The consensus was developed by experts from the Russian Scientific Medical Society of Internal Medicine, the Russian Society for the Prevention of Noncommunicable Diseases, the National Nephrology Association, the Professional Nephrology Association, the Russian Society of Cardiology, the Russian Medical Society for Arterial Hypertension, the Heart Failure Society, the National Atherosclerosis Society, the Russian Endocrinology Association, and the Russian Gerontology and Geriatrics Association.The expert consensus opinion was compiled on the basis of the relevant sections of national and international clinical guidelines on chronic kidney disease, prevention and treatment of atherosclerosis, hypertension, diabetes and heart failure.

Background: Kidney involvement in infective endocarditis (IE) has a huge contribution in failure of the antimicrobal therapy and in rejection of the surgical treatment. Frequency of kidney lesions is still high and is diagnosed in 50–80% cases intravitaly, and in 91,6% post-mortem. Materials/Methods: 28 patients with verified IE (DUKE 2009, 2015), hospitalized and treated in clinical hospital from 2010 to 2018, were included in the study. Kidney function was assessed using CKD-EPI formula. Acute kidney injury (AKI) was diagnosed according to current guidelines (KDIGO 2012). Intravital nephrobiopsy was performed in 2 (7,1%) patients, in 26 patients (92,9%) morphological assessment was made on the autopsy tissue specimens. Autopsy material was assessed grossly and microscopically with H&E staining. Morphological changes in kidney were estimated based on standart histological criteria. Results: Majority of patients with IE (92.9%) had structural changes in kidney tissue: 3 (12%), 16 (64%) and 6 (24%) patients had respectively isolated glomerular, tubular and mixed lesions. Significantly higher is rate of tubular lesion than glomerular (p=0.014). Main pattern in glomerular damage was mesangial proliferation, we didn't found any cases of crescentic GN. Herewith, proliferation was mainly diffuse (87.5%) rather than focal (12.5%). Glomerular damage in subacute IE (>56 days) appears more often than in acute IE (<56 days) (p=0.057 χ2=3.63). When studying the influence of various factors on the involvement of the glomeruli or tubules, no statistically significant group differences were obtained, except for the gram-negative flora as the causative agent, in which the tubules are significantly more likely to be affected (p=0.019) Morphological diagnosis n (%) Morphological diagnosis n (%) Glomerulonephritis 8 (28.6) Tubulointerstitial nephritis 3 (10.7) Membranoproliferative glomerulonephritis 3 (10.7) Allegrgic tubulointerstitial nephritis 2 (7.2) Mesangioproliferative glomerulonephritis 5 (17.9) Infective tubulointerstitial nephritis 1 (3.6) Extracapillar crescentic glomerulonephritis 0 (0) Kidney abscess 3 (10.7) Acute tubular necrosis 22 (78.6) Kidney infarction 1 (3.6) Acute tubular necrosis (ischaemic) 11 (39.3) Renal artery embolism 1 (3.6) Acute tubular necrosis (toxic) 11 (39.3) Shock kidney 4 (14.3) Conclusions: A morphological study of patients with IE revealed a wide range of kidney damage, however, the frequency of tubular lesions, mediated by nephrotoxic drugs and hemodynamic disorders significantly exceeds the frequency of immune complex glomerular lesions, as previously thought.

