretion rate? Kidney Int 1998; 54: 303-304.  

  57. Huber W, Conradt C, Dangl C et al. Organische Lösemittel und chronische Glomerulonephritis.  Nieren Hochdruckkrankheiten 2000; 29:.41-53. 

  58. Hultberg B, Ravnskov U. The excretion of N-acetyl-b-glucosaminidase in glomerulonephritis. Clin Nephrol 1981; 15: 33-38.

  59. Johansson BG, Ravnskov U. The serum level and urinary excretion of a2-microglobulin, b2-microglobulin and lysozyme in renal disease. Scand J Urol Nephrol  1972; 6: 249-256.

  60. Klavis G, Drommer W. Goodpasture-syndrom und Benzineinwirkung. Arch Toxicol 1970; 26: 40-55.

  61. Lagrue G, Kamalodine T, Hirbec G, Bernaudin JF, Guerrero J, Zhepova. Rôle de l´inhalation de substances toxiques dans la genèse des glomérulonéphrites. Nouv Presse Med 1977; 6: 3609-13.

  62. Larsen S. Glomerular immune deposits in kidneys from patients with no clinical or light microscopic evidence of glomerulonephritis. Acta Path Microbiol Scand (Sect A) 1979; 87: 313-319.

  63. Lee HS, Koh HI. Nature of progressive glomerulosclerosis in human membranous nephropathy. Clin Nephrol 1993; 39: 7-16

  64. Lerner RA, Dixon FJ. Spontaneous glomerulonephritis in sheep. Lab Invest 1966; 1279-1289.

  65. Lerner RA, Dixon FJ, Lee S. Spontaneous glomerulonephritis in sheep. II. Studies on natural history, occurrence in other species, and pathogenesis. Am J Pathol 1968; 53: 501-512.

  66. Markham RV, Sutherland JC, Mardiney MR. The ubiquitous occurrence of immune complex localization in the renal glomeruli of normal mice. Lab Invest  1973; 29: 111-120.

  67. Miettinen A. Nephritogenic antibodiews against kidney brush border glycoproteins in rabbits injected with Freund´s adjuvant.  Lab Invest 1982; 47: 67-75.

  68. Mosinger M, Fiorentini H. Intoxication expérimentale par le trichloréthyléne. Annal Med Leg Crim Pol Scient Toxicol 1958; 38: 319-324.

  69. Mutti A, Alinovi R, Bergamaschi E, Biagini C, Cavazzini S, Franchini I, Lauwerys RR, Bernard AM, Roels H, Gelpi E, Rosello J, Ramis I, Price RG, Taylor SA, de Broe M, Nuyts GD, Stolte H, Fels LM, Herbort C. Nephropathies and exposure to perchloroethylene in dry-cleaners. Lancet 1992; 340: 189-193.

  70. Nakajima H. Tubulo-interstitial nephritis in guinea pigs sensitized to 2,4-dinitrochlorobenzen. Osaka City Med J. 1981;27:93-100.

  71. Nakajima H, Nishiwaki S, Shimada I. Induction of anti-tubular- and anti-glomerular-basement-membrane antibodies in guinea pigs sensitized to 2,4-dinitrochlorobenzen with reference to tubulo-interstitial and glomerular nephritis. Osaka City Med J 1982; 28: 59-65.

  72. Navas-Palacios JJ, Usera-Sárraga G, Gil-Martin R. Pathology of the kidney in “toxic oil epidemic syndrome”. J Toxicol Environ Health 1984; 13: 1-18.

  73. Neale TJ, Woodroffe AJ, Wilson CB. Spontaneous glomerulonephritis in rabbits: role of a glomerular capillary antigen. Kidney Internat  1984; 26: 701-711

  74. Nelson NA, Robins TG, Port FK. Solvent nephrotoxicity in humans and experimental animals. Am J Nephrol 1990; 10: 10-20.

  75. Nuyts GD, van Vlem E, Thys J, et al. New occupational risk factors for chronic renal failure. Lancet 1995; 346: 7-11.  

  76. Ogawa M, Mori T, Mori Y, Ueda S, Azemoto R, Makino Y, Wakashin Y, Ohto M, Wakashin M, Yoshida H, Iesato K . Study on chronic renal injuries induced by carbon tetrachloride: selective inhibition of nephrotoxicity by irradiation. Nephron 1992; 60: 68-73.

  77. Pai P, Stevenson A, Mason H, Bell GM. Occupational hydrocarbon exposure and nephrotoxicity: a cohort study and literature review. Postgrad Med J 1998; 74: 225-228.

  78. Pascal RR, Iannaccone PM, Rollwagen FM, Harding TA, Bennett SJ. Electron microscopy and immunofluorescence of glomerular immune complex deposits in cancer patients. Cancer Res 1976; 36: 43-47

  79. Poon-King T, Mohammed I, Cox R, Potter EV, Simon NM, Siegel AC, Earle DP . Recurrent epidemic nephritis in South Trinidad. N Engl J Med 1967; 277: 728-733.

