Drug-induced nephrotic syndrome

Many drugs may produce a syndrome closely resembling spontaneous systemic lupus erythematosus (SLE). Those most commonly implicated are hydrallazine, isoniazid, and procainamide. Drugs less commonly implicated include the following. Antimicrobials-sulphonamides, penicillins, tetracycline, strepto-`mycin, and para-amino salicylic acid; Antithyroid drugs-methylthiouracil and propylthiouracil; Anticonvulsants-phenytoin, methoin, primidone, troxidone, and ethosuximide; Antihypertensives reserpine and methyldopa; Oral contraceptives; Miscellaneous drugs-griseofulvin, phenylbutazone, and practolol. The mechanism of drug-induced SLE is not clear, but genetic predisposition may be important. Hydrallazine, isoniazid, and some sulphonamides are metabolised by acetylation in the liver. The rate of acetylation by the enzyme acetyltransferase is genetically controlled; some people are "slow" acetylators and others "fast." Druginduced SLE develops more commonly in phenotypically slow acetylators of hydrallazine and antinuclear factor is more commonly found in slow acetylators of isoniazid. Clinically, renal involvement is usually less common in the druginduced as opposed to the spontaneous form of SLE. About twothirds of patients with spontaneous SLE have renal disease, but the incidence falls to about 20% in hydrallazine-induced SLE and to about 2 % in procainamide-induced SLE. Drug-induced SLE may be reversible on withdrawal of the drug, but this is not always so.