Related Experiment Videos
Defect in urinary acidification in nephrotic syndrome and its correction by furosemide
Insights
Children with nephrotic syndrome exhibit impaired distal urinary acidification, especially when sodium excretion is low. Furosemide administration revealed enhanced hydrogen ion secretion, suggesting reduced sodium delivery to the distal nephron.
Area of Science:
- Pediatric Nephrology
- Renal Physiology
Background:
- Idiopathic nephrotic syndrome (INS) in children can affect renal function.
- Disturbances in acid-base balance and sodium handling are observed in INS.
Purpose of the Study:
- To investigate the relationship between distal urinary acidification and urinary sodium excretion in children with INS during relapse.
- To explore the impact of furosemide on these parameters.
Main Methods:
- Studied 6 children with INS during clinical relapse.
- Administered ammonium chloride loading followed by furosemide.
- Measured plasma bicarbonate, urinary pH (UPH), and urinary ammonium/hydrogen ion excretion (UTAV, UNH4V) before and after furosemide.
Main Results:
- A defect in urinary acidification was observed during low sodium excretion.
- Furosemide induced natriuresis, significantly decreasing UPH and increasing UTAV and UNH4V.
- No overall correlation between urinary acidity and sodium excretion, but significant correlations with specific ion transport.
Conclusions:
- The observed defect in distal urinary acidification in INS is likely due to reduced sodium delivery to the distal nephron.
- Enhanced hydrogen ion secretion post-furosemide may relate to increased sodium delivery and altered reabsorption in the collecting duct.
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 UNH4V: 12.6 +/- 3.1 and 36.4 +/- 15.8 mumol/min/1.73 m2, respectively.) Following furosemide-induced natriuresis UPH fell to 4.81 +/- 0.25 (p less than 0.0005), and UTA2V and UNH4V increased to 46.3 +/- 15.8 and 125.6 +/- 49.5 mumol/min/1.73 m2, respectively (p less than 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 less than 0.05), and UC1V - (UNaV + UKV) (r = 0.64, p less than 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.