[Analgesic nephropathy]

Abstract

Analgesic nephropathy, its morphology, development and pathogenesis are described. The earliest analgesic-caused lesion is capillary sclerosis of the urinary tract mucosa. Later focal necroses can be found in the papillae surrounding the collecting ducts. Foci of necrosis progress and become confluent, resulting in complete papillary necrosis. Later renal cortical lesions develop due to retained areas of papillary necrosis. The cortical changes include chronic interstitial nephritis with cortical atrophy in the suprapapillary region as well as hypertrophy of the columnae Bertini with segmental, focal glomerulosclerosis. The analgesic-related lesions are the result of toxic damage to endothelial, tubular and interstitial cells. Analgesic-induced kidney and urinary tract changes are quite specific. Frequent complications include hypertension, pyelonephritis, hydro- or pyonephrosis and urinary tract tumors. The clinical picture is characterized by the consequences of distal tubular damage: impairment of urine concentrating capacity, acidosis, electrolyte loss. Analgesic nephropathy is an example of an absolutely preventable drug induced nephropathy. It is the most important single manifestation of the analgesic syndrome. It is recommended that prescriptions for mixed analgesics (multi-component analgesics) should be made obligatory. Monocomponent analgesics could be sold over-the-counter.