JAMES P. KNOCHEL, M.D.; LARRY N. DOTIN, M. D.; RICHARD J. HAMBURGER
Twenty-two men were studied serially to examine the possible mechanism of acute renal failure during intense physical training in hot climates. By day eleven, hyperuricemia was prevalent and uric acid excretion rose, suggesting overproduction. Creatinuria, abnormal serum creatine Phosphokinase activity, and depressed serum calcium and elevated serum phosphorus concentrations suggested muscle injury and occurred with maximal muscle tenderness. In hot weather, urine volumes were smaller and contained higher concentrations of uric acid. As these abnormalities improved, glomerular filtration rate and extracellular volume rose to levels clearly above normal. These results suggest that muscle injury caused overproduction of uric acid and that hyperuricemia and uricosuria may play a role in heat stress nephropathy. The rarity of heat stress nephropathy in trained men under comparable conditions might be the result of resistance to muscle injury, decreased uric acid production, expansion of extracellular volume, and supercompensation of glomerular filtration rate.
KNOCHEL JP, DOTIN LN, HAMBURGER RJ. Heat Stress, Exercise, and Muscle Injury: Effects on Urate Metabolism and Renal Function. Ann Intern Med. 1974;81:321–328. doi: 10.7326/0003-4819-81-3-321
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Published: Ann Intern Med. 1974;81(3):321-328.
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