Abstract: PO1428
A Case of Central Diabetes Insipidus due to Pituitary Adenoma Complicated by Amphotericin-Induced Nephrogenic Diabetes Insipidus
Session Information
- Fluid, Electrolyte, and Acid-Base Disorders: Clinical - 1
October 22, 2020 | Location: On-Demand
Abstract Time: 10:00 AM - 12:00 PM
Category: Trainee Case Report
- 902 Fluid, Electrolyte, and Acid-Base Disorders: Clinical
Authors
- Sambharia, Meenakshi, University of Iowa, Iowa City, Iowa, United States
- Noureddine, Lama A., University of Iowa, Iowa City, Iowa, United States
Introduction
Amphotericin B (Amph B) is an anti-fungal agent that exhibits its action by binding to ergosterol, the main component of the fungal cell wall and shares a similar structure to the human cell membrane. Its main site of action is the principal cell where it causes an increase in membrane permeability by insertion of pores into the membrane, causing leaking of potassium into tubular lumen leading to hypokalemia. It also causes nephrogenic diabetes insipidus (NDI) by preventing insertion of vasopressin-induced aquaporin 2 (AQP-2). Reports in the literature have suggested that liposomal formulations might be less nephrotoxic than conventional ones.
Case Description
A 37-year-old male with history of pituitary adenoma s/p trans-sphenoidal resection of pituitary tumor with subsequent central diabetes insipidus (CDI) on maintenance desmopressin DDAVP 1mcg BID presented to hospital for suspected meningitis. He was started on liposomal Amph B 5mg/kg (550mg) for empiric fungal coverage. Lumbar drain cultures returned positive for Candida albicans on Hospital Day (HD) 1 and Amph B was continued. Renal was consulted for evaluation of worsening polyuria. Increased dose of DDAVP was recommended. He continued to be polyuric despite this dose adjustment. Amph B induced NDI was suspected secondary to refractory polyuria and hypokalemia. Amph B was discontinued on HD 7, after which his polyuria improved gradually. He was switched to fluconazole to complete the remainder of the treatment duration.
Discussion
Our patient with h/o CDI developed worsening polyuria on Amph B treatment, unresponsive to escalating DDAVP. Improvement with cessation of Amph B supports causality of concurrent drug-induced NDI. Amph B renal toxicity frequently presents with AKI with potassium wasting. NDI induced by Amph B is rare. A high index of suspicion is required for diagnosis of NDI occuring on top of CDI. Early discontinuation of Amph B usually leads to resolution of symptoms.
Hospital Day(HD) | Urine Osm (mOsm/kg) | Urine Output(L/day) | Ampho-B |
1 | 118 | 3.8 | started |
5 | 191 | 14.7 | continued |
7 | 471 | 8.6 | discontinued |
14 | 590 | 3.8 |