Drug-Induced Renal Lesions
In the symposium on Drug Effects on the Kidney held in Sidney in 1979, practically all the papers delt with various aspects of nephrotoxicity. To my knowledge, there was not a session dedicated to renal injury related to drug-induced hypersensitivity reactions. The chapters in this section address this topic, a task made very difficult by the ignorance that still persists in this area of nephropathology. During the last decade, but especially during the last 3–4 years, drug-induced hypersensitivity has received increasing attention due to its importance in clinical medicine and the accelerated pace of progress in basic research. There is evidence, based on experimental models, human disease, or both, that the four main mechanisms of hypersensitivity, namely (1) antibody reacting with renal antigens, (2) immune complex formed in situ or in the circulation, (3) cell-mediated hypersensitivity, and (4) immediate IgE-type hypersensitivity, may by activated, independently or synergistically, by drugs and that the kidney may be a target organ.
KeywordsImmune Complex Mercuric Chloride Interstitial Nephritis Tubular Basement Membrane Accelerate Pace
Unable to display preview. Download preview PDF.
- Bariety, J., Druet, P., Laliberte, F., and Sapin, C., 1971, Glomerulonephritis with γ-and β1C-globulin deposits induced in rats by mercuric chloride, Am. J. Pathol. 65:293.Google Scholar
- Palosuo, T., Provost, T. T., and Milgrom, F., 1976, Gold nephropathy: Serologic data suggesting an immune complex disease, Clin. Exp. Immunol. 25:311.Google Scholar
- Roman-Franco, A. A., Turiello, M., Albini, B., Ossi, E., and Andres, G. A., 1976, Anti-basement membrane antibody and immune complexes in rabbits injected with mercuric chloride (HgCl2), Kidney Int. 10:549.Google Scholar
- Sapin, C., Druet, E., and Druet, P., 1977, Induction of anti-glomerular basement membrane antibodies in the Brown-Norway rat by mercuric chloride, Clin. Exp. Immunol. 28:173.Google Scholar
- Tan, E. M., 1974, Drug-induced autoimmune disease, Fed. Proc. 33:1894.Google Scholar