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An elevated serum uric acid (UA) causes kidney damage: evidence for a novel crystal independent mechanism
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An elevated serum uric acid (UA) causes kidney damage: evidence for a novel crystal independent mechanism
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Journal Article
An elevated serum uric acid (UA) causes kidney damage: evidence for a novel crystal independent mechanism
2000
Overview
Controversy exists over whether an elevated UA is a true cardiovascular risk factor. We hypothesized that the known association between an elevated UA and increased renal vasoconstriction was causal and not secondary. Rats were placed on a low sodium (0.05%) diet with oxonic acid to block endogenous uricase (OA rats); control rats received a low sodium diet alone (LS). OA rats developed modest hyperuricemia (4.0 vs 1.5 mg/dl) and maintained normal renal function (CrCl) at 7 wks. Renal histology showed no crystal deposition; however, mild tubulointerstitial fibrosis was present, with an increase in markers of tubular injury (osteopontin), macrophage infiltration, and collagen III deposition. LS rats maintained normal histology. To better understand the pathogenesis, we examined several vasoactive mediators, and found that OA treated rats had significantly less NOS1 expression in the macula densa, a decrease in medullary NOS3 expression, and an increase in renin staining than LS controls. As these changes are similar to what is observed with cyclosporine (CSA) administration, we examined the effect of an elevated UA in experimental CSA nephropathy. CSA-OA treated rats had an increase in UA compared to CSA alone (5.9 vs 3.2 mg/dl) and significantly worse renal histology at 7 weeks, in terms of tubular damage (osteopontin), macrophages and collagen III deposition. No crystals were demonstrated in the kidneys. CSA rats were similar to OA alone rats with respect to effects on NOS1, NOS3 and renin; however, CSA-OA rats showed greater decreases in NOS1 and NOS3 and a greater increase in renin. Thus, an elevated UA directly causes renal injury through a crystal-independent mechanism that involves alterations in nitric oxide and renin levels; this has significant implications on the role of uric acid in cardiovascular disease, hypertension, and renal disease.
Publisher
Elsevier Inc,Oxford University Press
Subject
