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Kidney Week

Abstract: PO0277

Too Much of a Good Thing: A Case Report of Suspected Acute Tubular Necrosis Potentiated by Hypervitaminosis D

Session Information

Category: Acute Kidney Injury

  • 102 AKI: Clinical, Outcomes, and Trials

Authors

  • Benavente, Kevin V., Marian University College of Osteopathic Medicine, Indianapolis, Indiana, United States
  • Peesapati, Meghna Priyanka, Marian University College of Osteopathic Medicine, Indianapolis, Indiana, United States
  • Knox, Mark, Hilo Medical Center, Hilo, Hawaii, United States
Introduction

While Vitamin D deficiency is prevalent in the United States, vitamin D toxicity remains a rare pathology. More novel is the incidence of acute kidney injury facilitated by calcitriol toxicity, with a Pubmed search yielding less than twenty results, a majority of which come from foregin journals. Tubular injury propagated by calcitriol has been demonstrated both in vivo, and from biopsies in even fewer case reports.

Case Description

A middle age man presented to the ED after routine labs demonstrated an acute kidney injury approximately four times his baseline creatinine, with mildly elevated hypercalcemia. Creatinine was within normal limits 1 year prior. Workup for his hypercalcemia revealed a markedly elevated 25 vitamin D >480, exceeding the quantifiable limit of the lab equipment. The patient reported a two week history of vitamin D supplementation of approximately 210,000 IU daily. Even with stabilization of his hypercalcemia, fluid resuscitation, and cessation of his supplements, the patient did not recover his baseline kidney function at discharge, nor at follow-up three months later. The patient had no medical history predisposing him to chronic kidney disease, with labs non-contributory for any other nephritic or nephrotic process, but suggesting an intrinsic, tubular pathology. With other etiologies essentially ruled out, in the setting of recent consumption of massive amounts of Vitamin D, the diagnosis of ATN secondary to hypervitaminosis D was suspected.

Discussion

Hypercalcemic AKI, at calcium levels as high as 19.9 mg/dL, typically resolves with treatment within 1-2 weeks; this patient failed to resolve, suggesting an additional insult. In calcitriol-induced AKI, toxicity of excess free Vitamin D metabolites exceeds the capacity of neutralizing vitamin D binding proteins. In vitro, calcitriol potentiates ATP depletion, and cytotoxicity of renal tubular cells even in the absence of hypercalcemia. In vivo, excess calcitriol exacerbates cellular azotemia by 2-3 times even with only modest hypercalcemia. Similar case reports describe biopsy evidence of tubular injury caused by vitamin D toxicity, with recovery of baseline creatinine taking between 3 months to 2 years. As incidence of vitamin intoxication increases, vigilance toward the harms of these supplements are important to recognize in healthy patients presenting with AKI.