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. 2008;28(3):391-6.
doi: 10.1159/000112271. Epub 2007 Dec 7.

Uric acid excretion and dopamine-induced glomerular filtration response in patients with IgA glomerulonephritis

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Uric acid excretion and dopamine-induced glomerular filtration response in patients with IgA glomerulonephritis

Beata Sulikowska et al. Am J Nephrol. 2008.

Abstract

Background/aim: It is unknown to what extent uric acid (UA) may affect vessel function and participate in tubulointerstitial damage. We examined the relationship between intrarenal vessel function and serum UA and its excretion in association with urinary N-acetyl-beta-D-glucosaminidase (NAG).

Methods: In 50 IgA patients (mean age 34.7 +/- 9.3 years) and 15 controls (mean age 33.5 +/- 6.9 years) with a creatinine clearance of 99.4 +/- 21.6 and 118.1 +/- 17.2 ml/min, respectively, the renal vascular function was estimated based on the dopamine-induced glomerular filtration response (DIR; see text). The DIR was measured using two 120-min creatinine clearance values (before and after intravenous administration of 2 g/kg/min dopamine). Serum UA, triglycerides and cholesterol and urinary NAG (24 h) and protein and UA excretion were measured.

Results: Patients with IgA nephropathy versus controls: DIR 8.80 +/- 6.6 vs. 12.83% (p < 0.01), NAG 7.25 +/- 3.30 vs. 4.69 +/- 1.12 U/g creatinine (p < 0.01), and fractional UA excretion 7.80 +/- 2.20 versus 6.29 +/- 1.80% (p < 0.01). A negative correlation between DIR and NAG was found; regression analysis showed a more prominent relationship in the patients (NAG = 9.99 - 0.29x DIR) than in the controls (NAG = 5.50 - 0.06x DIR). UA and urate excretion and NAG in the patients correlated with DIR (r = -0.39, p < 0.02; r = -0.29, p < 0.04, and r = 0.59, p < 0.001, respectively). Multivariate analysis showed an association of DIR (R(2) = 0.39) with NAG but not with proteinuria and UA and UA excretion; the NAG excretion (R(2) = 0.56) correlated significantly with UA and DIR.

Conclusion: It is suggested that UA plays a role, associated with tubular dysfunction, in the regulation of intrarenal vessel function.

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