Hyperuricemia and renal function

Abstract

Increased serum urate concentration is commonly seen in clinical practice. It does not represent a specific disease, nor is it an indication for therapy. Hyperuricemia can be the consequence of increased uric acid production and/or decreased renal capacity to excrete uric acid. In essential hypertension, it has been described in up to one third of patients and is directly related to an increase in renal vascular resistance and inversely correlated with renal plasma flow. In other words, abnormal renal hemodynamics, commonly seen in the initial stages of the disease, account for the increased serum urate concentration. This can be maintained if a decrease in glomerular filtration rate takes place. The increase in uric acid has been shown to be a potent predictor of the development of cardiovascular events and death. In addition, uric acid, particularly when elevated, could represent an independent risk factor. On the other hand, an altered renal function predicts in an independent manner a higher cardiovascular risk. For this reason, the predictive capacity of uric acid could be partly dependent on the fact that hyperuricemia runs in parallel with a deranged renal function.

Comparing the Effects of Inorganic Nitrate and Allopurinol in Renovascular Complications of Metabolic Syndrome in Rats: Role of Nitric Oxide and Uric Acid

“…Recent epidemiological evidence indicated that hyperuricemia might be a risk factor for renal dysfunction [43,44]. In accordance with the previous studies, the current study showed that fructose resulted in hyperuricemia and attenuated renal function manifested by increase in serum creatinine and urea.…”

“…Although the role of uric acid in the metabolism of triglycerides remains unknown, uric acid might be involved in either the overproduction or the reduction of clearance of triglycerides. A decrease in the clearance of triglycerides in fructose-fed rats has been attributed to a reduction in lipoprotein lipase activity in endothelial cells [44]. An alternative explanation is the possibility that the de novo increase in purine synthesis observed in fructose-fed rats may be pathogenetically linked to hepatic fatty acid synthesis, resulting in overproduction of triglycerides [46].…”

Uric Acid and the Development of Hypertension

“…A population definition of hyperuricemia in men is an SUA Ͼ7.0 mg/dL, whereas a physical chemical definition of hyperuricemia is Ͼ6.5 mg/dL, as serum is supersaturated for monosodium urate at concentrations above this. 22 A SUA level Ͼ7.0 mg/dL (416 mol/L) was associated with a RR for hypertension of 1.36 (95% CI: 1.07 to 1.74) and 1.08 (95% CI: 0.83 to 1.39) in age-adjusted and multivariable-adjusted analyses, respectively. A SUA level Ͼ6.5 mg/dL (387 mol/L) was associated with an RR for hypertension of 1.34 (95% CI: 1.16 to 1.55) and 1.25 (95% CI: 1.08 to 1.45) in age-adjusted and multivariable-adjusted analyses, respectively.…”

Nephroprotective Effects of Berberis Vulgaris L. Total Extract on Lead Acetate-induced Toxicity in Mice

“…PbAC could increase blood urea by more than one mechanism, including enhancement of proteins catabolism, conversion of ammonia to urea by induction of arginase-enzyme synthesis [33] , and inhibition of amino acids incorporation in proteins [34] . The hyperuricemia induced by PbAc treatment might result from over-production and/or reduced renal excretion of uric acid [35] , and elevation of endogenous oxygen species levels [36] . Co-treatment with BV extract inhibited PbAc-induced nephrotoxicity, as indicated by significant restoration of serum creatinine, urea and uric acid.…”