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Right Heart Failure—Unrecognized Cause of Cardiorenal Syndrome

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Right Heart Failure—Unrecognized Cause of Cardiorenal Syndrome PERSPECTIVE www.jasn.org Right Heart Failure—Unrecognized Cause of Cardiorenal Syndrome Shweta Bansal,1,2 Anand Prasad,3 and Stuart Linas4,5 Divisions of 1Nephrology and 3Cardiology, University of Texas Health at San Antonio, San Antonio, Texas; 2Renal Section, South Texas Veterans Healthcare System, San Antonio, Texas; 4Renal and Hypertension Division, University of Colorado School of Medicine, Aurora, Colorado; and 5Nephrology Division, Denver Health Medical Center, Denver, Colorado J Am Soc Nephrol 29: 1795–1798, 2018. doi: https://doi.org/10.1681/ASN.2018020224 The cardiorenal syndromes (CRSs) are de- compromised, leading to activation of classified PH into five groups on the basis fined as disorders of the heart and kidneys, baroreceptors residing in the high-pressure of etiology and mechanisms7 (Table 1). whereby acute or chronic dysfunction of system, which results in activation of neu- RHF encompasses right heart dysfunc- one organ induces acute or chronic dys- rohormones, including the sympathetic tion due to any of above etiologies of function of the other.1 Generally, CRSs are nervous system, renin-angiotensin- PH. Among all, PH due to LHF (group classified into five subtypes, which are aldosterone system (RAAS), and vaso- 2 PH) remains the most common cause conceptual and largely on the basis of pressin.3 These neurohormones cause of RHF, and pathophysiology of CRS in expert opinion. Since the recognition of systemic and renal vasoconstriction thisgroupissharedwiththepatients CRS as an entity, multiple studies have de- and stimulation of sodium retention with LHF. However, there is a paucity of scribed its magnitude and pathophysiol- throughout the nephron to compensate data regarding the prevalence of renal ogy. However, the majority of the patients for arterial underfilling and reduced BP disease in patients with PH and isolated in these trials have had left heart failure but at the expense of increased systemic RHF. In retrospective analyses of hospi- (LHF) with reduced ejection fraction.2 vascular resistance and higher plasma vol- talized patients and PH registries, acute There is a dearth of information regarding ume. Initially, the GFR is maintained with kidney diseases and CKDs exist in 4%– pulmonary hypertension (PH) and isola- increased filtration fraction; however, after 50% of patients and significantly asso- ted right heart failure (RHF) as a cause of the autoregulatory capacity is exhausted, ciate with worse outcomes.8,9 However, CRS. Here, we discuss the potential path- decreases in GFR ensue. On the basis of it is not clear whether PH and RHF are ophysiology of renal disease in patients associations between increases in central the primary causes of kidney disease. To with PH and isolated RHF with the pur- venous pressure (CVP) and reduced GFR answer this question, it is necessary to pose to stimulate further investigation in in patients with heart failure, venous show that PH/RHF can contribute to re- this understudied topic. Tounderstand re- congestion has been recognized as an ad- nal dysfunction in the absence of LHF. nal dysfunction in PH and RHF,it is useful ditional important determinant of renal In sleep apnea, severity of nocturnal hyp- to review the pathophysiology of CRS in dysfunction.4,5 Venous congestion, in oxemia, and in chronic obstructive pul- LHF, because mechanisms of renal dys- addition to causing hemodynamics pertur- monary disease (COPD), degree of functions are better studied in LHF, and bances on transglomerular pressure gradi- hypercapnia closely associate with de- some of these are shared by RHF. ent, also causes release of inflammatory creasedRBFandGFR,suggestingapos- mediators, neurohormones, and activation sible causal association between renal of endothelial cells, resulting in decompen- dysfunction and COPD/sleep apnea PATHOGENESIS OF CRS IN LHF sation of heart and kidney function.4,6 (group 3 PH). In mechanistic studies of The main mechanisms behind renal dys- function in LHF involve (1)reducedrenal ETIOLOGY AND PATHOGENESIS Published online ahead of print. Publication date blood flow (RBF) as a result of neurohor- OF CRS IN RHF available at www.jasn.org. monal activation and (2) increased central Correspondence: Dr. Shweta Bansal, Division of and renal venous pressure. Concisely, in PH is a syndrome characterized by the Nephrology, Department of Medicine, University of Texas Health at San Antonio, 7703 Floyd Curl Drive, heart failure with reduced ejection frac- presenceof mean pulmonary artery pres- MSC 7882, San Antonio, TX 78229. Email: ban- tion, as a result of decreases in stroke vol- sure .25 mm Hg at rest measured [email protected] ume and cardiac output, arterial