Sodium-lithium countertransport in children with nephrotic syndrome

Abstract

The mechanisms of sodium retention in edema-forming minimal change nephrotic syndrome (MCNS) have not been completely evaluated. The aim of this study was to characterize the transmembrane sodium transport in nephrotic syndrome by measuring the erythrocyte sodium-lithium countertransport (SLC) in vitro. Eighteen children with MCNS were studied in the edema-forming state, and subsequently at the beginning of remission. Nephrotic children with edema retained sodium (10+/-12 micromol/day) and had a higher SLC [426+/-118 vs. 281+/-60 micromol/l red blood cells (RBC) per hour, P=0.003). The intracellular sodium concentration of nephrotics was 6.1+/-2.1 mmol/l RBC, which did not differ from that of controls (6.42+/-2.24, n=13). In remission sodium balance became negative (-30+/-21 mmol/day), and the SLC decreased but still differed significantly from control values (P=0.009). The intracellular sodium content decreased to 4.4+/-0.9 mmol/l RBC (P=0.002). There was a negative correlation between erythrocyte SLC and plasma albumin concentration (r=0.48, P=0.003), and urinary sodium excretion rate (r=0.66, P=0.001). In conclusion, erythrocyte SLC is high in the edema-forming state of childhood nephrotic syndrome and decreases with the onset of remission. A role for the SLC in the altered sodium homeostasis of nephrotic syndrome is suggested.

Role of sodium during formation of edema in children with nephrotic syndrome

“…Results of this study demonstrated the importance of sodium reabsorption in proximal tubuli for the development of edema. Previous studies indicating the impact of sodium reabsorption in proximal tubule on the pathogenesis of NS supported these results 8,28–31 . In healthy individuals, sodium reabsorption also occurs in distal and collecting tubules.…”

“…Previous studies indicating the impact of sodium reabsorption in proximal tubule on the pathogenesis of NS supported these results. 8,[28][29][30][31] In healthy individuals, sodium reabsorption also occurs in distal and collecting tubules. During follow up of cases with edema, resolution of edema without any change in distal K-Na exchange rates has failed to demonstrate any role of sodium reabsorption of the distal tubule on the pathogenesis of edema.…”