The severe cardiorenal syndrome: ‘Guyton revisited’

Abstract

The incidence of cardiac failure and chronic renal failure is increasing and it has now become clear that the co-existence of the two problems has an extremely bad prognosis. We propose the severe cardiorenal syndrome (SCRS), a pathophysiological condition in which combined cardiac and renal dysfunction amplifies progression of failure of the individual organ, so that cardiovascular morbidity and mortality in this patient group is at least an order of magnitude higher than in the general population. Guyton has provided an excellent framework describing the physiological relationships between cardiac output, extracellular fluid volume control, and blood pressure. While this model is also sufficient to understand systemic haemodynamics in combined cardiac and renal failure, not all aspects of the observed accelerated atherosclerosis, structural myocardial changes, and further decline of renal function can be explained. Since increased activity of the renin-angiotensin system, oxidative stress, inflammation, and increased activity of the sympathetic nervous system seem to be cornerstones of the pathophysiology in combined chronic renal disease and heart failure, we have explored the potential interactions between these cardiorenal connectors. As such, the cardiorenal connection is an interactive network with positive feedback loops, which, in our view, forms the basis for the SCRS.

Renal Damage after Myocardial Infarction Is Prevented by Renin-Angiotensin-Aldosterone-System Intervention

“…Several mechanisms have been hypothesized, including hemodynamic alterations, involvement of the RAAS and sympathetic nervous system, endothelial dysfunction, and inflammation (27), which also are thought to interact with each other. First, as far as the role of hemodynamics in explaining the observed cardiorenal interaction is concerned, reduced cardiac output after MI may lead to reduced renal perfusion, which in turn could lead to compensatory RAAS activation.…”

Decrease of Urotensin II activity can impact on the volume status in predialysis chronic kidney disease

“…As GFR decreases by worsening CKD, blood pressure rises and is more difficult to control due to aberrant activation of the RAS and sympathic nervous system (SNS). 17 Overhydration, the resulting hyper inflammation, is one of the results of biochemical processes. The increase in inflammatory reaction, the effect is well known in CKD progression.…”

Concept and therapeutic approach to cardiorenal insufficiency

“…8 Klasični koncept adaptacije organizma na HSI i HBI podrazumeva koncept hemodinamske kontrole u kome glavnu ulogu imaju bubrezi, kao regulator volumena ekstracelularne tečnosti, i sistem renin-angiotenzin-aldosteron sa pripadajućim biohemijski aktivnim jedinjenjima (endotelin, natriuretski peptidi, azot oksid). Ovim modelom se mogu objasniti promene volumena ekstracelularne tečnosti, krvnog pritiska i minutnog volumena u bolesnika sa popuštanjem srca i bubrega.…”