Renal failure in COVID-19 patients is reportedly related to multiple factors such as a direct SARS-CoV-2 cytopathic effect, cytokine storm, the association of pulmonary and/or cardiovascular lesions, the presence of thrombotic microangiopathy, endothelial damage, or the use of potentially nephrotoxic medications.

We retrospectively analyzed 466 cases of SARS-CoV-2 infection, comparing 233 patients with acute kidney injury (AKI) with 233 patients without AKI in terms of their demographic characteristics, comorbidities, clinical background, laboratory investigations, time of AKI onset, therapy, and outcomes after using univariate analysis and a CART decision-tree approach. The latter was constructed in a reverse manner, starting from the top with the root and branching out until the splitting ceased, interconnecting all the predictors to predict the overall outcome (AKI vs. non-AKI).

There was a statistically significant difference between the clinical form distribution in the two groups, with fewer mild (2 vs. 5) and moderate (54 vs. 133) cases in the AKI group than in the non-AKI group and more severe and critical patients in the AKI cohort (116 vs. 92 and 60 vs. 3). There were four deaths (1.71%) in the non-AKI group and 120 deaths in the AKI group (51.5%) (p-value < 0.001). We noted statistically significant differences between the two study groups in relation to different tissue lesions (LDH), particularly at the pulmonary (CT severity score), hepatic (AST, ALT), and muscular levels (Creatine kinase). In addition, an exacerbated procoagulant and inflammatory profile in the study group was observed. The CART algorithm approach yielded decision paths that helped sort the risk of AKI progression into three categories: the low-risk category (0-40%), the medium-risk category (40-80%), and the high-risk category (>80%). It recognized specific inflammatory and renal biomarker profiles with particular cut-off points for procalcitonin, ferritin, LDH, creatinine, initial urea, and creatinine levels as important predictive factors of AKI outcomes (93.3% overall performance).

Our study revealed the association between particular risk factors and AKI progression in COVID-19 patients. Diabetes, dyspnea on admission, the need for supplemental oxygen, and admission to the intensive care unit all had a crucial role in producing unfavorable outcomes, with a death rate of more than 50%. Necessary imaging studies (CT scan severity score) and changes in specific biomarker levels (ferritin and C-reactive protein levels) were also noted. These factors should be further investigated in conjunction with the pathophysiological mechanisms of AKI progression in COVID-19 patients.

Severe acute respiratory syndrome coronavirus-2 acute kidney injury is a condition that in many ways resembles classical acute kidney injury. The pathophysiology appears to be multifactorial, and accordingly, our main objective was to review possible components of this form of acute kidney injury.

Literature review.

Our principal observation was that the various components of severe acute respiratory syndrome coronavirus-2 acute kidney injury appear to be relatively similar to the classical forms. Temporality of injury is an important factor but is not specific to severe acute respiratory syndrome coronavirus-2 acute kidney injury. Several insults hit the kidney at different moments in the course of disease, some occurring prior to hospital admission, whereas others take place at various stages during hospitalization.

Treatment of severe acute respiratory syndrome coronavirus-2 acute kidney injury cannot be approached in a "one-size-fits-all" manner. The numerous mechanisms involved do not occur simultaneously, leading to a multiple hit model that may contribute to the prevalence and severity of acute kidney injury. A personalized approach to each patient with acute kidney injury based on the timing and severity of disease is necessary in order to provide appropriate treatment. Although data from the literature regarding the previous coronavirus infections can give some insights, more studies are needed to explore the different mechanisms of acute kidney injury occurring as a result of severe acute respiratory syndrome coronavirus-2.