Pathophysiology of cardiorenal syndrome in decompensated heart failure: Role of lung–right heart–kidney interaction

Guazzi, Marco; Gatto, Pamela; Giusti, G; Pizzamiglio, Francesca; Previtali, I.; Vignati, Carlo; Arena, Ross

doi:10.1016/j.ijcard.2013.09.014

Cited by 66 publications

(59 citation statements)

References 54 publications

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“…In the face of this, RV adapts to maintain output, primarily by the development of hypertrophy and eventually, if the overload persists, of dilatation, tricuspid regurgitation, loss of contractility (by muscle mass unit), and an irreversible decrease in RV function may follow. 38 RV dysfunction and tricuspid regurgitation further complicate HF syndrome by central venous pressure elevation, which affects the release of natriuretic peptides, impairs renal function, definitively causing congestion and a high degree of neural and hormonal activation. 38 Renal dysfunction and renal associated mortality seem to be higher in HFpEF compared with HFrEF.…”

Section: Rv Dysfunction and Failurementioning

confidence: 99%

“…38 RV dysfunction and tricuspid regurgitation further complicate HF syndrome by central venous pressure elevation, which affects the release of natriuretic peptides, impairs renal function, definitively causing congestion and a high degree of neural and hormonal activation. 38 Renal dysfunction and renal associated mortality seem to be higher in HFpEF compared with HFrEF. 39 Although, together with PH, the development…”

Section: Rv Dysfunction and Failurementioning

confidence: 99%

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Pulmonary Hypertension in Heart Failure Preserved Ejection Fraction

Guazzi

2014

Circ: Heart Failure

103

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Section: Rv Dysfunction and Failurementioning

confidence: 99%

Section: Rv Dysfunction and Failurementioning

confidence: 99%

Pulmonary Hypertension in Heart Failure Preserved Ejection Fraction

Guazzi

2014

Circ: Heart Failure

103

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“…During an AHF event, systemic vasoconstriction and decreased cardiac function can lead to increased cardiac pre-and after load and increased left ventricular filling pressures [24]. This, in turn, leads to congestion and hypoperfusion, with neurohormonal activation, inflammation, oxidative stress and haemodynamic abnormalities, leading to organ dysfunction, including renal dysfunction [24,25].…”

Section: Discussionmentioning

confidence: 99%

Can chronic heart failure induce kidney function damage?

Kimak

Dziedzic

Kimak

et al. 2016

Current Issues in Pharmacy and Medical Sciences

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events, hospitalisation, and more cardiovascular complications following a myocardial infarct [4,5]. Even microalbuminuria, in the absence of an apparent decrease in renal function or diabetes, predicts more cardiovascular disease (CVD) and death [6]. The impact of CVD in CKD is illustrated by reports on the natural history of patients with early CKD. These indicate that the risk of premature CVD death is much higher than the risk of dialysis/transplantation progress [7,8]. Such observations are significant not only because of a high incidence and prevalence of end stage CKD, but because the number of patients with early CKD far exceeds those with end stage CKD. This trend is continuing to rise [9].Patients with CKD, have the highest risk for atherosclerotic CVD. Current interventions have been insufficiently Accelerated atherosclerosis and increased cardiovascular events have been extensively documented in patients with end stage chronic kidney disease. The aim of our work was to find evidence supporting the theory that chronic heart failure (CHF) induces renal function damage. In our work, lipids, apolipoprotein (apo)AI, NTproBNP, hsCRP, lipid hydroperoxide (LPO) and creatinine levels were determined in patients with CHF. A total of 37 patients who were diagnosed with CHF, as well as 15 healthy persons, were recruited for the study. The patients were placed into 2 groups: patients with NYHA class 2 and NYHA class 3. Using routine laboratory methods, NTproBNP level, and lipids were measured by way of employing a Cobas Integra analyser, while the concentration of hs-CRP was measured by immunonephelometric methods. Moreover, serum LPO concentration was measured using Cayman's Assay Kit (LPO). The statistical analysis of the obtained results was performed using the nonparametric Kruskal-Wallis test and Spearman's correlation analysis. Our work demonstrated that the CHF patients had significantly decrease concentration of HDL cholesterol and apoAI, but increased NT-pro-BNP, hsCRP and LPO levels. In all CHF patients, a significant positive correlation between NTproBNP concentration and creatinine levels, and a significant negative correlation between NTproBNP concentration and apoAI levels, as well as between concentration of creatinine and apoAI levels, was shown. The study results suggest that variation in the concentration of NTproBNP, LPO, hsCRP, apoAI, creatinine, in addition to chronic heart failure progression, gradually accompany the progress of chronic renal failure. What is more, the disorders may lead to the occurrence of cardiovascular events, consequently, to patient death.

