Abstract: SA-PO0590
Turns Out You Can Fix Renal Tubular Acidosis with a Scalpel
Session Information
- Fluid, Electrolyte, and Acid-Base Disorders: Case Reports - 2
October 24, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Fluid, Electrolytes, and Acid-Base Disorders
- 1102 Fluid, Electrolyte, and Acid-Base Disorders: Clinical
Authors
- Evans, Neil Asn, UC Davis Health, Sacramento, California, United States
- Beck, Natalie M., UC Davis Health, Sacramento, California, United States
Introduction
Type 1 distal renal tubular acidosis (dRTA) involves impaired H+ secretion, causing hyperchloremic non-anion gap metabolic acidosis (NAGMA). Primary hyperparathyroidism (PHPT) is an under-recognized, potentially reversible trigger for dRTA. We report a case of symptomatic NAGMA definitively treated with parathyroidectomy.
Case Description
A young, previously healthy female presented with NAGMA, fatigue, muscle aches, and brain fog. Labs showed serum bicarbonate ranging 18-21 mmol/L, anion gap of 10-12, serum albumin 4.3 – 4.5 g/dL and normal renal function. Metabolic acidosis was confirmed with venous blood gas. Distal RTA was suspected due to positive urine anion gap on two occasions (14 and 42) while serum bicarbonate was 20 mmol/L. The patient never took supplemental alkali throughout testing. Other workup included negative SSA and SSB antibodies, normal kappa/lambda ratio and no paraproteinemia on serum electrophoresis. The patient then developed hypercalcemia ranging 10.2 to 10.9 mg/dL and hypophosphatemia at 2.3 mg/dL. Parathyroid hormone (PTH) was elevated at 76 pg/mL and 25-hydroxy vitamin D was 25 ng/mL. A 24-hour urine collection showed pH 6.37, phosphorous 1353 mg (ref 600-1200 mg/24hr) and calcium 252 mg (ref <200 mg/24hr). A renal ultrasound showed bilateral nephrolithiasis. A 4D-CT suggested a parathyroid adenoma, a right upper parathyroidectomy was performed, and pathology confirmed a hypercellular parathyroid gland. Post-parathyroidectomy, the PTH and calcium normalized and the metabolic acidosis resolved. The patient reported resolution of prior constitutional symptoms.
Discussion
The proposed mechanism of dRTA due to PHPT is hypercalciuria causing medullary nephrocalcinosis and structural damage to α-intercalated cells of the collecting duct, disrupting the H+-ATPase functionality which is required for H+ secretion. Our case suggests a functional defect transiently decreasing the apical H+-ATPase activity prior to parathyroidectomy, in the absence of overt radiographic nephrocalcinosis. Additionally, in the proximal tubule, PTH also exerts several effects which inhibit proximal bicarbonate reabsorption that cannot be compensated for in the distal nephron. Hypophosphatemia from hyperparathyroidism can also independently impair proximal tubular bicarbonate reabsorption through ATP depletion. This case illustrates the physiology that can cause a reversible dRTA following surgical cure of PHPT.