Figure 630

A, Intratubular deposits of uric acid. B, Gouty tophus in the renal medulla. The kidney is the major organ of urate excretion and a primary target organ affected in disorders of its metabolism. Renal lesions result from crystallization of urate in the urinary outflow tract or the renal parenchyma. Depending on the load of urate, one of three lesions result: acute urate nephropathy, uric acid nephrothiasis, or chronic urate nephropathy. Whereas any of these lesions produce tubulointerstitial lesions, it is those of chronic urate nephropathy that account for most cases of chronic TIN.

The principal lesion of chronic urate nephropathy is due to deposition of microtophi of amorphous urate crystals in the inter-stitium, with a surrounding giant-cell reaction. An earlier change, however, probably is due to the precipitation of birefringent uric acid crystals in the collecting tubules, with consequent tubular obstruction, dilatation, atrophy, and interstitial fibrosis. The renal injury in persons who develop lesions has been attributed to

hyperacidity of their urine caused by an inherent abnormality in the ability to produce ammonia. The acidity of urine is important because uric acid is 17 times less soluble than is urate. Therefore, uric acid facilitates precipitation in the distal nephron of persons who do not overproduce uric acid but who have a persistently acidic urine.

The previous notion that chronic renal disease was common in patients with hyperuricemia is now considered doubtful in light of prolonged follow-up studies of renal function in persons with hyperuricemia. Renal dysfunction could be documented only when the serum urate concentration was more than 10 mg/dL in women and more than 13 mg/dL in men for prolonged periods. The deterioration of renal function in persons with hyperuricemia of a lower magnitude has been attributed to the higher than expected occurrence of concurrent hypertension, diabetes mellitus, abnormal lipid metabolism, and nephrosclerosis.

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