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Abstract: PO0586

Severe Hypercalcemia in a Patient with Acute Lobar Nephronia

Session Information

Category: Bone and Mineral Metabolism

  • 402 Bone and Mineral Metabolism: Clinical

Authors

  • Ilkun, Olesya, University of Utah Health Hospitals and Clinics, Salt Lake City, Utah, United States
  • Gregory, Martin C., University of Utah Health Hospitals and Clinics, Salt Lake City, Utah, United States
  • Cho, Monique E., University of Utah Health Hospitals and Clinics, Salt Lake City, Utah, United States
  • Abraham, Josephine, University of Utah Health Hospitals and Clinics, Salt Lake City, Utah, United States
Introduction

Acute lobar nephronia is a form of focal acute bacterial pyelonephritis without abscess formation or liquefaction.

Case Description

A 62-year-old Native American woman with a childhood history of left nephrectomy and treatment for tuberculosis was admitted for sepsis due to pyelonephritis and pan-sensitive E. coli bacteremia. Her creatinine was 5.2 mg/dL on admission, improved to 3.5 mg/dL with intravenous ceftriaxone, then increased to 4.2 mg/dL after transitioning to oral antibiotics six days later. At the same time, she developed hypercalcemia, which peaked at 13.7 mg/dL (ionized calcium 1.83 mmol/L). PTH was undetectable. Her 1,25-dihydroxy vitamin D (1,25-Vit D) was elevated at 120 pg/mL. The ultrasound showed right kidney hypertrophy to 16.3 x 9.9 x 10.5 cm, but no perinephric abscess or hydronephrosis. MRI abdomen showed wedge-shaped and cortical hyperintense striations through the kidney, the largest measuring 2.3 cm (Figure 1). Imaging showed no osteomyelitis, lytic lesions or suspicious masses. Kappa/lambda ratio was at 0.8 and IFE gel showed a faint band in lambda suggestive of a specific immune response or an early monoclonal protein. QuantiFERON Gold was indeterminate but imaging did not show pulmonary tuberculosis. Seven separate urine samples had negative acid fast stain and culture. Mycobacterium Tuberculosis PCR in urine was negative. She completed a prolonged course of antibiotics and over the six months of follow-up, her serum calcium and albumin normalized, and 1,25-Vit D fell to 16 pg/mL. Her serum creatinine decreased to 2.17 mg/dL. Right kidney size decreased to 9.8 x 5.7 x 5.4 cm and had normal contour and sonographic appearance.

Discussion

Acute hypercalcemia was likely due to a rare pathological activation of 1-alpha-hydroxylase (CYPb27b1) in renal proximal tubule cells due to inflammatory response. Common causes of severe hypercalcemia were ruled out. Supporting this etiology, resolution of hypercalcemia correlated with resolution of renal inflammation.

Figure 1.