  80. Porro A, Lomonte C, Coratelli P, Passavanti G, Ferri GM, Assennato G. Chronic glomerulonephritis and exposurte to solvents: a case-referent study. Brit J Industr. Med 1992; 49: 738-42.

  81. Ramzy MH, Cameron JS, Turner DR, Neild GH, Ogg CS, Hicks J. The long-term outcome of idiopathic membranous nephropathy. Clin Nephrol 1981; 16: 13-19.

  82. Ravnskov U. Exposure to organic solvents - a missing link in acute poststreptococcal glomerulonephritis? Acta Med Scand 1978; 203: 351-356

  83. Ravnskov U, Forsberg B, Skerfving S. Glomerulonephritis and exposure to organic solvents. A case-control study. Acta Med Scand 1979; 205: 575-9.

  84. Ravnskov U, Lundström S, Nordén Å. Hydrocarbon exposure and glomerulonephritis: Evidence from patients' occupation. Lancet 1983; 2: 1214-6.

  85. Ravnskov U. Possible mechanisms of hydrocarbon-associated glomerulonephritis. Clin Nephrol 1985; 23:294-298.

  86. Ravnskov U. Influence of hydrocarbon exposure on the course of glomerulonephritis. Nephron 1986; 42: 156-60

  87. Ravnskov U. Focal glomerular lesions in glomerulonephritis may be secondary to tubulo-interstitial damage. Am J Kidney Dis 1988; 12: 250-251

  88. Ravnskov U. Non-systemic glomerulonephritis: Exposure to nephro- and immunotoxic chemicals is primary and predisposes to immunologic harassment. Med Hypotheses 1989; 30: 115-122. 

  89. Ravnskov U. The subepithelial formation of immune complexes in membranous glomerulonephritis may be harmless and secondary to allergic or toxic factors. Scand J Immunol 1998; 48: 469-474. 

  90. Ravnskov U. Glomerular, tubular and interstitial nephritis associated with non-steroidal antiinflammatory drugs. Evidence of a common mechanism. Brit J Clin Pharmacol 1999; 47: 203-210.

  91. Ravnskov U. Hydrocarbons may worsen renal function in glomerulonephritis: a meta-analysis of the case-control studies. Am J Indust Med 2000a; 37: 599-606.

  92. Ravnskov U. Hydrocarbon exposure may cause glomerulonephritis and worsen renal function:evidence based on Hill´s criteria for causality.Q J Med 2000b; 93: 551-556.

  93. Riemenschneider T, Mackensen-Haen S, Christ H, Bohle A. Correlation between endogenous creatinine clearance and relative interstitial volume of the renal cortex in patients with diffuse membranous glomerulonephritis having a normal serum creatinine concentration. Lab Invest 1980; 43: 145-49

  94. Rodriguez-Iturbe B, Garcia R, Rubio L, Cuenca L, Treser G, Lange K. Epidemic glomerulonephritis in Maracaibo. Evidence for progression to chronicity. Clin Nephrol 1976; 5: 197-206.

  95. Rosenberg HG, Martinez PS, Vaccarezza AS, Martinez LV. Morphological findings in 70 kidneys of living donors for renal transplant. Pathol Res Pract 1990; 186: 619-624.

  96. Roy AT, Brautbar N, Lee DBN. Hydrocarbons and renal failure. Nephron 1991;58:385-92

  97. Sakaguchi H, Dachs S, Mautner W, Grisham E, Churg J. Renal glomerular lesions after administration of carbon tetrachloride and ethionine. Lab Invest 1964; 13: 1418-1426.

  98. Savige JA, Baker C, Gallicchio M, Varigos G. Circulating anti-glomerular basement membrane antibodies in coeliac disease and epidermolysis bullosa acquisita. Aust N Z J Med 1991; 21: 867-70

  99. Seligson G, Lange K, Majeed HA, Deol H, Cronin W, Bovie R. Significance of endostreptosin antibody titers in poststreptococcal glomerulonephritis. Clin Nephrol 1985; 24: 69-75

  100. Sesso R, Stolley PD, Salgado N, Pereira AB, Ramos OL. Exposure to hydrocarbons and rapidly progressive glomeru­lonephritis. Brazilian J Med Biol Res 1990; 23: 225-33.

  101. Steblay RW. Glomerulonephritis induced in sheep by injections of heterologous glomerular basement membrane and Freund´s complete adjuvant. J Exp Med 1962; 116: 253-272.

  102. Steblay RW, Rudofsky U. Spontaneous renal lesions and glomerular deposits of IgG and complement in guinea pigs. J Immunol 1971; 107: 1192-1196.

  103. Steenland NK, Thun MJ, Ferguson W, Port FK.  Occupational and other exposures associated with male end-stage renal disease. A case/control study. Am J Public Health 1990; 80: 153-9.

  104. Stengel B, Cénée S, Limasset J-C, et al. Organic solvent exposure may increase the risk of glomerular nephropathies with chronic renal failure. Int J Epidemiol 1995; 24: 427-34.  

