THE CONTENTS OF SCD40 AND INDICATORS OF DAMAGED ENDOTHELIUM IN PATIENTS WITH CHRONIC KIDNEY DISEASE
Abstract
Introduction. Impairments of endothelial structure and functions of renal vessels are regarded as important factors of progression and chronization of chronic kidney disease (CKD). It is well known that the CD40/CD40L interaction is responsible for the aggregation of blood cells and their adhesion to the vascular wall, as well as its effect on the state of immune response. We investigated whether this interaction could be altered in patients with CKD and impaired immune status.
Materials and methods. We examined 48 patients with chronic glomerulonephritis (CGN), 38 patients with chronic pyelonephritis and 42 patients with essential hypertension (EH) - control group. All patients received standard therapy with an ACE inhibitor perindopril in combination with a calcium channel
antagonist amlodipine. Along with standard therapy the patients intravenously administered injections of "Kardioarginine." The degree of endothelial damage was assessed by the number of CEC and VE-cadherin content in blood plasma. In order to estimate changes in the immune status we determined the content of sCD40 in serum.
Results. Increase in the content of serum sCD40 was shown for the CGN patients compared with healthy subjects and EH patients. The level of sCD40 in serum correlated with the number of CEC and VE-cadherin content in plasma. The use of kardioarginine combined with standard therapy led to reduction of sCD40 and stabilized the structure of endothelium. The loss of endothelial integrity in patients with CKD is apparently due to the activation of apoptosis with subsequent accelerated desquamation under the influence of activated white blood cells and the system of cytokines.
Conclusions. The increase of sCD40 in patients with CKD may be a compensatory mechanism aimed to reduce the inflammatory activity by blocking the CD40/CD40L interaction at the cellular level.
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Уровень и фенотипические особенности липиднагруженных лейкоцитов у больных хроническим гломерулонефритом в сочетании с ишемической болезнью сердца / Гальчинская В.Ю., Топчий И.И., Семеновых П.С. [и др.] // Научные ведомости БЕЛГУ. – 2012. - №10. – В.18. – с. 46.
Топчий И.И. Взаимосвязь содержания асимметричного диметиларгинина с нарушением регенерации клеток эндотелия и уменьшением биодоступности оксида азота у больных хронической болезнью почек в сочетании с атеросклерозом / Топчий И.И. // Сімейна медицина. – 2011. – №4. – С. 81-88.
Chronic Kidney Disease Prognosis Consortium. Association of estimated glomerular filtration rate and albuminuria with all-cause and cardiovascular mortality in general population cohorts: a collaborative meta-analysis. // Lancet. – 2010. – V. 375. – P. 2073-2081.
Macrophage/monocyte depletion by clodronate, but not diphtheria toxin, improves renal ischemia/ reperfusion injury in mice / David A., Ferenbach B., Sheldrake A.Тага [et al.] // Kidney International. – 2012. – V. 2. – P. 928-933.
B cells regulate expression of CD40 ligand on activated T cells by lowering the mRNA level and through the release of soluble CD40 / Van Kooten C., Gaillard C., Galizzi J.P. [et al.] // Eur J Immunol. – 1994. – V. 24. – Р. 787–792.
Lee S. Distinct macrophage phenotypes contribute to kidney injury and repair / Lee S., Huen S., Nishio H. // J Am Soc Nephrol.-2011.-Vol.22.-P.317-326.
Mobilized human hematopoietic stem/progenitor cells promote kidney repair after ischemia/reperfusion injury. / Li B., Cohen A., Hudson T.E. [et al.] // Circulation. – 2010. – Vol. 121(20). – Р. 2211-2220.
Serum Level of sCD40 Ligand and Monocyte Chemoattractant Protein-1 in cases of Acute Ischemic Coronary and Cerebral Events / Naglaa M. El Khayat, Ahmed Khashaba, Samar Refaat, Mervat El-Fiky // Egypt J Neurol Psychiat Neurosurg. – 2010. – Vol. 47(4). – Р. 665-672.
CD40/CD154 interactions at the interface of tolerance and immunity / Quezada S.A., Jarvinen L.Z., Lind E.F., Noelle R.J. // Annu Rev Immunol. – 2004. –Vol. 22. – Р. 307-328.
Cell adhesion dynamics at endothelial junctions: VE-cadherin as a major player / Vestweber D., Winderlich M., Cagna G., Nottebaum A.F. // Trends Cell Biol. – 2008. – Vol. 19(1). – Р. 8-15.
