Chemical-Induced Nephropathy: A Review of the Renal Tubulointerstitial Lesions in Humans

Abstract

It is almost ironic that one of the major organs that serves to maintain the “internal milieux” by secretion of various toxic agents, can itself become injured in the process. The pattern of morphologic renal injury is nonspecific and can involve any of the components of the kidney, although the injury and subsequent morphologic changes are most commonly noted in the tubules and/or interstitium. Of course, unless the drug/toxin is commonly or regularly noted to be associated with tubular and/or interstitial injury, the association of the drug with the renal changes may be missed and the correlation may not necessarily identify causation. For example, if a drug is associated with a renal injury in a given individual, it may be quite difficult to prove that the drug is the cause of the injury. This scenario is somewhat reminiscent of the test question—is it “true-true-related,” or “true-true-unrelated”? Sometimes it is only by the accrual of a great many examples or correlations, and or dissection of the pathophysiology, can it be shown that the drug is directly related to the observed morphologic (and subsequent clinical) injury. Renal changes induced by chemicals can affect the tubules, interstitium or both. This review of chemically induced nephropathy in humans considers acute tubular necrosis, interstitial nephritis , and tubulointerstitial nephritis or nephropathy. Because the tubules and the interstitium are so intimately related, injury to 1 of these 2 components may eventually lead to injury of the other, resulting in tubulointerstitial disease.