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Kidney Week

Abstract: PUB035

Hypercalcemia in the Recovery Phase of Pigment-Induced Acute Tubular Necrosis

Session Information

Category: Acute Kidney Injury

  • 102 AKI: Clinical, Outcomes, and Trials

Authors

  • Kumari, Usha, The University of Tennessee Health Science Center, Memphis, Tennessee, United States
  • Maheshwari, Sanjana Kumari, Dow University of Health Sciences, Karachi, Pakistan
  • Raza, Syed Muhammad Mohsin, The University of Tennessee Health Science Center, Memphis, Tennessee, United States
Introduction

Acute tubular necrosis (ATN) is a common intrinsic cause of renal failure. Common etiologies are severe hypovolemia, nephrotoxins, or sepsis. Rhabdomyolysis or skeletal muscle injury leads to pigment induced ATN. Hypercalcemia has been described in cases of rhabdomyolysis. However, in this case, hypercalcemia occurred well after a decline in creatine phosphokinase (CPK) levels, possibly related to post ATN diuresis and prolonged immobility.

Case Description

We describe a case of a 23-year-old Hispanic male with a history of travel through the desert who presented with abdominal discomfort, myalgias, and respiratory distress. He initially developed an oliguric acute kidney injury due to rhabdomyolysis, followed by recovery by the end of the second week, marked by polyuria. He then developed symptoms of nausea and headaches, besides polyuria. Laboratory values showed increasing total calcium, as shown in figure (A) The trend of serum calcium and CPK levels is shown in figure (B). The vitamin D 25-OH level was low, and the parathyroid gland was appropriately suppressed. The electrocardiogram was unremarkable. Hypercalcemia was initially unresponsive to increasing volume replacement and calcitonin. Patients eventually received pamidronate with a gradual decline in calcium to a normal level. The alkaline phosphate was normal initially and peaked at 145 U/L when calcium started to trend down. Hypercalcemia was presumed to be related to dehydration during the polyuric phase of ATN. On the 22nd day of stay, the polyuria and hypercalcemia had resolved, and the patient was discharged. Lab values were normal on the 2-week follow-up post-hospital discharge.

Discussion

ATN is a very common acute illness in hospitalized patients. This case highlights that life-threatening hypercalcemia can present late with a prolonged course in the setting of acute kidney injury. It is crucial to closely monitor patients with ATN following their discharge.