[Molecular and cellular mechanisms of damage to renal parenchyma in renal warm ischemia].

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.

[Biomarkers of acute hypoxia-reoxygenation injury to nercycites during laparoscopic resection of renal parenchyma].

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.