  105. Stevenson A. Yaqoob M, Mason H, Pai P, Bell GM. Biochemical markers of basement membrane disturbances and occupational exposure to hydrocarbons and mixed solvents. Q J Med 1995; 88: 23-28

  106. Suganuma T. Glomerular IgA deposits in an autopsy study. Nippon-Jinzo-Gakkai-Shi  1994; 36: 813-22.

  107. Sugisaki T, Klassen J, Andres GA et al. Passive transfer of Heymann nephritis with serum. Kidney Int 1973; 3: 66-73.

  108. Sutherland JC, Markham RV, Mardiney MR. Subclinical immune complexes in the glomeruli of kidneys postmortem. Am J Med 1974; 57: 536-541.

  109. Unanue ER, Dixon FJ. Experimental glomerulonephritis: immunological events and pathogenetic mechanismss. Adv Immunol 1967; 6: 1-90.

  110. Waldherr R, Rambausek M, Duncker WD, Ritz E. Frequency of mesangial IgA deposits in a non-selected autopsy series. Nephrol Dial Transplant 1989; 4: 943-946.

  111. van der Laan G. Chronic glomerulonephritis and organic solvents. A case-control study. Int Arch Occup Environ Health 1980; 47: 1-8.

  112. Watson JI, Dixon FJ, Feldman JD. The effect of complete Freund´s adjuvant on rat kidneys. Lab Invest 1965; 14: 1559-1567.

  113. Wehrmann M, Bohle A, Bogenschütz O, Eissele R, Freislederer A, Öhlschlegel C, Schumm G, Batz C, Gärtner HV. Long-term prognosis of chronic idiopathic membranous glomerulonephritis. An analysis of 334 cases with particular regard to tubulo-interstitial changes. Clin Nephrol 1989; 31: 67-76.

  114. Viau C, Bernard A, Gueret F, Maldague P, Gengoux P, Lauwerys R. Isoparaffinic solvent-induced nephrotoxicity in the rat. Toxicology 1986; 38:227-240.

  115. Viau C, Bernard A, Lauwerys R, Buchet JP, Quaeghebeur L, Cornu ME, Phillips SC, Mutti A, Lucertini S, Franchini I. A cross-sectional survey of kidney function in refinery employees. Amer J Industr Med 1987; 11: 177-187.

  116. Wilson CB, Dixon FJ. The renal response to immunological injury. In Brenner, Rector (eds.): The Kidney, 2.ed. Saunders, Philadelphia 1981, pp. 237-1350

  117. Yaqoob M, Bell GM, Percy DF, Finn R. Primary glomerulone­phritis and hydrocarbon exposure: a case-control study and literature review. Q J Med 1992; 83: 409-18.

  118. Yaqoob M, Bell GM, Stevenson A, Mason H, Percy DF. Renal impairment with chronic hydrocarbon exposure. Q J Med 1993a; 86: 165-174.

  119. Yaqoob M, Stevenson A, Mason H, Bell GM. Hydrocarbon exposure and tubular damage: additional factors in the progression of renal failure in primary glomerulonephritis. Q J Med 1993b: 86: 661-7

  120. Yaqoob M, Bell GM. Occupational factors and renal disease. Renal Failure 1994a; 16: 425-34.

  121. Yaqoob M, Patrick AW, McClelland P, et al. Occupational hydrocarbon exposure and diabetic nephropathy. Diabetic Med 1994b; 11: 789-93  

  122. Zanetti M, Druet P. Passive Heymann's nephritis as a model of immune glomerulonephritis mediated by antibodies to immunoglobulins. Clin Exp Immunol 1980; 41:189-195

  123. Zimmerman SW, Groehler K, Beirne GJ. Hydrocarbon exposure and chronic glomerulonephritis. Lancet, 1975; 2: 199-201.

  124. Zimmerman SW, Varanasi UR, Hoff B. Goodpasture´s syndrome with normal renal function. Am J Med 1979a; 66: 163-171.

  125. Zimmerman SW. Characterization of chronic N,N´-diacetylbenzidine-induced nephropathy. Am J Pathol 1979b;94:285-300.

  126. Zimmerman SW, Norback DH, Powers K. Carbon tetrachloride nephrotoxicity in rats with reduced renal mass. Arch Pathol Lab Med 1983; 107: 264-9.

  127. Churchill DN, Fine A, Gault MH. Association between hydrocarbon exposure and glomerulonephritis. Nephron 1983; 33: 169-172.

  128. Rosenman KD, Moore-Fuller M, Reilly MJ. Kidney disease and silicosis. Nephron 2000; 85: 14-19.

  129. Calvert GM, Steenland K. End-stage renal disease among silica-exposed gold miners. JAMA 1997; 277: 1219-1223.

  130. Ng TP, Ng YL, Lee HS, Chia KS, Ong HY. A study of silica nephrotoxicity in exposed silicotic and non-silicotic workers. Brit J Indust Med 1992; 49: 35-37.

