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Abstract: TH-PO824

Acute Phosphate Nephropathy: A Preventable Cause of AKI Among Kidney Transplant Recipients

Session Information

Category: Transplantation

  • 2102 Transplantation: Clinical


  • Orejo, Johanna Marie Sedicos, Boston Medical Center, Boston, Massachusetts, United States
  • Ghai, Sandeep, Boston Medical Center, Boston, Massachusetts, United States
  • Francis, Jean M., Boston Medical Center, Boston, Massachusetts, United States
  • Solomon, Melinda K., Boston Medical Center, Boston, Massachusetts, United States

Acute Kidney Injury (AKI) after a kidney transplant is an extreme emergency. It is associated with allograft loss and increased morbidity. Prompt recognition of reversible causes of AKI is important to prevent graft loss. We present a case of a kidney transplant patient who developed AKI secondary to acute phosphate nephropathy.

Case Description

A 37-year-old male with end-stage renal disease secondary to hypertension underwent a deceased donor kidney transplant. His pre-operative laboratory results include calcium of 8.2 mg/dl, phosphorus of 6.6 mg/dl, PTH of 855 pg/ml, and 25-hydroxyvitamin D of 18.6 ng/ml. His phosphate binder Sevelamer was discontinued after the transplant. He had an immediate graft function and an uncomplicated post-operative course. He was discharged on hospital day 4 with a creatinine of 1.1 mg/dl and phosphorus of 2 mg/dl. His immunosuppressants include Tacrolimus 7 mg twice daily, Myfrotic 720mg twice daily, and Prednisone 5mg daily. On follow-up, his blood work showed stable renal function but worsening hypophosphatemia of 1.4 mg/dl. He was initiated on oral phosphate supplementation. Two weeks later, he has a progressive worsening of AKI with creatinine trending up to 3 mg/dl. Due to concern for acute rejection, a kidney biopsy was performed which showed acute tubular injury with focal tubular necrosis, focal tubular subepithelial tubular calcium phosphate deposition, and calcium phosphate casts. There was no evidence of T-cell or Anti-body mediated rejection. Phosphate supplementation was discontinued which subsequently improved the patient’s allograft function with his creatinine reaching a nadir of 1.8 mg/dl 3 months later.


Hypophosphatemia is commonly seen after kidney transplantation. This case highlights that acute phosphate nephropathy secondary to oral phosphate repletion may cause AKI among kidney transplant patients. Nephrologists should be vigilant in managing hypophosphatemia following a kidney transplant. Unless hypophosphatemia is life-threatening, we recommend conservative management including high dietary phosphate intake. Oral phosphate supplementation should only be considered in patients who are symptomatic with persistent severe hypophosphatemia and once a patient is initiated, careful monitoring of serum phosphate level and kidney function is recommended.