An Unusual Dietary Cause of Hyperphosphatemia and Hypocalcemia Mimicking Tumor Lysis Syndrome
- Fluid, Electrolyte, Acid-Base Disorders: Clinical - II
November 04, 2023 | Location: Exhibit Hall, Pennsylvania 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
- Kwon, Alvin G., Cleveland Clinic, Cleveland, Ohio, United States
- Baker, Melissa, Cleveland Clinic, Cleveland, Ohio, United States
- Sawaf, Hanny, Cleveland Clinic, Cleveland, Ohio, United States
In healthy individuals, high dietary phosphate intake is rarely emphasized since there is no correlation proven between phosphate intake and serum inorganic phosphate concentration. Hyperphosphatemia has a variety of etiologies other than traditionally focused cellular shifts. High phosphorus could cause more acute kidney injury (AKI) events and acute phosphate nephropathy can cause AKI in rare cases. Additionally, COVID-19 infection can alter the physiology of phosphate regulation and the severity of AKI. Here we present a patient with COVID-19 infection and sudden onset severe hyperphosphatemia and hypocalcemia in the setting of AKI who was revealed to have a substantial dietary intake of phosphate that improved with the improvement of AKI.
The patient is a 52-year-old male who presented with shock in the setting of COVID-19 pneumonia. Further laboratory tests found that he had severe hyperphosphatemia (10.0 mg/dL), hypocalcemia (6.5 mg/dL), and AKI with a serum creatinine that peaked at 8.53 mg/dL. Ionized calcium was also low at 0.96 mmol/L and his uric acid level was elevated at 11.1 mg/dL. These electrolyte derangements initially raised concern for tumor lysis syndrome (TLS). However, there was no evidence of malignancy on physical examination or imaging. It was noted after further history taking that the patient drank 2 liters of soft drinks daily. This unusual diet in the setting of severe AKI likely led to hypocalcemia. The patient’s renal function improved with the improvement of his shock. The resolution of the patient’s AKI also normalized his hyperphosphatemia and hypocalcemia.
In the setting of AKI, dysregulation of the phosphate transporter may interfere with phosphate balance. Although hyperphosphatemia is commonly seen in patients with severe AKI, a dietary cause of severe hyperphosphatemia leading to hypocalcemia is not well recognized. This patient’s phosphate intake through soda alone was 300-400 mg a day and phosphorous from food additives is absorbed at a much higher rate than natural sources. This intake likely precipitated a sudden hyperphosphatemia in the setting of the patient’s AKI which resulted in hypocalcemia, mimicking TLS. Further studies investigating hyperphosphatemia being the cause of hypocalcemia in instances other than TLS should be followed.