  131. Ng TP, Lee HS, Phoon WH. Further evidence of human silica nephrotoxicity in occupationally exposed workers. Brit J Indust Med 1993; 50: 907-912.

  132. Boujemaa W, Laywerys R, Bernard A. Early indicators of renal dysfunction in silicotic workers. Scand J Environ Health 1994; 20: 180-183.

  133. Hotz P, Gonzales-Lorenzo J, Siles E, Trulillano G, Lauwerys R, Bernard A. Subclinical signs of kidney dysfunction following short exposure to silica in the absence of silicosis. Nephron 1995; 70: 438-442.

  134. Nuyts GD, van Vlem E, de Vos A et al. Wegener granulomatosis is associated to exposure to silicon compounds: a case-control study. Nephrol Dial Transpl 1995; 10: 1162-1165.

  135. Parks CG, Conrad K, Cooper GS. Occupational exposure to crystalline silica and autoimmune disease. Environ Health Perspect. 1999;107 Suppl 5:793-802.

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About the Author

Born 1934 in Copenhagen, Denmark. Graduated 1961 from the University of Copenhagen with an M.D.  1961-1967 various appointments at surgical, roentgenological, neurological, pediatric and medical departments in Denmark and Sweden.  1968-79 various appointments at the Dept. of Nephrology, and the Dept. of Clinical Chemistry, University Hospital, Lund, Sweden;1975-79 as an assistant professor at the Dept. of Nephrology. 1973 PhD at the University of Lund.  1979-2000 a private practitioner. Since 1979 an independent researcher. 

Honoured by The Skrabanek Award 1998.

On the Swedish medical web-journal The Rondel, you will find a personal view  of me by Bo Norberg, MD, PhD, and a review of my career. My own story is available in Swedish

Address: Magle Stora Kyrkogata 9, S-223 50 Lund, Sweden  Tel: +46 46 145022   

My publications in inverse chronologically order:

Papers on Glomerulonephritis

  1. Ravnskov U. Suicide of the nephron is preventable. The Lancet 2001;357 (May 12).

  2. Ravnskov U. Glomerulonefrit – en yrkessjukdom – nya rön om en sjukdom associerad med exposition för njurtoxiska  ämnen. Läkartidningen 2000; 97: 3978-9.

  3. Ravnskov U. Hydrocarbon exposure may cause glomerulonephritis and worsen renal function:evidence based on Hill´s criteria for causality. Quarterly Journal of Medicine 2000; 93: 551-556.

  4. Ravnskov U. Hydrocarbons may worsen renal function in glomerulonephritis: a meta-analysis of the case-control studies. American Journal of Industrial Medicine 2000; 37: 599-606.

  5. Ravnskov U. Glomerular, tubular and interstitial nephritis associated with non-steroidal antiinflammatory drugs. Evidence of a common mechanism. British Journal of Clinical Pharmacology 1999; 47: 203-210.

  6. Ravnskov U. Lösningsmedel och drivmedel orsakar kronisk njursvikt. Tidskriften Medikament 1999; 2: 80-84.

  7. Ravnskov U. The subepithelial formation of immune complexes in membranous glomerulonephritis may be harmless and secondary to allergic or toxic factors. Scandinavian Journal of Immunology 1998; 48: 469-474.

  8. Ravnskov U. Renal complement synthesis in glomerulonephritis. Lancet 1994; 343: 235-6.

  9. Ravnskov U. Hydrocarbons and renal failure: Primary damage in glomerulonephritis is tubular, not glomerular. Nephron 1992; 61: 243

  10. Ravnskov U. Glomerulonephritis, renal carcinoma, and solvent exposure: bias from choice of referents. British Journal of Industrial Medicine 990; 47: 791-92., 1990

  11. Ravnskov U. Non-systemic glomerulonephritis: Exposure to nephro- and immunotoxic chemicals is primary and predisposes to immunologic harassment. Medical Hypotheses 989; 30: 115-122. 

  12. Ravnskov U. Focal segmental glomerulosclerosis in acute renal failure. New England Journal of Medicine 1989; 320: 1218-1219.

  13. Ravnskov U. Focal glomerular lesions in glomerulonephritis may be secondary to tubulointerstitial damage. American Journal of Kidney Diseases 1988; 12: 250-251.

  14. Ravnskov U. Hepatitis B virus and glomerulonephritis. The Lancet 1987; 2: 691.

  15. Ravnskov U. Influence of hydrocarbon exposure on the course of glomerulonephritis. Nephron 1986; 42: 156-160.

  16. Ravnskov U. Glomerulonefrit och organiska lösningsmedel. Läkartidningen 1986; 83: 1080-1083

  17. Ravnskov U. Possible mechanisms of hydrocarbon-associated glomerulonephritis. Clinical Nephrology 1985; 23: 294-298.

  18. Ravnskov U. Glomerulonephritis and organic solvents. The Lancet 985; 2: 566.

  19. Ravnskov U. Hydrocarbon exposure and glomerulonephritis. Nephron 1983; 36: 143.

  20. Ravnskov U, Lundström S, Nordén Å. Hydrocarbon exposure and glomerulonephritis: evidence from patients' occupations. The Lancet 1983; 2: 1214-1216.

