NITRIC-OXIDE IN IGA NEPHROPATHY PATIENTS WITH OR WITHOUT HYPERTENSION

Nitric oxide (NO) is claimed to have a role in the pathogenesis of imm une-mediated glomerulonephritis and in the regulation of blood pressur e (BP). NO rapidly converts to NO2-/NO3- which is excreted in the urin e. 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 c ontrols (999.1 +/- 66.8 vs. 1,051.2 +/- 53.0 mu mol/day). The urinary excretion of NO2-/NO3- in IgA NP patients whose mean diastolic BP rema ined above 85 mm Hg in spite of antihypertensive therapy, was signific antly decreased (n = 8; 734.38 +/- 87.83 mu mol/day; p < 0.05). There was a significant inverse correlation between mean diastolic BP and ur inary 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 ther e was no difference between the urinary NO2-/NO3- excretion of IgA NP patients and controls argues against the idea that NO production in im mune-mediated IgA NP can be increased. The decrease of urinary NO2-/NO 3- in hypertensive and in older IgA NP patients may be correlated with the impaired NO production of the endothelium.