Факторы риска и механизмы развития острого пиелонефрита после контактной уретеролитотрипсии

Abstract

of the study is to identify risk factors for the development of acute pyelonephritis after contact urethrolithotripsy (URLLT) and to establish the mechanisms for maintaining inflammation after the withdrawal of NSAIDs.The study included 21 patients who underwent contact ureterolithotripsy (URLT). The severity of leukocyturia was assessed 1 day after URLT, 2 days (the last appointment of NSAIDs, the total duration of the drug was 9 days) and 3 days (24 hours after NSAID discontinuation). The number of circulating platelet-leukocyte aggregates (PLA) was calculated by microscopy of stained blood smears. Analysis of the functional activity of platelet receptors involved in the modulation of the acute inflammatory response was performed by the turbidimetric method on a ChronoLog analyzer (USA).Statistical analysis was performed using the MedCalc package.After URSL, when NSAIDs were prescribed to patients, the level of leukocyturia decreased (p<0.05) compared to that at the time of hospitalization. A similar dynamics was found by analyzing the amount of TLA in the blood. Similar dynamics was found in the analysis of the amount of TLA in the blood. After 24 hours of NSAIDs cancellation, an increase in the severity of leukocyturia was detected (p<0.001). At the same time, normoreactivity of the 2-adrenergic receptor, GPVI receptor, AT1 receptor, PAT receptor, P2X1 receptor and A2A receptor, as well as hyporeactivity of the 2-adrenergic receptor and P2Y receptors, were revealed. An analysis of correlations made it possible to establish that the 2-adrenoreceptor, AT1 receptor, and GPVI receptor play a key role in the formation of TPA. Incubation of blood cells in vitro with agonists made it possible to establish that the maximum effect of TLA formation was reproduced during the interaction of the 2-adrenergic receptor and the AT1 receptor.With the abolition of NSAIDs, activation of the sympathetic-adrenal and renin-angiotensin systems, as well as remodeling of the basement membrane of the vascular wall are risk factors for the development of acute pyelonephritis after URLS.