  21. Ravnskov U, Forsberg B. Improvement of glomerulonephritis after discontinuation of solvent exposure. The Lancet 1979; 1: 1194.

  22. Ravnskov U, Forsberg B, Skerfving S. Glomerulonephritis and hydrocarbon exposure - a case control study. Acta Medica Scandinavica 1979; 205: 575-579.

  23. Ravnskov U. Acute glomerulonephritis and exposure to organic solvents in father and daughter. Acta Medica Scandinavica 1979; 205: 581-582

  24. Ravnskov U. Exposure to organic solvents - a missing link in acute poststreptococcal glomerulonephritis? Acta Medica Scandinavica 1978; 203: 351-356

  25. Ravnskov U, Dahlbäck O, Messeter L. Treatment of glomerulonephritis with drainage of the thoracic duct and plasmapheresis. Acta Medica Scandinavica 202, 489-494, 1977.

  26. Ravnskov U. Exposure to organic solvents in acute poststreptococcal glomerulonephritis. The Lancet 1977; 2: 258

Papers on Proteinuria and/or Renal Function

  1. Hultberg B, Ravnskov U. The excretion of N-acetyl-ß-glucosaminidase in glomerulonephritis. Clinical Nephrology 1981; 15: 33-38.

  2. Ekman R, Johansson BG, Ravnskov U. Renal handling of Zn alfa2-glycoprotein as compared with that of albumin and the retinol-binding protein. Journal of Clinical Investigation 1976; 57: 945-954.

  3. Ravnskov U. Serum ß2-microglobulin and glomerular function. New England Journal of Medicine 1976; 294: 611.

  4. Ravnskov U, Johansson BG. Isolation and partial characterization of a porcine low molecular weight protein occurring in plasma and urine. International Journal of Biochemistry 1976; 7: 579-583.

  5. Ravnskov U, Johansson BG, Ljunger L. Proteinuria in pigs with experimentally induced renal damage. Contributions to Nephrology 1975; 1:  50-61.

  6. Ravnskov U, Karatson A. Renal handling of human ß2-microglobulin in the rat: The importance of sham-operation. Acta Physiologica Scandinavica 1975; 94: 467-471.

  7. Ravnskov U. Low molecular weight proteinuria in association with paroxysmal myoglobinuria. Clinical Nephrology 1975; 3: 65-69.

  8. Ravnskov U. Proteinuria after renal transplantation. 2. A functional identification of two types of rejection crisis. Scandinavian Journal of Urology and Nephrology 1974; 8: 45-49. 
    Ravnskov U, Johansson BG. Renal handling of ß2-microglobulin. Protides of the biological fluids. 1974; 21: 513-517.

  9. Ravnskov U. On renal handling of plasma proteins. Scandinavian Journal of Urology and Nephrology 1973; 7 suppl 20. [Thesis]

  10. Johansson BG, Ravnskov U. Urinproteinanalys vid kadmiumförgiftning. Läkartidningen 1973; 70: 2310.
    Ravnskov U. Albuminuria in acute and chronic renal failure. Acta Medica Scandinavica 1973; 194: 59-64.

  11. Ravnskov U. Proteinuria after renal transplantation. 1. Excretion of α2-microglobulin, ß2-microglobulin, lysozyme and albumin. Scandinavian Journal of Urology and Nephrology 1974; 8: 37-44.

  12. Johansson BG, Ravnskov U. The serum level and urinary excretion of α2-microglobulin, ß2-microglobulin and lysozyme in renal disease Scandinavian Journal of Urology and Nephrology 1972; 6: 249-256.

  13. Ravnskov U, Johansson BG, Göthlin J. Renal extraction of ß2-microglobulin. Scandinavian Journal of Clinical and Laboratory Investigation 1972; 30: 71-75.

  14. Ravnskov U. Muramidase and acute rejection of kidney grafts. The Lancet 1972; 2: 716.

  15. Johansson BG, Ravnskov U. Analyses of proteins in urine. Aids and limitations. Scandinavian Journal of Clinical and Laboratory Investigation 1972; 29,suppl 126.

Papers on Urinary Tract Infection

  1. Ravnskov U. Behandlingstidens längd vid urinvägsinfektion. Läkartidningen 1987; 84: 1339.

  2. Ravnskov U. Avvisa inte singeldosbehandlingen vid urinvägsinfektion! Läkartidningen 1987; 84: 1535.
    Ravnskov U. Singeldos vid urinvägsinfektion fungerar med rätt dos och rätt preparat. Läkartidningen 1987; 84: 2946.

  3. Ravnskov U. Singeldos-behandling av okomplicerad cystit och asymtomatisk bakteriuri. En översikt. Läkartidningen 1986; 83: 45-47.

