Background: Acute kidney injury (AKI) is a significant complication of Coronavirus Disease 2019 (COVID-19), with no effective therapy. Niacinamide, a vitamin B3 analog, has some evidence of efficacy in non-COVID-19-related AKI. The objective of this study is to evaluate the association between niacinamide therapy and outcomes in patients with COVID-19-related AKI. Methods: We implemented a quasi-experimental design with non-random, prospective allocation of niacinamide in 201 hospitalized adult patients, excluding those with baseline estimated glomerular filtration rate <15 ml/min/1.73m2 on or off dialysis, with COVID-19-related AKI by Kidney Disease Improving Global Outcomes (KDIGO) criteria, in two hospitals with identical COVID-19 care algorithms, one of which additionally implemented treatment with niacinamide for COVID-19-related AKI. Patients on the niacinamide protocol (B3 patients) were compared against patients at the same institution before protocol commencement and contemporaneous patients at the non-niacinamide hospital (collectively, non-B3 patients). The primary outcome was a composite of death or renal replacement therapy (RRT). Results: 38/90 B3 patients and 62/111 non-B3 patients died or received RRT. Using multivariable Cox proportional hazard modeling, niacinamide was associated with a lower risk of RRT or death (HR 0.64, 95% CI 0.40 to 1.00, p=0.05), an association driven by patients with KDIGO stage 2/3 AKI (HR 0.29, 95% CI 0.13 to 0.65, p=0.03; p interaction with KDIGO stage 0.03). Total mortality also followed this pattern (HR 0.17, 95% CI 0.05-0.52 in KDIGO 2/3 patients, p=0.002). Serum creatinine following AKI increased by 0.20 (SE 0.08) mg/dL/day among non-B3 patients with KDIGO 2/3 AKI but was stable among comparable B3 patients (+0.01 (SE 0.06) mg/dL/day; p interaction 0.03). Conclusions: Niacinamide was associated with lower risk of RRT/death and improved creatinine trajectory among patients with severe COVID-19-related AKI. Larger randomized studies are necessary to establish a causal relationship.
BackgroundDenosumab and abiraterone were approved by the United States Food and Drug Administration in 2011 for the treatment of metastatic castration-resistant prostate cancer. Neither denosumab nor abiraterone is known to cause rhabdomyolysis.Case presentationA 76-year-old Caucasian man with metastatic prostate cancer presented with non-oliguric severe acute kidney injury (AKI) 3 weeks after receiving simultaneous therapy with denosumab and abiraterone. The patient had been on statin therapy for more than 1 year with no recent dose adjustments. His physical exam was unremarkable. Blood work on admission revealed hyperkalemia, mild metabolic acidosis, hypocalcemia, and elevated creatine kinase (CK) at 44,476 IU/L. Kidney biopsy confirmed the diagnosis of rhabdomyolysis-induced AKI. The patient responded well to intravenous isotonic fluids and discontinuation of denosumab, abiraterone, and rosuvastatin, with normalization of CK and recovery of kidney function.ConclusionWe report the first case of biopsy-proven rhabdomyolysis-induced AKI in a cancer patient acutely exposed to denosumab and abiraterone. Whether one of these drugs individually, or the combination, was the bona fide culprit of muscle breakdown is unknown. Nonetheless, our report is hypothesis-generating for further investigations on the effect of these drugs on muscle cells.
Renal tubular acidosis (RTA) is a known complication of anti-retroviral medications. The presence of RTA in treatment naive-HIV patients is rare. A 49-yearold Caucasian woman presented with recurrent non-anion gap metabolic acidosis, AKI, rhabdomyolysis and hypokalemia on several occasions. Diagnosis of acquired distal RTA due to HIV was made given the history and laboratory data. To the best of our knowledge, this is the first case of HIV diagnosed with an initial presentation of rhabdomyolysis. We believe that acute renal failure was due to hypokalemia precipitating rhabdomyolysis caused by HIVinduced dRTA which was further exacerbated by amphetamine use.
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