Refractoriness of Hyperkalemia and Hyperphosphatemia in Dialysis-Dependent AKI Associated with COVID-19.

Background: Persistent hyperkalemia (hyperK) and hyperphosphatemia (hyperP) despite renal replacement therapy (RRT) was anecdotally reported in COVID-19 and acute kidney injury (AKI) requiring RRT (CoV-AKI-RRT). However, observation bias could have accounted for the reports. Thus, we systematically examined the rate and severity of hyperK and hyperP in patients with CoV-AKI-RRT in comparison with the pre-COVID-19 era. Methods: We identified patients with CoV-AKI-RRT treated with sustained low-efficiency dialysis (SLED) for ≥2 days in March-April 2020. As pre-COVID-19 control, we included patients with AKI treated with SLED in December 2019. We examined the rates of hyperK (serum potassium [sK] ≥5.5 mEq/L), severe hyperK (sK ≥6.5 mEq/L), hyperP (serum phosphate [sP] ≥4.5 mg/dl), and moderate or severe hyperP (sP ≥7-10 and >10 mg/dl, respectively) as %SLED-days with an event. Results: Along the duration of SLED, the incidence of hyperK was greater in CoV-AKI-RRT (n=64; mean 19%±2% versus 14%±3% SLED-days, P=0.002) compared with control (n=60). The proportion of patients with one or more event of severe hyperK was greater in CoV-AKI (33% versus 7%, P<0.001). The incidence of hyperP was similar between groups (mean 56%±4% versus 53%±5% SLED-days, P=0.49). However, the proportion of patients with one or more event of moderate and severe hyperP was greater in CoV-AKI-RRT (86% versus 60%, P=0.001, and 50% versus 18%, P<0.001, respectively). Among those with CoV-AKI-RRT, sK and sP correlated with lactate dehydrogenase (LDH; r=0.31, P=0.04, and r=0.31, P=0.04, respectively), whereas hyperP also correlated with shorter SLED runs (hours/run; r=-0.27, P=0.05). Conclusions: Refractory hyperK and hyperP were more frequent in CoV-AKI-RRT compared with the pre-COVID-19 era. Because of the correlation of sK and sP with higher LDH and sP with shorter SLED runs, intracellular ion release from cell injury due to cytokine storm and RRT interruptions may account for the findings.

Acute Kidney Injury Associated with Coronavirus Disease 2019 in Urban New Orleans.

Background: AKI is a manifestation of COVID-19 (CoV-AKI). However, there is paucity of data from the United States, particularly from a predominantly black population. We report the phenotype and outcomes of AKI at an academic hospital in New Orleans. Methods: We conducted an observational study in patients hospitalized at Ochsner Medical Center over a 1-month period with COVID-19 and diagnosis of AKI (KDIGO). We examined the rates of RRT and in-hospital mortality as outcome measures. Results: Among 575 admissions (70% black) with COVID-19 [173 (30%) to an intensive care unit (ICU)], we found 161 (28%) cases of AKI (61% ICU and 14% general ward admissions). Patients were predominantly men (62%) and hypertensive (83%). Median body mass index (BMI) was higher among those with AKI (34 versus 31 kg/m2, P<0.0001). AKI over preexisting CKD occurred in 35%. Median follow-up was 25 (1-45) days. The in-hospital mortality rate for the AKI cohort was 50%. Vasopressors and/or mechanical ventilation were required in 105 (65%) of those with AKI. RRT was required in 89 (55%) patients. Those with AKI requiring RRT (AKI-RRT) had higher median BMI (35 versus 33 kg/m2, P=0.05) and younger age (61 versus 68, P=0.0003). Initial values of ferritin, C-reactive protein, procalcitonin, and lactate dehydrogenase were higher among those with AKI; and among them, values were higher for those with AKI-RRT. Ischemic acute tubular injury (ATI) and rhabdomyolysis accounted for 66% and 7% of causes, respectively. In 13%, no obvious cause of AKI was identified aside from COVID-19 diagnosis. Conclusions: CoV-AKI is associated with high rates of RRT and death. Higher BMI and inflammatory marker levels are associated with AKI as well as with AKI-RRT. Hemodynamic instability leading to ischemic ATI is the predominant cause of AKI in this setting.