Summary
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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) |
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section: What to do?