Therapeutic Options for the Management of the Cardiorenal Syndrome

Abstract

Patients with heart failure often present with impaired renal function, which is a predictor of poor outcome. The cardiorenal syndrome is the worsening of renal function, which is accelerated by worsening of heart failure or acute decompensated heart failure. Although it is a frequent clinical entity due to the improved survival of heart failure patients, still its pathophysiology is not well understood, and thus its therapeutic approach remains controversial and sometimes ineffective. Established therapeutic strategies, such as diuretics and inotropes, are often associated with resistance and limited clinical success. That leads to an increasing concern about novel options, such as the use of vasopressin antagonists, adenosine A1 receptor antagonists, and renal-protective dopamine. Initial clinical trials have shown quite encouraging results in some heart failure subpopulations but have failed to demonstrate a clear beneficial role of these agents. On the other hand, ultrafiltration appears to be a more promising therapeutic procedure that will improve volume regulation, while preserving renal and cardiac function. Further clinical studies are required in order to determine their net effect on renal function and potential cardiovascular outcomes. Until then, management of the cardiorenal syndrome remains quite empirical.

Cardiorenal Syndrome - A Review Article

“…When patients have low blood pressure and poor renal perfusion, positive inotropes such as dobutamine or phosphodiesterase inhibitors may be required. 54 Chronic Cardiorenal Syndrome: Type II Preventive Approaches Pharmacologic therapies that have been beneficial for chronic CVD have been either neutral or favorable to the kidneys including use of RAAS antagonists, beta-adrenergic blocking agents and statins. Furthermore, other strategies include glycemic control in diabetes and blood pressure control in those with hypertension.…”

Cardio-renal syndrome type 2: Etiopathogenesis, diagnosis and therapy

“…Pored diuretika i ultrafiltracije u lečenju naglog popuštanja hronične zastojne srčane slabosti, u cilju održavanja zapremine arterijske krvi koja obezbeđuje perfuziju organa i sprečavanja razvoja akutnog oštećenja bubrega, primenjuju se i drugi lekovi, kao što su: vazodilatatori, inotropni lekovi, sintetski natriuretski peptidi, antagonisti receptora za vazopresin i antagonisti A1 receptora za adenozin (8,28,29). Vazodilatatori (nitroglicerin) popravljaju hemodinamski status bolesnika sa naglim popuštanjem hronične zastojne srčane slabosti (smanjuju pritisak punjenja u kapilarima pluća, sistemski i plućni vaskularni otpor, smanjuju opterećenje volumenom i povećavaju srčani indeks) (8).…”

“…(8). Sintetski natriuretski peptidi (nesiritid) dovode do vazodilatacije arterijskog i venskog sistema, a selektivni antagonisti V2 receptora za vazopresin (tolvaptan) povećavaju klirens osmotski slobodne vode i koncentraciju natrijuma u serumu bolesnika sa naglim popuštanjem hronične zastojne srčane slabosti i hiponatriemijom (Na + = 120-125 mmol/L) (8,28,29). Antagonisti A1 receptora za adenozin su novi agensi koji popravlaju bubrežni protok krvi, podstiču diurezu i povećavaju izlučivanje natrijuma (30).…”

Cardiorenal interaction during the acute phase of experimental <i>Trypanosoma cruzi</i> infection: the influence of aldosterone and the AT1 receptor on mortality

“…The term "cardiorenal syndrome" (CRS) includes a vast array of interrelated complications, highlighting the bidirectional nature of the interactions between the heart and kidneys [13]. Neurohormonal activation is a very important contributor to CRS pathophysiology, leading to exaggerated abnormalities in the activation of the renin-angiotensin-aldosterone system (RAAS) [14].…”