integrity by right-sided cardiac catheterization. Copyright © 2018 by the American Society of (or effective arterial blood volume) is The World Health Organization has Nephrology J Am Soc Nephrol 29: 1795–1798, 2018 ISSN : 1046-6673/2907-1795 1795 PERSPECTIVE www.jasn.org Table 1. Classification of pulmonary hypertension/right heart failure and potential pathophysiologic mechanisms of cardiorenal syndrome in the respective groups PH/RHF Etiology Potential Pathophysiologic Mechanism Group 1 Pulmonary arterial hypertension PH → ventricular dyssynchrony and leftward ventricular septal bowing → impaired LV filling →↓LV cardiac output → neurohormonal activation Central venous congestion Group 2 Left heart failure ↓ LV cardiac output → neurohormonal activation Central venous congestion Group 3 Lung disease and/or hypoxemia Hypercapnia →↓in SVR → neurohormonal activation Hypoxia →↓RBF and renal oxidative stress PH → ventricular dyssynchrony and leftward ventricular septal bowing Group 4 Chronic thromboembolic disease PH → ventricular dyssynchrony and leftward ventricular septal bowing →↓LV cardiac output Central venous congestion Group 5 Miscellaneous PH → ventricular dyssynchrony and leftward ventricular septal bowing →↓LV cardiac output Central venous congestion PH, pulmonary hypertension; RHF, right heart failure; LV, left ventricle; SVR, systemic vascular resistance; RBF, renal blood flow. COPD, hypercapnia is associated with de- sodium and water retention.13 Because independently predicted GFR.16,17 It is creases in systemic vascular resistance and pulmonary baroreceptors were not acti- possible that, compared with LHF, pa- thereby, threatening arterial pressure, re- vated, the cause for neurohormonal tients with RHF are more prone to renal sulting in unloading of arterial barorecep- activation and renal dysfunction was consequence of venous congestion, be- tors and increases in NE and RAAS. The unclear. Recent work has shown that cause central venous congestion may net effect is reduced RBF as well as sodium LV cardiac output can be reduced in pa- develop earlier in the course without and water retention just as in low left ven- tients with PH as a consequence of two significant prior sodium and water re- tricle (LV) cardiac output state.10 mechanisms. First, increased right ven- tention from high RVafterload and re- The cause of kidney disease in patients tricle (RV) afterload leads to decreases in duced RV output. These changes in with pulmonary arterial hypertension RV output and thus, decreases in left right-sided hemodynamics result in (PAH; group 1 PH) or chronic thrombo- atrial and LV filling. Second, as a result increased renal venous pressure and embolic disease (group 4 PH) is more of direct ventricular interaction, (1)be- decreased GFR. Further studies are complex, because neither hypercapnia cause both ventricles are enclosed clearly required to prove this hypothe- nor decreased ejection fraction are pre- within a relatively nondistensible peri- sis. The potential pathogenesis of renal sent in these patients. Peripheral edema cardium, increase in RV volume may oc- dysfunctioninPH/RHFisillustratedin and ascites are common, and resistance cur at the expense of reduced LV volume; Figure 1. to diuretics often occurs as the disease also, (2) RV pressure overload may lead progresses in advanced PAH. Do these to prolonged contraction of RV free wall, patients have neurohormonal activation, causing a right to left trans-septal pres- CLINICAL PRESENTATION AND impaired natriuresis, or reduced RBF to sure gradient at the early diastolic phase DIAGNOSIS explain salt and water retention? If so, of LV, and thus, results in dyssynchrony what is the stimulus? One study of pa- and leftward ventricular septal bowing. The clinical manifestations are nonspe- tients with PAH showed increases in The consequence is not only ineffective cificandusuallyreflect the underlying plasma endothelin, atrial natriuretic RVend systolic contraction but also, im- cause of PH/RHF (i.e.,COPD,PAH,or peptide, and NE concentrations but nor- paired LV early diastolic filling, causing signs and symptoms related to volume mal plasma renin levels.11 In an experi- decreased left stroke volume and re- overload and congestion). The diagnosis mental model of pulmonary stenosis in duced cardiac output, despite normal of CRS should be considered in patients dogs, as the pulmonary artery pressure LV ejection fraction.14,15 In 46 patients with PH/RHF presenting with worsen- was increased, LV cardiac output and with PAH, the LV stroke volume index ing renal function either at the time of mean arterial pressure (MAP) de- and the LV end diastolic volume index presentation or during hospitalization. creased, and the RAAS was activated. were 25% lower compared with in con- Multiple biomarkers reflecting neuro- Salt and water retention occurred over trol healthy
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