Nitric oxide in IgA nephropathy patients with or without hypertension.

Nitric oxide (NO) is claimed to have a role in the pathogenesis of immune-mediated glomerulonephritis and in the regulation of blood pressure (BP). NO rapidly converts to NO2-/NO3- which is excreted in the urine. We determined the daily NO2-/NO3- excretion in 26 IgA nephropathy (NP) patients and 20 healthy controls, recording the BP in each. There was no difference in NO2-/NO3- excretion between IgA NP patients and controls (999.1 +/- 66.8 vs. 1,051.2 +/- 53.0 mumol/day). The urinary excretion of NO2-/NO3- in IgA NP patients whose mean diastolic BP remained above 85 mm Hg in spite of antihypertensive therapy, was significantly decreased (n = 8; 734.38 +/- 87.83 mumol/day; p < 0.05). There was a significant inverse correlation between mean diastolic BP and urinary NO2-/NO3- (p < 0.006). NO2-/NO3- excretion decreased with aging (p < 0.01) in IgA NP patients, but not in controls. The fact that there was no difference between the urinary NO2-/NO3- excretion of IgA NP patients and controls argues against the idea that NO production in immune-mediated IgA NP can be increased. The decrease of urinary NO2-/NO3- in hypertensive and in older IgA NP patients may be correlated with the impaired NO production of the endothelium.