  4. Ravnskov U. Dysuri kan orsakas av tvål. Läkartidningen 1985; 82: 836

  5. Ravnskov U. Dysuri skyldes som regel sæbe. Ugeskrift for Læger 1985; 147: 1493-1494.

  6. Ravnskov U. Sæbe og dysuri. Ugeskrift for Læger 1985; 147: 2093.

  7. Ravnskov U. Soap is the major cause of dysuria. The Lancet 1983; 1: 1027-1028.

  8. Ravnskov U. Strikta indikationer, kort tids terapi - lösningen på sulfaproblemet. Läkartidningen. 1982; 79: 1350.

  9. Ravnskov U. Bakteriuri og vejen til iatrogenese. Ugeskrift for Læger 1978; 140: 2256-2257.

  10. Ravnskov U. Medikaliserat samhälle?. Läkartidningen 1976; 73: 1298.

  11. Ravnskov U. Långtidsprognosen vid urinvägsinfektion och asymtomatisk bakteriuri. Läkartidningen 1975; 72: 1796-1798.

  12. Ravnskov U. Urinary tract infection with disappearance of urinary creatinine. Scandinavian Journal of Urology and Nephrology 1973; 7: 94-95.

  13. Lindholm T, Ravnskov U. Bakteriuri och pyuri - är det farligt? Läkartidningen 1972; 69: 3538-3541.

Papers on Ochratoxin-Nephropathy

  1. Krogh P, Elling F, Friis C, Hald B, Larsen AE, Lillehøj EB, Madsen A, Mortensen HP, Rasmussen F, Ravnskov U. Porcine nephropathy induced by long-term ingestion of ochratoxin A. Veterinary Pathology 1979; 16: 466-475.

  2. Krogh P, Elling F, Gyrd-Hansen N, Hald B, Larsen AE, Lillehøj EB, A Madsen,HP Mortensen, Ravnskov U. Experimental porcine nephropathy: changes of renal function and structure perorally induced by crystalline ochratoxin A. Acta Pathologica Microbiologica Scandinavica 1976; 84 A: 429-434.

  3. Krogh P, Axelsen NH, Elling F, Gyrd-Hansen N, Hald B, Hyldgaard-Jensen J, Larsen AE, Madsen A, Mortensen HP, Møller T, Petersen OK, Ravnskov U, Rostgaard M, Aalund O. Experimental porcine nephropathy. Changes of renal function and structure induced by Ochratoxin A-contaminated feed. Acta Pathologica Microbiologica Scandinavica Suppl 246, 1974.

          Papers and Books Published in English on Cholesterol and the Diet-Heart Idea:

A popular-scientific review of my research about cholesterol and the diet-heart idea is available on

  1. Ravnskov U. The Cholesterol Myths. Washington: New Trends Publishing, 2000; ISBN 0-9670897-0-0

  2. Ravnskov U. Prevention of atherosclerosis in children. The Lancet 2000; 355: 69.

  3. Ravnskov U. VAT and fat. Evidence is contradictory. British Medical Journal 2000; 320: 1470

  4. Ravnskov U. Why heart disease mortality is low in France.Author´s hypothesis is wrong. British Medical Journal 1999; 319: 255. 

  5. Ravnskov U. The questionable role of saturated and polyunsaturated fatty acids in cardiovascular disease. Journal of Clinical Epidemiology 1998; 51: 443-460.   Read also a dissent to the paper: Golomb BA. Dietary fats and heart disease-dogma challenged? and my answer; same journal and same issue. This paper won the Skrabanek Award 1998

  6. Ravnskov U. What do angiographic changes after cholesterol lowering mean? The Lancet 1994; 344: 1297.

  7. Ravnskov U. American College of Physicians Guidelines on Cholesterol Screening. Annals of Internal Medicine 1996;125:1010

  8. Ravnskov U. Quotation bias in reviews of the diet-heart idea. Journal of Clinical Epidemiology 1995; 48: 713-719.

  9. Ravnskov U. Implications of 4S evidence on baseline lipid levels. The Lancet 1995; 346: 181.

  10. Ravnskov U. Beneficial effects of simvastatin may be due to non-lipid actions. British Medical Journal 1995; 311: 1436-1437.

  11. Ravnskov U. Hypercholesterolemia does not cause coronary heart disease - evidence from the nephrotic syndrome. Nephron 1994; 66: 356-35 7.

  12. Ravnskov U. Ischaemic heart disease and cholesterol. Optimism about drug treatment is unjustified. British Medical Journal 1994; 308: 1038.

  13. Ravnskov U. Is intake of trans-fatty acids and saturated fat causal in coronary heart disease? Circulation 1994; 90: 2568-2569.

  14. Ravnskov U. Doing the right thing: stop worrying about cholesterol. Circulation 1994; 90: 2572-2573.

  15. Ravnskov U. Is there a cause-effect relationship between high blood cholesterol and atherosclerosis? Workshop on cholesterol-lowering trials. National Heart, Lung and Blood Institute, Bethesda 1994.

