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      Hyperuricemic Nephropathies


      S. Karger AG

      Hyperuricemia, Urate, Nephropathy, Renal failure

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          This review explores the relationship between uric acid or urate and the pathogenesis of renal impairment. The following points and conclusions are emphasized: (1) uric acid is an end product of purine degradation in humans and normally depends upon renal excretion for the majority of its elimination from the body; (2) massive urate overproduction – usually occurring acutely because of tumor lysis, rhabdomyolysis, or some other cause of rapid nucleic acid turnover or tissue destruction – tends to cause acute renal failure because of an increase of intratubular uric acid precipitation and obstruction; (3) chronic urate overproduction (with increased urate excretion) is more likely to be associated with stones or gout than with acute renal failure; (4) chronic asymptomatic hyperuricemia is unlikely to cause renal disease, gout, or stones, but is associated with cardiovascular impairment over the long term, and (5) asymptomatic hyperuricemia may serve as an indicator of renal vascular disease, or, to the extent that it may reflect insulin-induced acceleration of renal tubule urate reabsorption, hyperuricemia may serve as an indicator of insulin resistance. Therefore chronic asymptomatic hyperuricemia may predict the adverse cardiovascular consequences of insulin resistance.

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          Effect of insulin on renal sodium and uric acid handling in essential hypertension.

          In normal subjects, insulin decreases the urinary excretion of sodium, potassium, and uric acid. We tested whether these renal effects of insulin are altered in insulin resistant hypertension. In 37 patients with essential hypertension, we measured the changes in urinary excretion of sodium, potassium, and uric acid in response to physiological euglycemic hyperinsulinemia (by using the insulin clamp technique at an insulin infusion rate of 6 pmol/min/kg). Glucose disposal rate averaged 26.6 +/- 1.5 mumol/min/kg, i.e., 20% lower than in normotensive controls (33.1 +/- 2.1 mumol/min/kg, P = .015) In the basal state, fasting plasma uric acid concentrations were higher in men than women (P < .001), were positively related to body mass index (r = 0.38, P = .02), waist/hip ratio (r = 0.35, P < .05), and serum triglyceride levels (r = 0.59, P = .0001), and negatively related to HDL cholesterol concentrations (r = -0.59, P = .0001) and glucose disposal rate (r = 0.42, P < .01). Uric acid clearance, on the other hand, was inversely related to body mass index (r = 0.41, P = .01), plasma uric acid (r = 0.65, P < .0001) and triglyceride concentrations (r = 0.39, P < .02), and directly related to HDL cholesterol levels (r = 0.52, P < .001). During insulin infusion, blood pressure, plasma uric acid and sodium concentration, and creatinine clearance did not change. In contrast, hyperinsulinemia caused a significant decrease in the urinary excretion of uric acid (2.67 +/- 0.12 to 1.86 +/- .14 mumol/min/1.73 m2, P = .0001), sodium (184 +/- 12 to 137 +/- 14 mumol/min/1.73 m2, P = .0001), and potassium (81 +/- 7 to 48 +/- 4 mumol/ min/1.73 m2, P = .0001). Both in absolute terms (clearance and fractional excretion rates) and percentagewise, these changes were similar to those found in normotensive subjects. Insulin-induced changes in urate excretion were coupled (r = 0.55, P < .0001) to the respective changes in sodium excretion. In hypertensive patients, higher uric acid levels and lower renal urate clearance rates cluster with insulin resistance and dyslipidemia. Despite insulin resistance of glucose metabolism, acute physiological hyperinsulinemia causes normal antinatriuresis, antikaliuresis, and antiuricosuria in these patients.
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            Serum uric acid. Its relationship to coronary heart disease risk factors and cardiovascular disease, Evans County, Georgia.

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              Correlates and consequences of asymptomatic hyperuricemia

               W. Fessel (1973)

                Author and article information

                S. Karger AG
                December 1998
                24 December 1998
                : 81
                : Suppl 1
                : 45-49
                University of Wisconsin, Madison, Wisc., USA
                46298 Nephron 1999;81(suppl 1):45–49
                © 1998 S. Karger AG, Basel

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                Page count
                References: 42, Pages: 5
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                Cardiovascular Medicine, Nephrology

                Renal failure, Nephropathy, Urate, Hyperuricemia


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