Abstract 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.