  16. Ravnskov U. Dietary fats and blood lipids as cardiovascular risk factors in the general population. A critical overview. Proceedings of the I. World Congress of Dairy Products in Human Health and Nutrition. Madrid 1993. Rotterdam: Balkema 1994, p 361-369.

  17. Ravnskov U. Reducing serum cholesterol. Lower cholesterol of doubtful benefit to anyone. British Medical Journal 1993; 307: 125.

  18. Ravnskov U. Coronary atherosclerosis on angiography-progress or regress and why? Circulation 1993; 88: 1358-1359.

  19. Ravnskov U. Cardiovascular disease in developing countries. British Medical Journal 1993; 306: 145-146.

  20. Ravnskov U. Cholesterol lowering trials in coronary heart disease: frequency of citation and outcome. British Medical Journal 1992; 305: 15-19. Letters: British Medical Journal 1992; 305: 420-422, and 717.

  21. Ravnskov U. The fragile links of the diet-heart chain. Nutrition Quarterly 1992; 16: 19-21.

  22. Ravnskov U. Atherogenicity and thrombogenicity indices. The Lancet 338, 1328, 1991.

  23. Ravnskov U. An elevated serum cholesterol is secondary, not causal, in coronary heart disease. Medical Hypotheses 1991; 36: 238-241.

  24. Ravnskov, U. Lowering cholesterol concentrations and mortality. British Medical Journal 1990; 301: 814. 

Papers and Books in Swedish, Danish or Finnish on Cholesterol and the Diet-Heart Idea

  1. Ravnskov U. Amerikansk kolesterol-policy kan leda till sjukförklaring av miljontals friska. Läkartidningen 2001;98:4574-4577.

  2. Ravnskov U. Koständringar förebygger inte hjärtinfarkt. Läkartidningen 2001;98:3926

  3. Ravnskov U. Statinbehandling vid akut hjärtinfarkt väl optimistiskt refererat i massmedierna. Läkartidningen 2001;98:2370

  4. Ravnskov U. Transfettsyra-den verkliga kostboven vid hjärtinfarkt? Läkartidningen 2001;98:4060.

  5. Ravnskov U. Är motion överlägsen statinbehandling? Läkartidningen 2000;97:2177

  6. Ravnskov U. Varför blir kranskärl aterosklerotiska? Läkartidningen 2000; 98: 41

  7. Ravnskov U. Myten om det mättade och det fleromättade fettet. Tidskriften Medikament 1998; 3(4): 44-51 och 1998; 3(5): 48-53.

  8. Ravnskov U. "Medelhavsdietens" förträfflighet är en myt. Läkartidningen 1998;95:4749-4750.

  9. Ravnskov U. Auktoriteter kräver tolkningsföreträde. Läkartidningen 1997;95:1024-1025.

  10. Ravnskov U. Är fleromättat fett en orsak till manlig sterilitet? Läkartidningen 1996; 93: 2040. 

  11. Ravnskov U. Fedtsyrer og forvirrende signaler. Ugeskrift for Læger 1995; 157: 1534-1535.

  12. Ravnskov U. Keys eller kaos.Ugeskrift for Læger 1995; 157: 3210.

  13. Ravnskov U. Slutreplik om kolesterol. Läkartidningen 1994; 91: 117-118.

  14. Ravnskov U. Kolesterolsænkende lægemidler. Ugeskrift for Læger 1994; 156: 329.

  15. Ravnskov U. Ukritisk referat af kolesterolartikler.Ugeskrift for Læger 1994; 156: 4479.

  16. Ravnskov U. Livet forkortes når kolesterolet sænkes. Ugeskrift for Læger 1993; 155: 3678-3679.

  17. Ravnskov U. Tveksamheter om kolesterol. Suomen Lääkarilehti 1993; 48: 1063-1064.

  18. Ravnskov U. Flera tveksamheter om kolesterol. Suomen Lääkarilehti 1993; 48: 1716-1717.

  19. Ravnskov U. Tvivlsomme råd om kolesterolscreening hos børn. Ugeskrift for Læger 1993; 155: 1886-1887.

  20. Ravnskov U. Nya tongånger från USA. Kolesterolkampanjen ifrågasättas. Läkartidningen 1993; 90: 2528-2529.

  21. Ravnskov U. Stoppa kolesterolkampanjen! Läkartidningen 1993; 90: 4587-4588.

  22. Ravnskov U. Kolesteroli. Helsinki: Art House, 1992 (Finnish translation of Kolesterolmyten); ISBN 951-884-078-4. 

  23. Ravnskov U. Hvad er det rigtige svar i kolesteroldebatten? Ugeskrift for Læger 1992; 154: 1716

  24. Ravnskov U. Kolesterol och hälsa: En titt under mattan. Livsmedelsteknik1992; 4: 7-8.

  25. Ravnskov U. Är fleromättat fett nyttigt? Läkartidningen 1991; 88: 1058.

  26. Ravnskov U. Kolesterolmyten. Månedsskrift for praktisk Lægegerning 1991; 70: 131-138.

  27. Ravnskov U. Kolesterolmyten (The Cholesterol Myth). Stockholm: Streifferts, 1991; ISBN 91-7886-085-7.

Papers on the Post-Myocardial-Infarction Syndrome

  1. Ravnskov U. Steroidbehandling av Dresslers syndrom? Läkartidningen 1978; 75: 768.Ravnskov U. Fluctuating pericardial effusion. New England Journal of Medicine 1969; 281: 854.

