Abstract: FR-PO487
Amlodipine-Induced Chylous Ascites in a Patient on Peritoneal Dialysis
Session Information
- Home Dialysis - 1
October 25, 2024 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Dialysis
- 802 Dialysis: Home Dialysis and Peritoneal Dialysis
Authors
- Yockey, Oliver Patrick, Corewell Health Southwest Michigan, Saint Joseph, Michigan, United States
- Kwon, Katherine Westin, Lake Michigan Nephrology, Saint Joseph, Michigan, United States
- Heeringa, Zachary K., Michigan State University College of Osteopathic Medicine, East Lansing, Michigan, United States
Introduction
Chylous ascites (CA) is the appearance of milky, lipid rich peritoneal fluid, often associated with portal hypertension, lymphatic obstruction, congenital abnormalities, infections, or post-operative complications. Previous studies have proposed that a triglyceride content of >187mg/dL confers a 95% specificity. CA has been associated with use of medications, including dihydropyridine (DHP) calcium channel blockers (CCBs). In this case we discuss the presentation of a peritoneal dialysis (PD) patient with amlodipine induced CA that resolved expeditiously on discontinuation of CCB.
Case Description
A 66-year-old man with history of end stage kidney disease secondary to uncontrolled hypertension presented to the hospital with milky, white PD fluid after request by his dialysis team. He was admitted three weeks prior for bacterial peritonitis and was completing a course of intraperitoneal ceftriaxone and vancomycin. CT abdomen and pelvis imaging at the first admission was negative for masses or abscesses. The etiology of his peritonitis was thought to be related to severe constipation with bacterial translocation, however, cultures remained negative. On this admission he was asymptomatic and vitals were unremarkable. Physical exam revealed a distended abdomen without tenderness; the PD site was without erythema or drainage. PD fluid showed 68 nucleated-cells/µL. Fungal culture, AFB culture and smear were negative. The PD fluid triglyceride level was 322mg/dL, consistent with CA. Antibiotics were continued. Review of the literature revealed case reports of other DHP CCB’s causing CA; therefore, amlodipine was suspected and discontinued in hospital. He was discharged the next day. On a follow up two days later, his PD fluid was noted to be entirely clear, without a milky appearance.
Discussion
Previous research has established other DHP CCB’s in the formation of CA in PD patients. However, despite widespread use of amlodipine as an anti-hypertensive, it accounts for one documented case of CCB-induced CA. Our case further implicates amlodipine as a rare etiology of CA. Furthermore, cessation of amlodipine led to rapid resolution, similar to other documented CCB-induced CA. This is the first report we have identified where CA developed months following CCB initiation; it is imperative that a careful review of medications be performed in patients with CA of unknown etiology.