Background: Infective endocarditis (IE) is frequently complicated by kidney damage of various pathogenesis. The essential differences in pathophysiological mechanisms of kidney lesions (glomerular and tubular damage, mixed mechanisms) create different therapeutical targets. Nowadays these mechanisms are only possible to differentiate with the use of nephrobiopsy or autopsy. Non-invasive methods to assess the genesis of kidney damage are eagerly wanted. It is possible that kidney biomarkers may be such method. Materials and methods: 209 patients with verified IE (DUKE 2009, 2015), hospitalized and treated in city clinical hospital named after V.V. Vinogradov in Moscow from January 2010 to June 2018, were included in the study. Kidney function was assessed using CKD-EPI formula. Acute kidney injury (AKI) and acute kidney disease (AKD) were diagnosed according to current guidelines (KDIGO 2012) and the work group consensus (ADQI 16 Workgroup 2017). Serum creatinine decrease on ≥26,5 mcmol/L in 48 hours after the hospitalization was counted as early-onset AKI. Patients with serum creatinine elevation on ≥26,5 mcmol/L in 48 hours during the hospitalization were diagnosed with late-onset AKI. Biomarkers were assessed at the admission. Cystatin C level was assessed in serum; neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule 1 (KIM-1), albumin levels were assessed in urine. Results: Kidney damage biomarkers' levels were analyzed in 65 patients with IE. Patients with kidney dysfunction (n=45) comparing to ones without AKI (n=20) had higher mean value of all kidney biomarkers, however, the significant difference was established only for cystatin C. (1.9 vs 1.3 mg/l respectively; p<0.001). Patients with early-onset AKI (n=11) next to patients without AKI had significantly higher cystatin C value at admission (1.9 vs 1.3 mg/l respectively; p=0,0186). In similar manner patients with late-onset had had significantly higher cystatin C value at admission (1.9 vs 1.3 mg/l respectively; p=0,002). Cystatin C appeared to be an independent AKI predictor with threshold value 1.35 mg/l (OR 14.0; 95% CI 1.74–112.2; p=0.013), and also cystatin C was an independent predictor of the in-hospital mortality with threshold 1.87 mg/l (OR 3.16; 95% CI 1.25–7.99; p=0.006). After analysis of patients with AKD it was established that they had significantly higher levels of cystatin C (1.7 vs 1.3 mg/l respectively; p=0.035) and NGAL (19 vs 1.9 ng/ml; p=0.05) in comparison with patients without AKD. Albumin and KIM-1 didn't show significant associations. Conclusions: The results of a study allow to consider serum cystatin C as AKI marker, AKI predictor and in-hospital mortality predictor in patients with IE, and urinal NGAL and serum cystatin C may be considered as AKD markers.

Aim. To evaluate the impact of acute kidney injury (AKI) on in-hospital (death) and long-term outcomes (rehospitalization or death within 30 days; death within 180 days) in hospitalized patients with coronavirus disease 2019 (COVID-19).Material and methods. The registry of patients with COVID-19 was analyzed to identify risk factors (RFs) for mortality. Discharged patients were included in a prospective study. Outcomes were assessed by telephone contacts.Results. The study included 1000 patients. The mortality rate was 20,8%, while AKI was registered in 29,6% of patients. According to multi­variate analysis, AKI, regardless of other risk factors, increased the risk of death (hazard ratio (HR), 1,62, 95% confidence interval (CI): 1,08-2,44, p=0,02). The prospective part included 691 patients. We revealed that 10% were rehospitalized or died within 30 days, while independent risk factors were age >65 years (HR, 2,72, 95% CI: 1,47-5,01, p=0,001) and AKI in the acute phase of COVID-19 (HR, 1,67, 95% CI: 1,00-2,80, p=0,05). In addition, 6% of patients died within 180 days, while AKI was the risk factor for death according to univariate analysis; the only independent predictor was age >65 years (HR, 5,96, 95% CI: 2,26-15,72, p<0,001).Conclusion. AKI during the acute period of COVID-19, independently of other risk factors, more than 1,5 times increases the risk of mortality and the risk of adverse outcome within 30 days after discharge.

Aim. To identify the relationship of different albuminuria levels with paraclinical signs of congestion on admission and discharge and with the prognosis of acute decompensated heart failure (ADHF).Material and methods. Patients hospitalized with ADHF were included. Albuminu­ria level was assessed on admission and discharge. Patients were divided into groups according to albuminuria level (A1, A2, A3) according to KDIGO guidelines. Among the congestion parameters, the following were assessed: N-terminal pro-brain natriuretic peptide (NT-proBNP), lung ultrasound examination (BLUE protocol), venous congestion according to the VExUS ultrasound protocol (inferior vena cava, portal, hepatic and renal veins). The primary endpoint was a composite of all-cause death and rehospitalization for ADHF within 180 days of discharge.Results. The final analysis included 180 patients. The prevalence of A1, A2 and A3 albuminuria at admission was 50%, 39%, 11%, respectively. A greater degree of albu­minuria was associated with worse renal function at admission and discharge. Pati­ents with increased albuminuria on admission had higher NT-proBNP and a greater number of B-lines on pulmonary ultrasound in on admission and discharge, and a higher degree of complex venous congestion and renal vein congestion on VExUS on admission. A3 albuminuria at admission and discharge was associated with an increased risk of poor long-term prognosis (hazard ratio (HR) 3,551; 95% confidence interval (CI) 1,593-7,914; p=0,002), (HR 4,362; 95% CI 1,623-11,726; p=0,004).Conclusion. In patients with ADHF, the albuminuria level on admission is associated with the severity of congestion upon admission and discharge. A3 albuminuria at admission and at discharge is a predictor of long-term poor prognosis within 180 days after discharge.