Chronic kidney disease (CKD) is a non-specific type of kidney disease that causes a gradual decline in kidney function (from months to years). CKD is a significant risk factor for death, cardiovascular disease, and end-stage renal disease. CKDs of different origins may have the same clinical and laboratory manifestations but different progression rates, which requires early diagnosis to determine. This review focuses on protein/peptide biomarkers of the leading causes of CKD: diabetic nephropathy, IgA nephropathy, lupus nephritis, focal segmental glomerulosclerosis, and membranous nephropathy. Mass spectrometry (MS) approaches provided the most information about urinary peptide and protein contents in different nephropathies. New analytical approaches allow urinary proteomic–peptide profiles to be used as early non-invasive diagnostic tools for specific morphological forms of kidney disease and may become a safe alternative to renal biopsy. MS studies of the key pathogenetic mechanisms of renal disease progression may also contribute to developing new approaches for targeted therapy.

SARS-CoV-2 causes thrombotic microangiopathy (TMA) through the activation of an alternative and lectin complement pathway. TMA is one of the main reasons for acute kidney injury development in patients with COVID-19. In this study, we present 3 TMA cases with severe kidney injury triggered by SARS-CoV-2. In the absence of other TMA causes, we diagnosed the atypical hemolytic uremic syndrome, triggered by SARS-CoV-2 due to abnormal complement activation. Because of both coagulation factors activation, and the high level of D-dimer in patients with COVID-19, it is crucial to differentiate disseminated intravascular coagulation from TMA. The use of anticomplement therapies such as eculizumab should be considered in refractory cases of progressive COVID-19. Controlled clinical trials are required before a definitive statement can be made.

Background — Acute kidney injury (AKI) reaches 29% in the intensive care unit (ICU). Our study aimed to determine the prevalence, features, and the main AKI factors in critically ill patients with coronavirus disease 2019 (COVID-19). Material and Methods — The study included 37 patients with COVID-19. We analyzed the total blood count test results, biochemical profile panel, coagulation tests, and urine samples. We finally estimated the markers of kidney damage and mortality. Result — All patients in ICU had proteinuria, and 80.5% of patients had hematuria. AKI was observed in 45.9% of patients. Independent risk factors were age more than 60 years, increased C-reactive protein (CRP) level, and decreased platelet count. Conclusion — Kidney damage was observed in most critically ill patients with COVID-19. The independent risk factors for AKI in critically ill patients were elderly age, a cytokine response with a high CRP level.