Pathophysiology of Cardiorenal Syndrome Type 2 in Stable Chronic Heart Failure: Workgroup Statements from the Eleventh Consensus Conference of the Acute Dialysis Quality Initiative (ADQI)

摘要: In cardiorenal syndrome (CRS) type 2, chronic heart failure (HF) results in the onset or progression of kidney disease (CKD). Examples CRS 2 (CRS2) include progressive CKD resulting from HF congenital acquired repeated bouts acute decompensated HF. Animal data and clinical studies indicate that extended periods result altered renal hemodynamics followed by pathology. Experimental CRS2 is characterized mild to moderate proteinuria, a decline glomerular filtration rate, an elevated expression injury biomarkers. Important pathophysiological triggers increases venous pressure, maladaptive activation renin-angiotensin-aldosterone axis sympathetic nervous system, as well inflammatory state. Intrarenal oxidative stress proinflammatory signaling precipitate structural injury, including glomerulosclerosis tubulointerstitial fibrosis. Yet, interventional trials directly test impact renin-angiotensin system antagonists β-blockers on are lacking. Secondary analyses designed assess these agents cardiovascular endpoints have failed show consistent benefit regarding functional parameters. contrast, left ventricular assist device placement cardiac resynchronization therapy patients consistently improved function, suggesting marked potential for reversibility many cases CRS2. Future research should be directed towards evaluation novel biomarkers improve diagnosis, severity grading our understanding pathophysiology addition, there need address long-term incorporating information measures function injury.