THE NEPHROPATHY OF GOUT

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Abstract
"Gouty nephritis" has long been known to exist, but has been considered a complication. Its true incidence and significance have not been fully realized. Careful study reveals that the metabolic error in gout produces not only arthritis but also, almost as frequently, kidney disease. The classification of gout as an arthritis rather than as kidney disease is due to the fact that the joint pains are outspoken even in mild cases. In contrast, the renal manifestations are usually insidious and silent until far advanced. The nephropathy of gout is quite variable in mode of onset and in extent and type of involvement This is illustrated by 3 cases. The first case was admitted with chronic gouty arthritis and advanced renal failure. One year prior he had had a right nephrectomy for massive calculus formation and complete renal destruction. Urate crystallization in tubules, calyses and pelvis of the right kidney had led to a staghorn calculus, internal obstruction, pyelonephriis, pyonephro-sis and eventually non-function. Three weeks after admission compensated renal function returned, presumably due to control of infection and/or relief of temporary internal renal obstruction by medical means. The 2d case demonstrated renal colic preceding joint manifestations. Here renal damage has been steadily progressive for years hand in hand with moderate chronic arthritis. After 25 years renal failure appeared in the absence of definite subjective symptoms. A careful regimen including continuous Benemid therapy, appears to have temporarily halted the destruction of renal tissue. The 3d case in unique in that both parents had gout His symptoms are due to almost continuous production of uric acid gravel. Joint pains are minor and atypical of gout, but in view of the genetic taint and response to therapy, a presumptive diagnosis of gout appears indicated. A Benemid plus alkali regimen may prevent calculus formation and renal damage. The metabolic error in gout results in overproduction of urates which overwhelms the renal excretory mechanisms and produces elevated blood and glomerular filtrate uric acid levels. The poorly soluble salts precipitate in many sites, especially the kidney. The renal tubules are the earliest, most frequent and often most severely affected of the parenchyma. The nephropathy of gout is divided into primary and secondary types. Under prim ary nephropathy are grouped the direct effects of uric acid crystallization, such as tubular blockage and necrosis, tophi formation with inflammatory and foreign body reactions and calculi in tubules and pelvis. The secondary nephropathies are sequelae such as pyelonephritis, hydronephrosis, pyonephrosis and arteriolarsclerosis. Recent work with isotopically labelled uric acid has shown that urate deposits may be mobilized by therapy with probenecid. It is felt that the renal lesions may be improved or held static by continuous probenecid therapy. At the first sign of nephropathy, patients should be "desalted" of urates by this method.