Abstract: SA-PO476
A Case Report on Unusual Idiopathic Central Diabetes Insipidus During the Polyuric Phase of AKI
Session Information
- Fluid, Electrolyte, and Acid-Base Disorders: Case Reports
November 05, 2022 | Location: Exhibit Hall, Orange County Convention Center‚ West Building
Abstract Time: 10:00 AM - 12:00 PM
Category: Fluid‚ Electrolyte‚ and Acid-Base Disorders
- 1002 Fluid‚ Electrolyte‚ and Acid-Base Disorders: Clinical
Authors
- Elhawary, Omar Nabil, SUNY Downstate Health Sciences University, New York City, New York, United States
- Bukhari, Syeda Sadia, SUNY Downstate Health Sciences University, New York City, New York, United States
- Puri, Isha, SUNY Downstate Health Sciences University, New York City, New York, United States
- Mallappallil, Mary C., SUNY Downstate Health Sciences University, New York City, New York, United States
- Agarwal, Sonalika, SUNY Downstate Health Sciences University, New York City, New York, United States
Group or Team Name
- Nephrology KCH
Introduction
Historically, classic Acute tubular injury (ATN) goes through an oliguric phase with urine output (UOP) ≤ 400 mL/24 hours for 1–2 weeks followed by a non-oliguric phase with UOP > 400 mL/24 hours for 10–14 days with eventual recovery of the kidney functions. Central diabetes insipidus (CDI) is caused by impairment in either the synthesis, transport, or release of antidiuretic hormone (ADH). Clinically, the patient with CDI presents with volume depletion, polyuria, and elevated serum sodium. We usually tend to consider polyuria following AKI as polyuric phase until proven otherwise. In our case the patient had diabetes insipidus that improved with desmopressin, so measuring the urine and serum osmolality in patients developing polyuria post ATN should be considered.
Case Description
75 y/o man with medical history of hypertension was admitted for encaphalopathy and hypoxemia. He was found to have anuric ATN secondary to volume depletion complicated with hyperkalemia. The patient was treated with aggressive hydration and electrolyte repletion. A week later he was hemodynamically stable, kidney functions improved without dialysis. As expected, he developed polyuria but surprisingly there was progressive increase in serum sodium despite aggressive free water replacement via the nasogastric tube and intravenous hypotonic fluids. We ordered urine and serum osmolality and serum Na. Labs were significant for serum Na 170, Serum osmolality 363 mOsm/kg, urine osmolality 203 mOsm/kg, therefore diabetes insipidus was highly suspected. Primary polydipsia was ruled out as patient was not conscious enough to drink water by himself. Subcutaneous desmopressin 2 mcg was administered. Diagnosis of CDI was confirmed since urine osmolality doubled at the end of 2 hours. He was started on desmopressin nasal spray and serum Na was checked twice daily. Serum Na improved from 170 to 144. MRI brain did not show pituitary/hypothalamic lesion. Additional diagnostic work up for CDI could not be performed as the patient passed away few days later.
Discussion
In cases with Acute Kidney Injury that present with persistent hypernatremia during polyuric phase, other causes should be considered. They should be screened for Diabetes Insipidus by measuring both serum and urine osmolality and a trial of desmopressin can be given if required.