Defect in Urinary Acidification in Nephrotic Syndrome and Its Correction by Furosemide

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Abstract
6 children with idiopathic nephrotic syndrome were investigated during clinical relapse to examine the interrelation between distal urinary acidification and urinary sodium excretion. Blood and urine studies were initiated 4 h after completion of ammonium chloride loading, prior to and following the intravenous administration of furosemide. Values for plasma bicarbonate before and after furosemide administration were not significantly different. In the control periods, when urinary sodium excretion was very low, a defect in urinary acidification was demonstrated (UpH : 6.09 ± (SD) 0.27; UTAV and UNHV: 12.6 ± 3.1 and 36.4 ± 15.8 µmol/min/1.73 m2, respectively.) Following furosemide-induced natriuresis UpHfell to 4.81 ± 0.25 (p < 0.0005), and UTA2V and UNH4V increased to 46.3 ± 15.8 and 125.6 ± 49.5 µmol/min/1.73 m2, respectively (p < 0.002). No overall correlation existed between urinary acidity, both considered as hydrogen ion concentration and as hydrogen ion excretion, and rate of urinary sodium excretion; but significant correlations were present between hydrogen ion concentration in the urine and both UC1V-UNaV (r = 0.38, p < 0.05), and UC1V – (UNaV + UkV) (r = 0.64, p < 0.01). These results indicate that the defect in distal urinary acidification observed in nephrotic syndrome is probably due to decreased delivery of sodium to the distal nephron. The enhanced secretion of hydrogen ion observed after furosemide administration may be related both to increased sodium delivery and to greater sodium than chloride reabsorption in the collecting duct.

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