Distal renal tubular acidosis in primary hyperparathyroidism

Primary hyperparathyroidism manifests biochemically as a disturbance in serum calcium homeostasis. The kidney appears to be the central organ that sets the serum calcium level. Hyperchloraemia, defective urinary acidification and renal tubular acidosis have been reported to be associated with primar...

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Bibliographic Details
Published in:BMJ case reports 2015-01, Vol.2015, p.bcr2014208120
Main Authors: Lo, Tom Edward Ngo, Tan, Iris Thiele Isip
Format: Article
Language:English
Subjects:
Acidification
Acidosis, Renal Tubular - etiology
Adenoma - complications
Adenoma - surgery
Adult
Asia
Electrolytes
Homeostasis
Humans
Hypercalcemia - etiology
Hypercalciuria - etiology
Hyperparathyroidism, Primary - etiology
Hypokalemia - etiology
Kidney Calculi - etiology
Kidney stones
Kidney Tubules, Distal
Male
Metabolism
Other Asian
Parathyroid Neoplasms - complications
Parathyroid Neoplasms - surgery
Phosphorus
Plasma
Potassium
Thyroid gland
Tumors
Ultrasonic imaging
Unusual Presentation of More Common Disease/Injury
Urinary tract diseases
Urinary tract infections
Urine
Urogenital system
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Summary:Primary hyperparathyroidism manifests biochemically as a disturbance in serum calcium homeostasis. The kidney appears to be the central organ that sets the serum calcium level. Hyperchloraemia, defective urinary acidification and renal tubular acidosis have been reported to be associated with primary hyperparathyroidism. Distal renal tubular acidosis due to primary hyperparathyroidism is rarely reported. Renal tubular dysfunction due to significant hypercalciuria appears to be one of the proposed mechanisms. This case report will highlight a case of primary hyperparathyroidism in a 26-year old Filipino man due to a solitary functioning parathyroid adenoma presenting with recurrent nephrolithiasis leading to distal renal tubular acidosis manifesting with hypokalaemia and hypomagnesaemia. The patient underwent a minimally invasive selective parathyroidectomy that resulted in full reversal of hypercalcaemia and hyperparathyroidism together with the features of distal renal tubular acidosis. He is currently on frequent follow-up for monitoring of electrolyte abnormalities and gradual resolution of nephrocalcinosis.
ISSN:1757-790X
1757-790X
DOI:10.1136/bcr-2014-208120