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Introduction: The choice of method of surgical treatment for endophytic kidney tumors depends on the precise definition of the location and size, the extent of invasion into adjacent tissues and the type of vascularization. Intraoperative ultrasound (IOUS) in combination with 3D-CT allow to receive this information. The aim of this study was to compare the laparoscopic-assisted extracorporeal partial nephrectomy and laparoscopic partial nephrectomy with IOUS and visualization in Full HD, 3D Full HD and 4K modes., Materials and Methods: A total of 77 patients aged 43-75 years with endophytic renal tumors were included in the study. They were undergone either extracorporeal partial nephrectomy or laparoscopic partial nephrectomy with IOUS. We compared the rate of positive surgical margins, early postoperative bleeding, de novo renal failure or aggravation of preexisting renal failure and stricture of vesico-ureteric anastomosis., Results: The rate of early postoperative bleeding, chronic kidney failure and pathologically-proven positive surgical margin in patients who underwent extracorporeal partial nephrectomy followed by kidney autotransplantation was 23.1%, 13.4% and 13.4%, respectively. After laparoscopic partial nephrectomy these values were 12%, 16.7% and 8.3%, respectively. The best outcomes were achieved in patients who underwent laparoscopic partial nephrectomy with IOUS and with a use of visualization in Full HD, 3D Full HD and 4K modes.

Currently, prostate biopsy remains the main method used to diagnose prostate cancer (PCa). The indication for the procedure is an elevated level of the serum level of the total prostate-specific antigen (PSA). However, the PSA test is organ- but not cancer-specific, and patients may undergo an unnecessary biopsy, which is an invasive procedure associated with a risk of complications. Additional tests have been developed aimed to improve the diagnostic performance of PSA for detecting PCa. They include PSA derivatives such as free PSA fraction, -2proPSA, PSA density, PHI and the free /total PSA fraction., Aim: To investigate the diagnostic accuracy of PSA and its derivatives in detecting benign and malignant diseases of the prostate after an initial prostate biopsy., Materials and Methods: The current study analyzed 65 initial biopsies performed due to an elevated serum PSA level and compared them with the results of extended PSA testing with the use of PSA derivatives., Results: The histological findings consistent with PCa were found in about 30% of initial biopsies performed due to elevated serum levels of total PSA. The incidence of histologically confirmed PCa increased with age, and 70-79 year old men were more likely to have it than 60-69 years old patients. PSA density in 85% of PCa cases exceeded that for benign prostatic hyperplasia (BPH). In all PCa patients, PHI and free /total PSA fraction were greater than 25 and less than 0.15, respectively. In most patients with BPH, the PHI and free /total PSA fraction did not exceed 25 and were greater than 0.15., Conclusions: 1. Initial biopsy triggered by elevated serum level of total PSA allows detection of PCa in about 30% of cases. 2. The age of 60 years and older should be regarded as a risk factor for PCa. The probability of malignant transformation of prostate epithelial cells in men over 70 years of age is greater than in 60-69-year-olds. 3. The density of PSA in men with morphologically verified PCa is statistically significantly greater than that in men with BPH and the threshold value in 85% of cases. 4. Determination of PHI and free/total PSA fraction can improve the accuracy of predicting malignant lesions of the prostate and adjust the indications for histological examination, reduce the number of unnecessary biopsies. 5. When defining indications for initial prostate biopsy in cases with serum PSA varying from 2 to 10 ng/ml, PSA derivatives should be used, including PSA density, prostate health index, and the free /total PSA fraction.

Intraoperative occlusion of the renal artery during laparoscopic partial nephrectomy results in warm ischemia and nonspecific hypoxia-reoxygenation alteration of the renal parenchyma cells with a predominant injury to epitheliocytes of the proximal segments of the tubular nephron system. The onset and development of acute kidney injury (AKI) syndrome, which requires immediate correction, is due to the typical pathological process of cell injury. In this regard, the issue of timely diagnosis of AKI remains highly relevant. In patients at high risk of developing acute renal failure, detection of AKI biomarkers enables early diagnosis. In cases with hypoxia-reoxygenation mediated destruction of epithelial cells of tt. renales, related to warm ischemia, the quality of diagnosis is significantly improved if the standard work-up is supplemented by measurements of the concentration and/or activity of cystatin C, interleukin-18, kidney injury molecule-1, neutrophil gelatinase-associated lipocalin, liver fatty acid binding protein, N-acetyl --glucosaminidase, glutathione S-transferase -isoform, -glutamyl transpeptidase and lactate dehydrogenase. This article provides an overview of published evidence on the properties and diagnostic capabilities of biomarkers of warm ischemia related AKI.

