Effects of allopurinol on gouty and non-gouty uric acid nephropathy.

The kidneys are probably the only vital organs that are commonly affected by the precipitation of uric acid in patients with gout. Microscopic crystals of uric acid can sometimes be demonstrated in the collecting tubules, along with macros^opic concretions or calculi in the medulla and pelvis (Lichtenstein, Scott, and Levin, 1956; Talbott and Terplan, 1960; Gonick, Rubini, Gleason, and Sommers, 1965). Deposits of urate in the renal parenchyma may lead to a granulomatous reaction with foreign body giant cells and accumulations of chronic inflammatory cells, comparable to tophaceous lesions in other sites and obliterating the normal architecture. These are the more specific lesions of gouty nephropathy. Less specific, but perhaps more common, are the secondary changes affecting the renal parenchyma, generally regarded as indistinguishable from chronic nephritis, nephrosclerosis, or pyelonephritis. Progressive impairment of renal function with proteinuria and hypertension may reach an incidence of 25 per cent. or more. However, it is the vascular complications of atherosclerosis rather than renal insufficiency that account for the greatest mortality in gout. More dramatic than these chronic renal changes is the acute uric acid nephropathy which frequently complicates myeloproliferative disorders during oncolytic therapy (Kritzler, 1958; Greenbaum and Stone, 1959; Frei, Bentzel, Reiselbach, and Block, 1963). Such cases are usually accompanied by an acute hyperuricaemia, resulting in the flooding of the urinary tract with excessive amounts of uric acid and giving rise to varying degrees of renal tubular obstruction or even complete urinary suppression, sometimes requiring haemodialysis (R.eiselbach, Bentzel, Cotlove, Frei, and Freireich, 1964). The present report concerns observations on