Abstract: PUB162
Severe Hyperphosphatemia in a Kidney Transplant Patient
Session Information
Category: Fluid, Electrolytes, and Acid-Base Disorders
- 1102 Fluid, Electrolyte, and Acid-Base Disorders: Clinical
Authors
- Ojike, Nwakile, Robert Wood Johnson University Hospital, New Brunswick, New Jersey, United States
- Shah, Mital, Robert Wood Johnson University Hospital, New Brunswick, New Jersey, United States
- Mondal, Zahidul H., Robert Wood Johnson University Hospital, New Brunswick, New Jersey, United States
Introduction
Hyperphosphatemia is rare complication of successful kidney transplant patients.
Case Description
A 54 y/o female with a past medical history of End stage renal disease secondary to IgA nephropathy, hypertension, deceased donor kidney transplant 1 year prior, hypophosphatemia who presented to the hospital with decreasing urine output and weight gain. She had been seen at our institution outpatient clinic 6 weeks ago for routine visit, where her serum phosphorus was 2.7. She was taking a combined sodium-phosphorus-potassium pill for low phosphorus levels for the past 2 months. Initial evaluation showed that she was afebrile, not hypoxic, not tachycardic, hypertensive with systolic blood pressure 160-185 mmHg. Initial laboratory results showed low sodium 132 mmol/L, elevated potassium 5.2 mmol/L, elevated blood urea nitrogen at 61 mg/Dl, SCr 5.3 mg/dL, Ca 7.4 mg/dL, and phosphorus 16.9 mg/dL, parathyroid hormone 198 pg/dL. Urinalysis had mild proteinuria and 6 white blood cells per high-power field, with a urine protein to creatinine ratio of 0.8 g/g. Doppler ultrasound of the transplant kidney showed increased echogenicity, and elevated restive indices, no hydronephrosis. Kidney biopsy showed acute tubular injury with calcium deposition in the tubules, no evidence of antibody mediated rejection or T cell mediated rejection. With phosphate binders and one (1) dialysis session, phosphorus level improved to normal level
Discussion
Post renal transplant occurs frequently die to high parathyroid hormone levels leading to abnormal renal phosphate dumping. In case, patient was initially hypophosphatemic, treated with phosphate supplements, and later became severely hyperphosphatemic. The mechanism of the elevated phosphate level was likely due to phosphate intake. Treatment of severe hyperphosphatemia requires saline infusion, phosphate binders and hemodialysis if symptomatic. This case show the importance of close follow-up in post-transplant patients with hypophosphatemia who are taking phosphorus supplements