Hypertension, mineralocorticoid-resistant hyperkalemia, and hyperchloremic acidosis in an infant with obstructive uropathy.
An 8-week-old infant with hypertension, hyperkalemia, and hyperchloremic acidosis, presumably due to chloride shunt type of distal renal tubular acidosis, is described. The patient's renin-aldosterone axis was intact. The infant was also found to have an obstructed solitary kidney. Despite correction of the obstruction and improvement in the glomerular filtration rate accompanied by normal development, hyperkalemia and renal tubular acidosis persisted. The defect was still demonstrable 9 months following relief of the obstruction. We conclude that neonatal obstructive uropathy can result in renal tubular acidosis of the chloride shunt type. The reversibility of this defect is, as yet, unknown.
D000136:Acid-Base Equilibrium; D000141:Acidosis, Renal Tubular / Q000188:drug therapy / Q000209:etiology*; D000450:Aldosterone / Q000378:metabolism; D002712:Chlorides / Q000097:blood*; D004351:Drug Resistance; D006801:Humans; D006869:Hydronephrosis / Q000150:complications* / Q000378:metabolism / Q000503:physiopathology; D006947:Hyperkalemia / Q000209:etiology*; D006977:Hypertension, Renal / Q000209:etiology*; D007223:Infant; D007668:Kidney / Q000002:abnormalities / Q000503:physiopathology; D008297:Male; D008901:Mineralocorticoids / Q000627:therapeutic use*; D012084:Renin-Angiotensin System
D002712:Chlorides; D008901:Mineralocorticoids; D000450:Aldosterone