Pathophysiology of human proximal tubular transport defects.
The generalized proximal tubular transport abnormalities comprising the Fanconi syndrome (glycosuria, generalized aminoaciduria, the proximal form of renal tubular acidosis, and increased renal clearance of phosphate, urate, calcium, magnesium, and potassium) may be ascribed to interference with "sodiumlinked" active transport. Evidence is presented that the majority of conditions known to cause Fanconi syndrome in man or experimental animals are associated with inhibitors of the renal Na-K-ATPase-ATP transport system.
D000255:Adenosine Triphosphate / Q000378:metabolism; D000328:Adult; D000818:Animals; D004195:Disease Models, Animal; D005198:Fanconi Syndrome / Q000188:drug therapy / Q000209:etiology / Q000503:physiopathology; D005260:Female; D006801:Humans; D008274:Magnesium / Q000627:therapeutic use; D011188:Potassium / Q000627:therapeutic use; D051381:Rats; D015499:Renal Tubular Transport, Inborn Errors / Q000150:complications*; D012964:Sodium / Q000378:metabolism; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism; D014807:Vitamin D / Q000627:therapeutic use
D014807:Vitamin D; D000255:Adenosine Triphosphate; D012964:Sodium; D000254:Sodium-Potassium-Exchanging ATPase; D008274:Magnesium; D011188:Potassium