Abstract: PO1879
Double Hit: A Case of Chromogranin A-Mediated Proximal Tubulopathy That Progressed to Full-Blown Fanconi Syndrome After Treatment with Everolimus
Session Information
- Cancer and Kidney Diseases: Nephrotoxins, RCC, and More
November 04, 2021 | Location: On-Demand, Virtual Only
Abstract Time: 10:00 AM - 12:00 PM
Category: Onco-Nephrology
- 1500 Onco-Nephrology
Authors
- Polani, Adnann Salim, Baylor College of Medicine, Houston, Texas, United States
- Workeneh, Biruh, The University of Texas MD Anderson Cancer Center, Houston, Texas, United States
Introduction
Hypophosphatemia is an independent risk factor for poor patient outcomes. We present a rare case of hypophosphatemia from a complication of a neuroendocrine tumor (NET) and the treatment for it.
Case Description
A 54-year-old female with metastatic NET presented with dyspnea. Patient had Pneumonia which was treated but a comprehensive electrolyte panel revealed profound hypophosphatemia (phosphorous levels < 1mg /dl). Initial suspicion was that poor nutritional status may be the underlying etiology, however despite aggressive intravenous phosphate supplementation, the hypophosphatemia was resistant. Workup revealed obvious evidence of Fanconi syndrome. Patient had profound glucosuria with normal serum glucose. 24 hours urine phosphorous excretion was markedly elevated at 900 mg. Vitamin D level was borderline low but activated (1,25-vitamin D) levels were markedly low at 1.8 pg/ml. PTH levels were only mildly elevated at 120 pg/ml. A deeper investigation into her course found that patient was diagnosed with a NET 8 months prior to this presentation and had evidence of mild glucosuria with mild-moderate hypophosphatemia at that time. Chromogranin A levels from her NET were substantially elevated at that time. Serial urine analyses during the course of her disease were reviewed, and it was evident that the glucosuria became markedly worse after the patient was started on everolimus therapy. We concluded that hypophosphatemia in this patient is from chromogranin A mediated proximal tubulopathy that developed to full blown Fanconi Syndrome after everolimus. We changed phosphorous supplementation to oral only and recommended holding everolimus provided it was appropriate from an oncological standpoint. Follow up of the patient in 4 weeks off everolimus showed continued improvement in phosphorous levels.
Discussion
Both chromogranin-A and mtor inhibitors have shown to cause acute tubular injury in proximal tubules.
Our case is unique in the sense that it presented as severe hypophosphatemia from Fanconi syndrome secondary to two uncommon culprit agents that acted in a sequential manner to worsen the proximal tubulopathy. Based on this case we recommend that in NET patients with high chromogranin A levels, we check for signs of proximal tubulopathy before starting mtor inhibitor therapy.