Aim: To investigate experimentally ultrastructural and biochemical signs of acute injury to the renal parenchyma after warm renal ischemia of various duration and subsequent reperfusion., Materials and Methods: The experiments were performed on 44 healthy conventional female rabbits of the "Chinchilla" breed weighted 2.6-2.7 kg, which were divided into four groups. In the first, control, group included pseudo-operated animals. In the remaining three groups, an experimental model of warm ischemia of renal tissue was created, followed by a 60-minute reperfusion. The renal warm ischemia time was 30, 60 and 90 minutes in the 2nd, 3rd and 4th groups, respectively. Electron microscopy was used to study ultrastructural disturbances of the renal parenchyma. Biochemical signs of acute kidney damage were detected by measuring the following blood serum and/or urine analytes: NGAL, cystatin C, KIM-1, L-FABP, interleukin-18. The glomerular filtration was evaluated by creatinine clearance, which was determined on days 1, 5, 7, 14, 21 and 35 of follow-up., Results: A 30-minute renal warm ischemia followed by a 60-minute reperfusion induced swelling and edema of the brush membrane, vacuolation of the cytoplasm of the endothelial cells of the proximal tubules, and microvilli restructuring. The observed disorders were reversible, and the epithelial cells retained their viability. After 60 minutes of ischemia and 60 minutes of reperfusion, the observed changes in the ultrastructure of the epithelial cells were much more pronounced, some of the epithelial cells were in a state of apoptosis. 90 min of ischemia and 60 min of reperfusion resulted in electron-microscopic signs of the mass cellular death of the tubular epithelium. Concentration in serum and/or biochemical urine markers of acute renal damage increased sharply after ischemic-reperfusion injury. Restoration of indicators was observed only in cases when the renal warm ischemia time did not exceed 60 minutes. The decrease in creatinine clearance occurred in the first 24 hours after the intervention, lasting not less than two weeks after a 30-minute warm ischemia, at least 3 weeks after a 60-minute warm ischemia and continued more than a month after a 90-minute renal artery occlusion., Conclusion: Intraoperative warm ischemia and subsequent reperfusion are the actual reasons for the alteration of the ultrastructure of the renal tissue and the impairment of the filtration function. The severity of the disorders depends on the duration of the damaging factors. After a 30-60-minute ischemia, the structural and functional changes in the renal tissue are reversible. The mass death of nephrocytes-effectors is possible only after warm renal ischemia longer than 60 min.

Warm ischemia of the renal parenchyma is a forced feature of laparoscopic partial nephrectomy. It is accompanied by oxygen deprivation of the organ and followed by re-oxygenation, which can cause additional damage to the renal tissue. This damage can result in acute functional and structural disorders of individual parts of the nephron, increasing the risk for a renal dysfunction. Timely diagnosis of the dysfunction is vital for the success of the treatment. The article provides an overview of current scientific data on the mechanisms of ischemic and reperfusion injuries at the molecular-cellular level and describes the current methods of their detection. Experimental and clinical study of the molecular-cellular mechanisms of ischemic-reperfusion injury of the renal tissue made it possible, first, to determine the main targets of alteration (cytolemma, mitochondria, lysosomes), and second, to establish its consequences, among which the most important are hypoergosis, DNA damage, simultaneous activation of intracellular systems of the suicidal program and induction of electrical breakdown of membranes of target nephrocytes; thirdly, to reveal the range of possibilities for limiting the consequences of hypoxia and/or re-oxygenation, among which interference in the metabolism of purines, measures ensuring the preservation of colloid osmotic pressure inside and outside the cell and membrane stabilization, antioxidant defense and inhibition of cysteine proteinases, etc. However, despite the advances in understanding the pathogenesis of cell damage, including ischemic-hypoxic injury, the problem of intraoperative ischemia-reperfusion safety remains relevant.