Renal handling of lysozyme in experimental Fanconi syndrome.
The relationship between lysozyme and sodium reabsorption by the kidney tubule was studied in the experimental Fanconi syndrome. Female, anesthetized Sprague-Dawley rats were injected intravenously with maleic acid (an inhibitor of sodium transport) neutralized with sodium hydroxide in doses of either 2 or 8 mmol/kg. Clearance studies were performed immediately afterward, and plasma and urine were analyzed for inulin, pH, sodium, glucose, and lysozyme. Two hours after the maleic acid injection, renal cortical tissue was removed and homogenized. Specific activity of Na-K-ATPase was assayed in the light microsomal fraction. The results showed that both concentrations of maleic acid caused significant increases in urinary volume, glucose excretion, and pH. There were significantly correlated decreases in TNafract and TLyfract. The slope of the regression line (TLyfract = 1.03 TNafract - 5.82; r = 0.92) approximated unity. Renal cortical Na-K-ATPase activity was significantly decreased by 25% in the animals receiving 2 mmol maleic acid and 43% in the animals receiving 8 mmol. The evidence suggests that lysozyme reabsorption in the proximal tubule might be mediated directly or indirectly by active tubular transport of sodium, a process that is related to the Na-K-ATPase transport system.
D000251:Adenosine Triphosphatases / Q000037:antagonists & inhibitors / Q000378:metabolism; D000818:Animals; D001693:Biological Transport, Active / Q000187:drug effects; D005198:Fanconi Syndrome / Q000378:metabolism*; D005260:Female; D007672:Kidney Cortex / Q000378:metabolism; D007687:Kidney Tubules, Proximal / Q000378:metabolism*; D008274:Magnesium / Q000378:metabolism; D008298:Maleates / Q000494:pharmacology; D009113:Muramidase / Q000378:metabolism*; D011188:Potassium / Q000378:metabolism; D051381:Rats; D012964:Sodium / Q000378:metabolism
D008298:Maleates; D012964:Sodium; D009113:Muramidase; D000251:Adenosine Triphosphatases; D008274:Magnesium; D011188:Potassium