Abstract: SA-PO0616
Obinutuzumab-Induced Acute Hypophosphatemia in Phospholipase A2 Receptor (PLA2R)-Positive Membranous Nephropathy
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
- Nemalidinne, Krishna Vani, University of Arkansas System, Little Rock, Arkansas, United States
- Vanteru, Abinay Siva kumar Reddy, University of Arkansas System, Little Rock, Arkansas, United States
- Alzghoul, Husam Mohammad, University of Arkansas System, Little Rock, Arkansas, United States
- Mahmoud, Saad Abdulrahim Talal, University of Arkansas System, Little Rock, Arkansas, United States
- Alqurini, Nadia Mustafa, University of Arkansas System, Little Rock, Arkansas, United States
Introduction
Obinutuzumab, a type II anti-CD20 monoclonal antibody, is increasingly used for membranous nephropathy (MN) refractory to rituximab. We describe a 42-year-old man with PLA2R-positive MN who developed abrupt, severe hypophosphatemia within 24 hours of a single 1-g dose of obinutuzumab.
Case Description
A 42-year-old man with biopsy-proven PLA2R-positive MN previously treated with rituximab without achieving partial or complete remission and was maintained on cyclosporine due to financial reasons. He presented with worsening nephrotic-range proteinuria and progressive chronic kidney disease after two years. Initial labs: creatinine: 2.9 mg/dl (baseline creatinine of ~1.7 mg/dL), 24-hour urine protein: 6.9 gms, sodium: 135 meq/l, potassium: 4.4 meq/l, bicarbonate: 18 meq/l, corrected calcium: 9.5 meq/l, phosphorus: 4.3 meq/l, serum albumin: 2.4 gm/dl, Anti-PLA2R Antibody titer: 8, and lisinopril and cyclosporine were held. we administered obinutuzumab 1000 mg intravenously.
The infusion was tolerated with mild chills and body aches. Within 24 hours, he developed muscle cramps and serum phosphorus decreased from 4.3 mg/dL to 1.0 mg/dL, confirmed on repeat testing at 1.7 mg/dL. Random urine phosphate was <5 mg/dL, indicating appropriate renal phosphate conservation. There was no evidence of gastrointestinal loss, insulin administration, respiratory alkalosis, refeeding syndrome, or tumor lysis syndrome. Creatine kinase was normal. Symptoms improved after intravenous sodium phosphate replacement.
At 5-month follow-up, proteinuria improved to 2.5 g/day and creatinine stabilized near 2.7 mg/dL without recurrent adverse effects.
Discussion
Hypophosphatemia has been described with obinutuzumab-based oncology regimens, although usually confounded by tumor lysis syndrome or concomitant chemotherapy. In this patient, absent renal phosphate wasting and lack of gastrointestinal losses suggest an acute intracellular phosphate shift temporally related to obinutuzumab infusion.
To our knowledge, this is the first reported case of isolated severe hypophosphatemia following obinutuzumab in PLA2R-positive MN. Clinicians should consider monitoring serum phosphate after obinutuzumab infusion in high-risk patients.