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Epithelioid cell granulomas within the renal interstitium are frequently found in drug-associated acute interstitial nephritis. Their presence is a strong argument in favour of an immunologically mediated nephropathy especially when extrarenal symptoms are absent and if the interstitial infiltrate does not contain eosinophils. They are probably due to a delayed hypersensitivity reaction. Unfortunately, there is no reliable experimental model. The high incidence of permanent renal damage observed in this type of nephritis indicates an early corticosteroid therapy, particularly when renal function does not rapidly improve after withdrawal of the offending drug.

Most glomerulopathies are immunologically-mediated. Their pathogenesis is now better understood. The role of cell-mediated immunity has recently been envisaged. The role of circulating antibodies now seems to be more important than that of circulating immune complexes. Antibodies may recognize structural or "planted" antigens in the kidney, the latter being non-renal molecules that may bind renal structures for non-immune reasons. The linear or granular pattern observed at immunofluorescence depends upon the regular or irregular distribution of the antigen. In susceptible individuals, various toxins (heavy metals such as mercury or gold, drugs with an SH group, non-steroidal anti-inflammatory agents) may induce an immune glomerulopathy. It has recently been shown that Brown-Norway rats exposed to one of the above-mentioned agents develop anti-self class II T lymphocytes that are responsible for a polyclonal activation of B cells. Among the various autoantibodies that are produced, some have a nephritogenic potential. Other drugs are responsible for glomerular lesions due to a direct toxic effect of the compound. Doxorubicin induces a nephrotic syndrome in the rabbit, while mitomycin induces a haemolytic uraemic syndrome in humans. Finally, drug addiction often leads to glomerulosclerosis.