Increased ammoniagenesis and the renal tubular effects of potassium depletion.
The cause of the morphological changes and functional defects in the renal tubule seen in patients with severe potassium depletion is unknown. In man and animals potassium status is a major factor regulating ammonia synthesis in the kidney and urinary ammonium excretion. A primary effect of potassium depletion is to cause an increase in ammoniagenesis by the renal tubular cells. It is proposed that the vacuolation of the renal tubular cells and the functional defects of tubular proteinuria, polyuria, resistance to arginine vasopressin, renal resistance to the action of parathyroid hormone, and increased urinary excretion of N-acetyl-beta-glucosaminidase found in potassium depletion are secondary effects caused by high concentrations of ammonia in the renal tubular cells.
D000118:Acetylglucosaminidase / Q000378:metabolism; D000641:Ammonia / Q000378:metabolism* / Q000652:urine; D002478:Cells, Cultured; D004705:Endocytosis; D006801:Humans; D006863:Hydrogen-Ion Concentration; D007684:Kidney Tubules / Q000187:drug effects / Q000378:metabolism*; D008247:Lysosomes / Q000378:metabolism; D011191:Potassium Deficiency / Q000378:metabolism* / Q000652:urine; D011506:Proteins / Q000378:metabolism; D000644:Quaternary Ammonium Compounds / Q000378:metabolism / Q000652:urine; D014617:Vacuoles
D011506:Proteins; D000644:Quaternary Ammonium Compounds; C018589:lysosomal proteins; D000641:Ammonia; D000118:Acetylglucosaminidase