Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pneumonia emerged in Wuhan, China in December 2019. Unfortunately, there is a lack of evidence about the optimal management of novel coronavirus disease 2019 (COVID-19), and even less is available in patients on maintenance hemodialysis therapy than in the general population. In this retrospective, observational, single-center study, we analyzed the clinical course and outcomes of all maintenance hemodialysis patients hospitalized with COVID-19 from March 12th to April 10th, 2020 as confirmed by real-time polymerase chain reaction. Baseline features, clinical course, laboratory data, and different therapies were compared between survivors and nonsurvivors to identify risk factors associated with mortality. Among the 36 patients, 11 (30.5%) died, and 7 were able to be discharged within the observation period. Clinical and radiological evolution during the first week of admission were predictive of mortality. Among the 36 patients, 18 had worsening of their clinical status, as defined by severe hypoxia with oxygen therapy requirements greater than 4 L/min and radiological worsening. Significantly, 11 of those 18 patients (61.1%) died. None of the classical cardiovascular risk factors in the general population were associated with higher mortality. Compared to survivors, nonsurvivors had significantly longer dialysis vintage, increased lactate dehydrogenase (490 U/l ± 120 U/l vs. 281 U/l ± 151 U/l, P [ 0.008) and C-reactive protein levels (18.3 mg/dl ± 13.7 mg/dl vs. 8.1 mg/dl ± 8.1 mg/dl, P [ 0.021), and a lower lymphocyte count (0.38 310 3 /ml ± 0.14 310 3 /ml vs. 0.76 310 3 /ml ± 0.48 310 3 /ml, P [ 0.04) 1 week after clinical onset. Thus, the mortality among hospitalized hemodialysis patients diagnosed with COVID-19 is high. Certain laboratory tests can be used to predict a worsening clinical course.

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Kidney transplant recipients are at increased risk of infection, including COVID-19, given ongoing immunosuppression. In individuals with COVID-19, complications including thrombosis and endothelial dysfunction, portend worse outcomes. In this report, we describe a kidney transplant recipient who developed severe thrombotic microangiopathy (TMA) with low platelet count (12 x 109 /L), anemia (7.5g/dL with 7% schistocytes on peripheral blood smear) and severe acute kidney injury concurrent with COVID-19. The clinical course improved following plasma exchange. Given this presentation, we hypothesize that COVID-19 triggered TMA.

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