The Cardiorenal Syndrome: What the Cardiologist Needs to Know

Abstract

Interactions between the heart and the kidneys are increasingly acknowledged among both cardiologists and nephrologists. The term cardiorenal syndrome now applies to the bidirectional nature of how disease in one organ system affects the function of the other organ system. Cardiovascular disease is a major threat to patients with chronic kidney disease, while renal dysfunction is prevalent in patients with cardiac disease and is a significant predictor of prognosis in cardiac patients. Still, renal patients with cardiac disease have largely been excluded from the clinical trials that have been the basis of modern cardiologic treatment. In this review, the current understanding of the pathophysiological mechanisms involved in the cardiorenal syndrome and potential therapeutic implications will be summarized from a nephrologist's point of view. Probably, fragile cardiorenal patients will benefit from an enhanced collaboration between cardiologists and nephrologists to secure the best treatment given under safe conditions.

Noncardiac Comorbidities in Heart Failure With Reduced Versus Preserved Ejection Fraction

“…The reports vary significantly in different datasets, depending on the specific criteria used, but the figures are similar in patients with HFrEF and HFpEF. The interdependence of heart and kidney dysfunction is captured by the recently described “cardiorenal syndrome” (7,80). Renal dysfunction may worsen HF through multiple mechanisms, including increased sodium and fluid retention, anemia, inflammation, and uremic toxins, as well as RAAS and sympathetic activation.…”

Pentoxifylline Decreases Dialysis Risk in Patients With Advanced Chronic Kidney Disease

“…Using ESRD as the primary outcome, our study showed that the addition of ACEI/ARB to pentoxifylline achieved no further benefits in ESRD risk reduction in predialysis stage 5 CKD, and, moreover, that pentoxifylline alone conferred a lower risk of initiation of long‐term dialysis than ACEI/ARB monotherapy. Consistent with clinical practice and especially in patients with cardiorenal syndrome, RAAS blockade for CKD is not always associated with an improvement in renal function . Although most patients have an attenuating reduction after the initial functional drop in GFR, a minority of patients have a conspicuous decrease in GFR or hyperkalemia that can often be ameliorated by withholding ACEI/ARB therapy.…”

Mechanisms in fluid retention – towards a mutual concept

“…In 2008, the CRS was subdivided into five types (Ronco et al, 2008;Ronco et al, 2010;Waldum & Os, 2013).…”

“…However, during an incident of total loss of kidney function, the fluid retention is caused by the loss of kidney function itself; in all other cases of CRS, type 3 and 4 fluid retention is most likely caused by interaction between changes in vasculature, pharmacodynamics, mineral and vitamin metabolism, as well as production of inflammatory cytokines (Waldum & Os, 2013;Clementi et al, 2015). However, during an incident of total loss of kidney function, the fluid retention is caused by the loss of kidney function itself; in all other cases of CRS, type 3 and 4 fluid retention is most likely caused by interaction between changes in vasculature, pharmacodynamics, mineral and vitamin metabolism, as well as production of inflammatory cytokines (Waldum & Os, 2013;Clementi et al, 2015).…”