Background: Calcitriol [1,25(OH)2D] plays a central role in endocrine regulation of bone and mineral metabolism. Low 1,25(OH)2D levels in chronic kidney disease (CKD) are associated with increased cardiovascular morbidity and mortality. However, the role of 1,25(OH)2D in acute kidney injury (AKI) is unclear, with very limited data. This pilot study examined the relationship between 1,25(OH)2D levels in critically ill patients with AKI and clinical outcomes.
Methods: Plasma 1,25(OH)2D, intact parathyroid hormone (iPTH), 25-OH Vitamin D (VitD), calcium and phosphorus were measured in 34 patients with AKI without pre-existing chronic kidney disease and 12 healthy controls.
Results: The mean 1,25(OH)2D levels were significantly lower in patients with AKI compared to controls, (42±5.6 pg/mL vs. 76.1±5.3 pg/mL, P <0.0001). The mortality in patients with AKI was 30%. 1,25(OH)2D levels were higher in non-survivors than survivors (62±41.4 pg/mL vs. 33.7±24.2 pg/mL respectively, P = 0.046) and serum phosphorus was also higher in non-survivors (6.2±2.1 mg/dL vs. 4.6±1.6 mg/dL, P = 0.019). However, on multivariate regression analysis, accounting for age and APACHE II score, higher levels of 1,25(OH)2D was not associated with mortality in critically ill patients with AKI.
Conclusion: Mineral metabolism is dysregulated within days of acute renal injury in critically ill patients. On univariate analysis, high levels of calcitriol were associated with adverse clinical outcome in AKI. This association was not apparent after adjusting for age and APACHE II. Large controlled studies are needed to confirm these results, and determine if higher 1,25(OH)2D mediates worse outcomes in AKI.
Keywords: Calcitriol; acute tubular necrosis; intact parathyroid hormone.