Refractory rickets caused by mild distal renal tubular acidosis.
10.6065/apem.2013.18.3.152
- Author:
Ji Ho LEE
1
;
Joo Hyun PARK
;
Tae Sun HA
;
Heon Seok HAN
Author Information
1. Department of Pediatrics, Chungbuk National University College of Medicine, Cheongju, Korea. hshan@chungbuk.ac.kr
- Publication Type:Case Report
- Keywords:
Distal renal tubular acidosis;
Rickets;
Nephrocalcinosis
- MeSH:
Acidosis;
Acidosis, Renal Tubular*;
Bicarbonates;
Bone Resorption;
Dehydration;
Failure to Thrive;
Follow-Up Studies;
Humans;
Hydrogen-Ion Concentration;
Hypercalciuria;
Kidney Tubules, Distal;
Nephrocalcinosis;
Protons;
Quaternary Ammonium Compounds;
Rickets*;
Vomiting
- From:Annals of Pediatric Endocrinology & Metabolism
2013;18(3):152-155
- CountryRepublic of Korea
- Language:English
-
Abstract:
Type I (distal) renal tubular acidosis (RTA) is a disorder associated with the failure to excrete hydrogen ions from the distal renal tubule. It is characterized by hyperchloremic metabolic acidosis, an abnormal increase in urine pH, reduced urinary excretion of ammonium and bicarbonate ions, and mild deterioration in renal function. Hypercalciuria is common in distal RTA because of bone resorption, which increases as a buffer against metabolic acidosis. This can result in intractable rickets. We describe a case of distal RTA with nephrocalcinosis during follow-up of rickets in a patient who presented with clinical manifestations of short stature, failure to thrive, recurrent vomiting, dehydration, and irritability.