  2. Ravnskov U. Aneurysm of the heart and the post-myocardial-infarction. Acta Medica Scandinavica  1968; 183: 393-395.

  3. Ravnskov U. Fall av PMI-syndrom. Läkartidningen 1967; 64: 436-438.

Other Publications 

  1. Ravnskov U. Beredskap mot forskningsfusk. Läkartidningen 1993; 90: 2116.

  2. Ravnskov U. Benskörhet kan vara iatrogen - skona äggstockarna! Läkartidningen 1993; 90: 3844.

  3. Ravnskov U. Kinesisk Mädchenfanger-metod bästa sättet att reponera en handledsfraktur? Läkartidningen 1989; 86: 3068-3069.

  4. Ravnskov U. Patientförsäkringen och Larssons arm. Läkartidningen 1989; 86: 3901-2.

  5. Ravnskov U. Accusation of fraud. The Lancet 1988; i: 539.

  6. Ravnskov U. Försäkringskassan, sparkniven och AIDS. Läkartidningen 1988; 85: 4583.

  7. Eksmyr R, Fex G, Jagell S, Johansson BG, Ravnskov U, Samuelsson G. Low molecular weight proteinuria and slight hyperlipoproteinemia in three mentally retarded brothers. Acta Pædiatrica Scandinavica 65, 521-525, 1976.

  8. Svensson L, Ravnskov U. α1-microglobulin, a new low molecular weight plasma protein. Clinica Chimica Acta 1976; 73: 415-422.

  9. Ekman R, Johansson BG, Ravnskov U. Gel chromatography on Sephadex gels with narrow particle size distribution obtained by dry elutriation. Analytical Biochemistry 1976; 70: 628-631.

  10. Ravnskov U. Uremic polyneuropathic motor paralysis and immobilization hypercalcemia. Scandinavian Journal of Urology and Nephrology 1973; 7: 63-67.

  11. Hegedüs V, Ravnskov U. Cortical volume in apparently normal kidneys. Scandinavian Journal of Urology and Nephrology  1972; 6: 159-165.

Newspaper Articles 

  1. Ravnskov U. Många är njursjuka i onödan. DN-debatt. Dagens Nyheter 11. april 1999

  2. Ravnskov U. Kritisk medicinjournalistik – finns det? Journalisten 29/30, 23-29 oktober 1997.

  3. Ravnskov U. Ingen risk med fett. DN-debatt. Dagens Nyheter 7. juli 1997

  4. Ravnskov U. Ny hjärtmedicin kan ge cancer. DN-debatt. Dagens Nyheter 22. april 1997

  5. Ravnskov U. Har Stakeberg och Redfors läst boken? Elfsborgs Läns Allehanda 28 feb 1992.

  6. Ravnskov U. Logik och kolesterol. Sundsvalls Tidning 2. maj 1992.

  7. Ravnskov U. Fortsat kolesterolgalskab. Information 26/6 1992

  8. Ravnskov U. Goddag kolesterol - økseskaft. Information 17/6 1992.

  9. Ravnskov U. Fedtkampanjen - humor eller kvaksalveri? Information 25/5 1992.

  10. Ravnskov U. Overlæge Færgeman ude at sejle. Jyllandsposten Oktober 1992.

  11. Ravnskov U. Kolesterolhypotesen pulveriseret. Jyllandsposten. Oktober 1992.

  12. Ravnskov U. Fats suffer from 'selective' research. Bulletin of the National Renderers Association Oct-Dec. 8, 1992.

  13. Ravnskov U. De äter världens fetaste mat - utan att få hjärtinfarkt. Land 12. juli 1991

  14. Ravnskov U. Kolesterol är ofarligt. DN-debatt. Dagens Nyheter 2. feb 1990.

  15. Ravnskov U. Kuren värre än sjukdomen. Sydsvenska Dagbladet 29. jan. 1984.

Humourous Stuff

  1. Ravnskov U. Högt blodtryck. Läkartidningen 1995; 92: 1296.

  2. Ravnskov U. Rosor för mullvadar. Sydsvenska Dagbladet Juli 1991.

  3. Ravnskov U. Gatfloran kremeras. Sydsvenska Dagbladet 4/7 1990.

  4. Ravnskov U. Don Quijotes hämnd. Läkartidningen. 1990; 87: 344.

  5. Ravnskov U. Häxdoktorn. Läkartidningen 1990; 87: 912.

  6. Ravnskov U. Ett (osakligt?) inlägg i kolesteroldebatten. Läkartidningen 1990; 87: 555.

  7. Ravnskov U. Intressekonflikt. Läkartidningen 1989; 86.