MECHANISMS OF NEPHROPATHY DEVELOPMENT AND PROGRESSION IN HEART FAILURE PATIENTS WITH CHRONIC CARDIORENAL SYNDROME
https://doi.org/10.24884/1561-6274-2011-15-2-20-29
Abstract
In the review modern data on a morphological picture, mechanisms of formation and approaches to drug therapy of chronic kidney disease (CKD) in patients with chronic cardiorenal syndrome are generalized. Principal causes of occurrence and progressing of chronic “heart” nephropathy – neurohumoral activation and infringement of system arterial and venous hemodynamics, starting
neurohumoral, hemodynamics and hypoxic mechanisms of renal sclerotic damage. Earliest of them is compensatory by the nature narrowing efferent glomerular arterioles, promoting increase in filtration fraction and occurrence of steady glomerularhypertension causing mechanical damage of fenestrial endothelium, podocytes and glomerular mesangial cells. In formation of this renal hemodynamics defect the mainly role is played with hyperactivity of circulating reninangiotensinaldosterone system
(RAAS) and renal tissue reninangiotensin system (RAS). In process of the further infringement postglomerular blood flow and occurrence in persons with expressed chronic heart failure (CHF) anemia syndrome the mechanism of renal sclerotic damage joins renal tissue hypoxia, the leader to development of hypoxic glomerulosclerosis and tubulointerstititial fibrosis, accelerating loss of kidney function. In CKD progression with CHF also participates to uremic toxin indoxyl sulfate, which possesses the expressive nephrotoxic action. For treatment of chronic kidney disease in patients with CHF, receiving usual drug therapy, various therapeutic approaches are used. They include prevention of intrarenal hemodynamics infringements (correction of dozes of angiotensin converting enzyme (ACE) inhibitors, purpose of preparations with mainly hepatic elimination, addition to ACE
inhibitors AT1angiotensin receptor blockers), easing hypoxic damage of renal tissue (treatment of an anemia by erythropoietin, darbepoetin and iron preparations) and decrease damaging actions on kidneys diuretics and aldosterone receptor antagonists.
neurohumoral, hemodynamics and hypoxic mechanisms of renal sclerotic damage. Earliest of them is compensatory by the nature narrowing efferent glomerular arterioles, promoting increase in filtration fraction and occurrence of steady glomerularhypertension causing mechanical damage of fenestrial endothelium, podocytes and glomerular mesangial cells. In formation of this renal hemodynamics defect the mainly role is played with hyperactivity of circulating reninangiotensinaldosterone system
(RAAS) and renal tissue reninangiotensin system (RAS). In process of the further infringement postglomerular blood flow and occurrence in persons with expressed chronic heart failure (CHF) anemia syndrome the mechanism of renal sclerotic damage joins renal tissue hypoxia, the leader to development of hypoxic glomerulosclerosis and tubulointerstititial fibrosis, accelerating loss of kidney function. In CKD progression with CHF also participates to uremic toxin indoxyl sulfate, which possesses the expressive nephrotoxic action. For treatment of chronic kidney disease in patients with CHF, receiving usual drug therapy, various therapeutic approaches are used. They include prevention of intrarenal hemodynamics infringements (correction of dozes of angiotensin converting enzyme (ACE) inhibitors, purpose of preparations with mainly hepatic elimination, addition to ACE
inhibitors AT1angiotensin receptor blockers), easing hypoxic damage of renal tissue (treatment of an anemia by erythropoietin, darbepoetin and iron preparations) and decrease damaging actions on kidneys diuretics and aldosterone receptor antagonists.
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For citations:
KUZMIN O.V. MECHANISMS OF NEPHROPATHY DEVELOPMENT AND PROGRESSION IN HEART FAILURE PATIENTS WITH CHRONIC CARDIORENAL SYNDROME. Nephrology (Saint-Petersburg). 2011;15(2):20-29. (In Russ.) https://doi.org/10.24884/1561-6274-2011-15-2-20-29
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