Abstract: FR-PO644
Hyperphosphatemia in a Patient with Mucormycosis and AKI
Session Information
- Fluid and Electrolytes: Clinical - Acid-Base, Magnesium, Calcium, Phosphorus
November 08, 2019 | Location: Exhibit Hall, Walter E. Washington Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Fluid and Electrolytes
- 902 Fluid and Electrolytes: Clinical
Authors
- Konanur venkataram, Raghu, Olive View-UCLA Medical Center, Los Angeles, California, United States
- Bader, Nada M., Olive View-UCLA Medical Center, Los Angeles, California, United States
- Pham, Jimmy T.H., Olive View-UCLA Medical Center, Los Angeles, California, United States
- Pham, Phuong-Thu T., UCLA Medical Center, Los Angeles, California, United States
- Pham, Phuong-Chi T., Olive View-UCLA Medical Center, Los Angeles, California, United States
Introduction
Hyperphosphatemia may arise from ingestion, extracellular shifts (e.g. cell death or alterations in acid-base status), bone resorption, hormonal dysregulations leading to reduced renal excretion, and/or poor kidney function. Pseudohyperphosphatemia has been well-described but may be under-recognized and/or not commonly seen in clinical practice.
Case Description
A 35-year-old 7-week-pregnant woman with type 1 diabetes mellitus was admitted for mucormycosis involving the clivus and cervical vertebrae. On day 1, she was initiated on liposomal amphotericin (10mg/kg) with normal saline support. On day 4, sulfamethoxazole/trimethoprim and ampicillin/sulbactam were added for methicillin-sensitive Staphylococcal Aureus and Prevotella Buccae from her fungating mass. On day 6, patient was noted to have acute kidney injury (AKI) when her creatinine increased from 0.4-0.5 mg/dL to 1.25 mg/dL. Nephrology was consulted for AKI and concurrent multiple electrolyte abnormalities. See Table for laboratory findings. Chart review was notable for a hypotensive episode when her blood pressure dropped from a baseline of 100/80 mmHg to 79/50 mmHg over 4 hours. Physical exam was unremarkable. Primary team replaced her potassium and magnesium and started sevelamer carbonate 2400 mg tidac.
Discussion
While the etiologies of AKI, hypokalemia, and hypomagnesemia were straightforward, hyperphosphatemia was out of proportion to the degree of AKI.
A full investigation for contributing factors of hyperphosphatemia other than AKI revealed that she had pseudohyperphosphatemia due to liposomal amphotericin. Methods for measuring Pi may differ among commonly used clinical analyzers, where some may read the organic phosphate contained in the lipid bilayer of the liposomes as Pi. Repeat phosphorus level on a different analyzer revealed a level of 5.8 mg/dL. Erroneous treatment of pseudohyperphosphatemia would have been detrimental in current case.
Laboratory findings
| Liposomal amphotericin | Creatinine (mg/dL) | Potassium (meq/L) | Magnesium (mg/dL) | Calcium (mg/dL)/Albumin (g/dL) | Phosphorus (mg/dL) | Alkaline phosphatase (IU/L) |
| Day 1 | 0.4 | 3.8 | 1.9 | 8.5/3.0 | 2.6 | 278 |
| Day 4 | 0.5 | 3.1 | 1.3 | 8.0/2.0 | 5.0 | 245 |
| Day 6 | 1.25 | 2.7 | 1.2 | 7.8/2.5 | 6.0 | 396 |
| Day 10 | 1.46 | 3.9 (after repletion) | 1.9 (after repletion) | 8.1/2.3 | 10.7 |
Others: Parathyroid hormone 26 pg/ml, vitamin D, 25-OH 33 pg/mL, lactate dehydrogenase 106 U/L, creatine phosphokinase 21 U/L, urinalysis was without protein, blood, or cellular casts.