Kidney Failure in Heart Failure

Tarik K*, Mehmet AK, Mehmet B and Ilgin K

Department of Cardiology, University of Firat, Turkey

*Corresponding author: Tarik Kivrak, Department of Cardiology, University of Firat, 23119, Turkey

Received: May 29, 2017; Accepted: June 15, 2017; Published: June 29, 2017

Abstract

The heart is closely related to the kidney. Cardiorenal syndrome with bidirectional heart-kidney signal in gare increasingly being recognized for the association with increased morbidity and mortality. This relationship is defined the cardiorenal syndrome. Pathophysiologically Our aim is to talk abou the effect and treatment of kidney failure in heart failure.

Keywords: Kidney failure; Heart failure; Cardiorenal syndrome

Introduction

The heart has strong relationships with other organs, the marriage to the kidneys is particularly unique. It is directly dependent on the regulation of salt and water content of the body by the kidneys. The kidneys are directly dependent on pressure and blood flow produced by the heart. This relationship is known as the cardiorenal syndrome [1]. The cardiorenal syndrome is not limited to patients with heart failure(HF), as cardiovascular disease (including HF) usually develops in patients with chronic and acute kidney disease, and signifies a poor outcome too [2].

Epidemiology

More or less 4.5% of people in the general population have a glomerular filtration rate (GFR), 60 mL/min/1.73 m², mean time across 50% of patients with acute and chronic HF (both preserved and reduced) have a steady reduction in GFR [3]. The prognostic importance of a decrease in GFR has only relatively recently been recognized 50 studies were published in the association between renaldys function and mortality [3].

To this background of kidney function disorder, growing worse kidney function has been identified as a clear identity. Especially during hospitalization, it was sighted that even a small, as little as 0.2 mg/dL remain in serum creatinine was associated with poor outcomes [4]. Worsening renal function (WRF) is associated with increased mortality in both in patients and outpatients with larger increases in serum creatin in predicting worse outcomes [5]. Sheerin, et al. lately advised changes in the definition of growing worse kidney function and discussed that growing worse kidney function in acute HF should be evaluated over the entirein-hospital period, and during three months after discharge, to assess possible transient WRF [6].

Pathophysiology of Renalimpairment in Heart Failure

The importance of attenuated renal blood flow (RBF) and enhanced central venous pressure as primary effector mechanisms for kidney failure were established early in the 20th century [7]. Cody and colleagues published land mark papers that further established the relationship between renal hemodynamics, GFR and the severity of HF. They demonstrated in ACEi naive patients that the reduction in RBF was out of proportion to the decrease in cardiac index, while GFR was relatively maintained; a phenomenon now easily explained by renal autoregulation [8]. These findings have been increased in patients on an ACE inhibitor, with the variation that RBF and GFR reduced in parallel since compensatory efferent arteriolar vasoconstriction is reduced by ACEi [9]. In the last few years, focused has shifted to venous congestion another important determinant of reduced GFR. It has now been convincingly shown in new patients with HF that, independent of a decreasein renal blood flow, there is an epidemiologic association between increased CVP or venous congestion and reduced GFR [10]. The importance of venous congestion in detection GFR is probably much greater in acute HF, but we have no information on RBF, venous congestion, and GFR in patients with acute HF.

Amultitude of factors influences the association between hemodynamics and GFR of particular attention are modulation of the rennin-angiotensin system, sympathetic nervous system (SNS) activation, inflammation, endothelial dysfunction, and anemia. Next, to the direct effect on renal blood flow, angiotensin II encourage renal parenchymal fibrosis, direct influences GFR, induces hyporesponsiveness to natriuretic peptide and mediates SNS activation [11-15]. Degenerated renal function in HF performs much more than elementarily a landing in GFR. Albuminuria is mostly observed in patients with chronic HF as was seen in retrospective analyses of CHARM and GISSI-HF [16,17]. Over 30% of patients have albuminuria, many of which have microalbuminuria. When present there is a stepwise increase in the risk of HF hospitalizations and mortality from normo-, to micro- and macro-albuminuria. In addition to increased glomerular permeability, decreased reabsorption in the tubules due to renal tubular damage most likely further contributes to the development of albuminuria. Tubular damage is now increasingly recognized in patients with acute and chronic HF [18,19]. Identification of patients at high risk of morbidity and mortality should contain ameasure of renal dysfunction: a GFR, and probably, albuminuria or a marker of renal tubular loss. New data have stated that blood urea nitrogen (BUN) could be an even better prognostic indicatorthat favors (some form) of GFR. In addition to this, BUN has been associated with factors beyond glomerular filtration, such as neurohormonal activation and hemodynamic status, which could be the cause for the fact that it retains powerful prognostic information even after controlling for GFR [20]. Unfortunately, phenotyping patients with renal dysfunction have proved a challenging endeavor since no gold standard consists by which HF-induced renal dysfunction can be distinguished from theintrinsic renaldisease. After all, it has been defined that the majority of risk related to renal dysfunction is limited to patients with eitheran elevated NT-proBNP or a high BUN to creatinine ratio (BUN/Creat), many markers which may help to define HF-induced renal dysfunction [21,22].

Treatment of Heart Failure Patients with Renal Dysfunction

RAAS inhibitors are related to a decline in eGFR with initiation, after which eGFR declines in parallel with placebo. For betablockersuniform, observations have been informed, though the magnitude of the impact was smaller. Biventricular pacing or left ventricular assist devices increase cardiac output and probably RBF, GFR has been advised to increase at least transiently in responders [23-25]. Many trials have been designed to treat or prevent WRF in acute HF specifically. The adenosine receptor antagonist rolofylline did not end up the expected benefit on renal function in acute HF [26]. In another study, low-dose nesiritide and dopamine were assessed in patients with renal damage. However, both treatments failed to provide a renal benefit [27]. In the end, therapies that attenuate congestion may affect renal function, too. Loop diuretics are the principalof the therapyof symptoms and signs of congestion in acute and chronic HF. After all, their impact on renal function is poorly understood and studied, and indication strongly confounds observational data since patientswith more severe HF (and renal dysfunction) are described more loop diuretics [28]. The DOSE trial laboured different dosages and intermittent vs. continuous prescription of loop diuretics in acute HF. The study did show that, though post-discharge outcomes were like, more high loop diuretics dosages were related to more fluid and weight loss but a higher incidence of WRF [29]. Since ultrafiltration direct decreases venous congestion, it could directaffect renal function by reducing venous pressure. After all, there was no evidence of improvement in renal function compared with loop diuretics in the UNLOAD and RAPIDCHF studies [30]. In the recent CARRESS-HF study in patients with WRF and persistent congestion admitted for acute HF, ultrafiltration was inferior to stepped pharmacologic therapy on changes in creatinine, and this was sustained after discharge [31].

Conclusion

Kidney failure is related to higher mortality and morbidity in HF. The reasonfor renal dysfunction is multifactorial but decreased renal blood flow, and venous congestion isfeatured factors, which are possiblymediated by a multitude of cardiorenal connectors. In the end, though much has been learned from the interaction between heart and kidney in HF, we need more assigned epidemiologic, mechanistic, and controlled trials in HF patients with reduced renal function. A newly updated classification of cardiorenal syndromes is needed which involves last evidence and milestones areas of attention and areas of uncertainties where progress is wanted. In the end, it should cause preventive and treatment strategies that can preserve renal function in patients with HF.