THE EFFECT OF pH ON THE FILTRATION, REABSORPTION, AND EXCRETION OF PROTEIN BY THE RAT KIDNEY*

Abstract

Urinary protein excretion and acid-base imbalances were studied in adult male rats drinking a 15% glucose in water solution to which 0.5% (NH4)2CO3, 1% NH4Cl, 5% NaHCO3, or 0.04% acetazol-amide was added. In rats on each solution, "protein absorption droplet" formation was studied microscopically in frozen kidney sections 24 hrs. after the intravenous (I-V) injection of 10 mg of T-1824 (Evans blue dye). Compared to the glucose controls (mean protein excretion 0.40 mg/hr.; droplet formation moderate) no significant difference in acid-base balance, proteinuria, or droplet formation accompanied (NH4)CO3 feeding. With NH4Cl ingestion, acidosis and aciduria developed, proteinuria rose significantly to 0.75 mg/hr, and droplet formation increased. Increased proximal convoluted tubule (PCT) protein re-absorption during NH4Cl ingestion was suggested by observing that dyed protein replaced undyed protein within PCT cells during continued NH4Cl feeding. Therefore, during NH4Cl ingestion the increased proteinuria apparently was the primary result of increased protein filtration. With NaHCO3 ingestion, alkalosis, alkaluria, and a significantly lowered rate of proteinuria (0.17 mg/hr) were observed; droplet formation was abolished. The observation that NaHCO3, reduced proteinuria in rats with PCT cells damaged by a prior I-V injection of 0.175 mg of uranyl acetate suggested that its action was independent of PCT cell integrity and protein reabsorption. Thus the decrease in proteinuria during NaHCO3 ingestion apparently was the primary result of decreased protein filtration. These results in rats indicate that physiological proteinuria can be influenced by changes produced in acid-base equilibrium with simple acid or alkali overloads and offer an explanation for the randomly recorded observations that a relationship exists between urinary pH and proteinuria in man.