BACKGROUND: Elevated serum uric acid experimentally stimulates renal vasoconstriction and activation of the renin- angiotensin system and consequently modulates erythropoietin (EPO) production. We used a dopamine-induced glomerular filtration response test (DIR) to assess whether elevated uric acid is associated with dopamine response and EPO levels in IgA patients. METHODS: In 46 non-nephrotic IgA patients (age: 33.7 ± 8.9 years) and 15 controls (age: 33.5 ± 6.9 years) with a glomerular filtration rate of 86.7 ± 17.4 and 118.1 ± 17.2 ml/min, respectively, renal vascular function was estimated based on DIR. DIR was measured using two 120-min creatinine clearances (before and after i.v. administration of 2 μg/kg/min dopamine) and at the same points EPO was measured. Uric acid, cholesterol, triglycerides, urinary uric acid and N-acetyl-β-D-glucosaminidase were measured. RESULTS: Basal EPO was the same in IgA patients and controls (13.5 ± 9.5 vs. 10.6 ± 4.3 mU/ml, respectively; NS); however, EPO correlated with uric acid clearance in IgA patients but not in controls (r = 0.45, p < 0.002 vs. r = 0.25, p < 0.361, respectively), and DIR tended to be lower in IgA nephropathy (p < 0.06). A more pronounced slope between EPO and DIR as well as lower DIR/EPO was found in IgA patients. CONCLUSIONS: These results are consistent with greater renal vasoconstriction in IgA nephropathy that would stimulate EPO and reduce urate clearance.
BACKGROUND: Elevated serum uric acid experimentally stimulates renal vasoconstriction and activation of the renin- angiotensin system and consequently modulates erythropoietin (EPO) production. We used a dopamine-induced glomerular filtration response test (DIR) to assess whether elevated uric acid is associated with dopamine response and EPO levels in IgA patients. METHODS: In 46 non-nephrotic IgA patients (age: 33.7 ± 8.9 years) and 15 controls (age: 33.5 ± 6.9 years) with a glomerular filtration rate of 86.7 ± 17.4 and 118.1 ± 17.2 ml/min, respectively, renal vascular function was estimated based on DIR. DIR was measured using two 120-min creatinine clearances (before and after i.v. administration of 2 μg/kg/min dopamine) and at the same points EPO was measured. Uric acid, cholesterol, triglycerides, urinary uric acid and N-acetyl-β-D-glucosaminidase were measured. RESULTS: Basal EPO was the same in IgA patients and controls (13.5 ± 9.5 vs. 10.6 ± 4.3 mU/ml, respectively; NS); however, EPO correlated with uric acid clearance in IgA patients but not in controls (r = 0.45, p < 0.002 vs. r = 0.25, p < 0.361, respectively), and DIR tended to be lower in IgA nephropathy (p < 0.06). A more pronounced slope between EPO and DIR as well as lower DIR/EPO was found in IgA patients. CONCLUSIONS: These results are consistent with greater renal vasoconstriction in IgA nephropathy that would stimulate EPO and reduce urate clearance.