Renal tubular dysfunction in transplanted kidneys.
We studied 15 renal transplant recipients for evidence of tubular dysfunction. Eight patients were hypophosphatemic, and two had systemic acidosis with a urinary acidification defect. Mild aminoaciduria and bicarbonaturia were present in four and 14 patients, respectively. Elevated parathyroid hormone level was found in only one patient. Tubular reabsorption of phosphorus was depressed in all eight hypophosphatemic patients, while no such abnormalities were observed in 14 control subjects. Defective tubular reabsorption of phosphorus was the most striking abnormality. None of the parameters studied, including immunosuppressant therapy, parathyroid hormone levels, creatinine clearance, or acid-base balance, clearly account for the pathogenesis of this abnormality.
D000138:Acidosis / Q000209:etiology; D000293:Adolescent; D000305:Adrenal Cortex Hormones / Q000627:therapeutic use; D000328:Adult; D006801:Humans; D007674:Kidney Diseases / Q000209:etiology / Q000503:physiopathology; D016030:Kidney Transplantation; D007684:Kidney Tubules / Q000378:metabolism / Q000503:physiopathology*; D008875:Middle Aged; D010281:Parathyroid Hormone / Q000097:blood; D010758:Phosphorus / Q000097:blood / Q000378:metabolism; D011183:Postoperative Complications; D014184:Transplantation, Homologous
D000305:Adrenal Cortex Hormones; D010281:Parathyroid Hormone; D010758:Phosphorus