Molecular mechanisms modulating hemostasis and development of acute pyelonephritis after contact ureteral lithotripsy

Abstract

BACKGROUND: Improving the efficiency and reducing the frequency of complications of surgical treatment of urolithiasis is an actual problem in urology.
 AIM: To establish the molecular mechanisms that modulate the hemostasis and development of acute pyelonephritis after percutaneous contact ureteral lithotripsy.
 MATERIALS AND METHODS: The study included 21 patients with urolithiasis and concretions in the upper third of the ureter in whom, after standard lithokinetic therapy for 7 days, according to imaging control data, the calculus did not move from the pyelo-ureteral zone to the middle third of the ureter. All patients underwent contact ureteral lithotripsy. After the operation, nonsteroidal anti-inflammatory drugs and antibiotics were used for 2 days. The severity of hematuria and leukocyturia was assessed 24, 48, and 72 h after contact ureteral lithotripsy. Functional activity receptors were analyzed in vitro on a platelet suspension. Platelet aggregation was assessed by the turbidimetric method using a ChronoLog analyzer (USA).
 RESULTS: At 24, 48, and 72 h after contact ureteral lithotripsy, a significant decrease was found in the severity of microhematuria (p 0.001). The leukocyturia level decreased over 48 h (p 0.05) and increased 72 h after surgery (p 0.001). The above dynamics of complications after hours indicates that two pathological processes simultaneously develop in the ureteral mucosa: induction of thrombogenesis and modulation of an acute inflammatory reaction. Аfter 24 h of NSAID discontinuation (3 days after contact ureteral lithotripsy), normoreactivity of the 2-adrenergic receptors, GPVI receptors, AT1 receptors, PAF receptors, P2X1 receptors, and A2A receptors was found, as well as hyporeactivity of purine P2Y receptors and 2-adrenergic receptors. The correlation between the severity of hematuria and the activity of GPVI receptors for collagen, 2-adrenergic receptors for adrenaline, and AT1 receptors for angiotensin-2 (p 0.05) makes it possible to specify the possible interaction of platelet receptors that maintain hemostasis during inhibition of the COXTxA2 axis. Maintaining the severity of pyelonephritis after contact ureteral lithotripsy is associated with the interaction of the PAF receptors, purine ionotropic P2X1 receptors, and 2-adrenergic receptors on blood cells.
 CONCLUSIONS: The analysis of targets receptors on platelets and leukocytes after contact ureteral lithotripsy in the upper third of the ureter with ineffective lithokinetic therapyallows us to outline ways to improve conservative therapy to limit the development of postoperative complications.