Abstract: SA-PO531
Hypercalcemia-Associated AKI and Nephrogenic Diabetes Insipidus in the Hospital Setting: A Cohort Study
Session Information
- Acid-Base, Calcium, Potassium, and Magnesium Disorders: Clinical
October 26, 2024 | Location: Exhibit Hall, 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
- Suman, Fnu, Ochsner Health, New Orleans, Louisiana, United States
- Velez, Juan Carlos Q., Ochsner Health, New Orleans, Louisiana, United States
Group or Team Name
- Ochsner Group.
Background
Hypercalcemia (hyperCa) can cause acute kidney injury (AKI) through a variety of mechanisms
that include renal vasoconstriction, a loop diuretic-like effect, nephrogenic diabetes insipidus, and
nephrocalcinosis. Although these clinical associations are well-recognized, their incidence and interrelationship
are sparsely reported. We examined the rate of AKI and hypernatremia (hyperNa) during episodes of hyperCa
in hospitalized patients.
Methods
A retrospective review of medical records was conducted searching for inpatient adults with hyperCa
at Ochsner Medical Center over a 1-year period. Hypercalcemia was defined as serum calcium (sCa) > 11.0
mg/dL. Etiology of hyperCa was determined based on history and available laboratory and imaging data. We
examined the rate of AKI (by KDIGO) registered during the hyperCa event, as well as the rate of hyperNa.
Patients with end-stage kidney disease or kidney transplant were excluded.
Results
A total of 102 patients with in-hospital hypercalcemia were included. Median age was 72, 35%
women, 48% White, 29% Black. Etiology of hyperCa was malignancy in 58 (57%) (multiple myeloma,
metastatic bone disease, PTH-related peptide production, or 1,25-vitamin D), exogenous calcium or vitamin D
supplements in 29 (28%), thiazide in 3 (3%), sarcoidosis in 3 (3%), and immobilization in 9 (9%). Median peak
sCa was 12.1 (11.2-17.8) mg/dL. Corrected sCa was available in 65%, with a median of 12.8 (11.7-15.4)
mg/dL. High ionized Ca was verified in 36%. AKI was present in 14 (14%). Hypernatremia was present in 8
(8%). The most severe case of hyperNa had a serum Na 168 mEq/L and a urine osmolality of 110 mOsm/kg,
suggesting nephrogenic diabetes insipidus. The second most severe case of hyperNa had a serum Na 150
mEq/L and a urine osmolality of 603 mOsm/kg, suggesting absence of ongoing water losses. Urine osmolality
was not measured in the remaining 6 hyperNa cases. Concomitant AKI and hyperNa only occurred in 2 (2%).
Conclusion
AKI occurred in 1 in 7 cases of hyperCa, whereas hyperNa occurred in 1 in 12 cases. Urine
osmolality is seldom obtained in cases of hyperNa. Because hyperNa was only present in 2/14 (14%) of AKI
cases, the primary mechanism of AKI in hyperCa may not relate to nephrogenic diabetes insipidus. Further
investigation is warranted.