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“…Right ventricular dilatation and dysfunction may adversely affect kidney function through an elevation in venous pressure, as discussed above (15), as well as through impairing left ventricular filling (16) and, therefore, forward output. Another mechanism that had previously been hypothesized to explain worsening kidney function in heart failure, as well as improvement in kidney function with diuresis, is the negative limb of the starling curve (Figure 1, D→E).…”

Section: Pathophysiologymentioning

confidence: 99%

A Patient with Heart Failure and Worsening Kidney Function

Sarnak¹

2014

Clinical Journal of the American Society of Nephrology

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There is high prevalence of CKD, defined by reduced GFR, in patients with heart failure. Reduced kidney function is associated with increased morbidity and mortality in this patient population. The cardiorenal syndrome (CRS) involves a bidirectional relationship between the heart and kidneys whereby dysfunction in either may exacerbate the function of the other, but this syndrome has been difficult to precisely define because it has many complex physiologic, biochemical, and hormonal abnormalities. The pathophysiology of CRS is not completely understood, but potential mechanisms include reduced kidney perfusion due to decreased forward flow, increased right ventricular and venous pressure, and neurohormonal adaptations. Treatment options include inotropic medications; diuretics; ultrafiltration; and medications, such as b-blockers, inhibitors of the renin-angiotensinaldosterone system, and more novel treatments that focus on unique aspects of the pathophysiology. Recent observational studies suggest that treatments that result in a decrease in venous pressure and lead to hemoconcentration may be associated with improved outcomes. Patients with CRS that is not responsive to medical interventions should be considered for ventricular assist devices, heart transplantation, or combined heart and kidney transplantation.Clin J Am Soc Nephrol 9: 1790-1798, 2014. doi: 10.2215/CJN.11601113 Case PresentationOur patient is a 56-year-old man with ischemic cardiomyopathy who has had several admissions for worsening shortness of breath, lower-extremity edema, and increased abdominal girth. He was readmitted with the same symptoms. His medical history is significant for coronary artery disease, coronary artery bypass surgery performed 9 years before admission, mitral and tricuspid valve repair, atrial fibrillation with failed cardioversion, nonsustained ventricular tachycardia with an implantable cardiac defibrillator, pulmonary hypertension, severe hyperlipidemia treated with lipid apheresis using an arteriovenous fistula, and CKD with a baseline creatinine level of 1.5-2 mg/dl.Outpatient oral medications included furosemide, 60 mg in the morning and 40 mg in the evening; carvedilol, 12.5 mg twice daily; hydrochlorothiazide, 25 mg daily; digoxin, 0.125 mg daily; aspirin, 81 mg daily; mexiletine, 150 mg three times daily; and warfarin, 3 mg daily. He had intolerance to angiotensin-converting enzyme (ACE) inhibitors and statins.Pertinent physical examination findings included BP, 130/74 mmHg; heart rate, 84 beats/min; respiratory rate, 18 breaths/min; and weight, 88.7 kg (increased .10 kg during the last few months). Jugular venous pressure was elevated to the angle of the jaw with the patient at 45 degrees. Heart rate was irregular, with a II/VI systolic murmur loudest at the left sternal border. There were bibasilar crackles, tense ascites, and 21 pitting edema bilaterally up to the knees. He had an arteriovenous fistula in his left arm.Laboratory results were as follows: sodium, 131 mEq/L; potassium, 3.8 mEq/L; chlori...

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Pathophysiology of cardiorenal syndrome in decompensated heart failure: Role of lung–right heart–kidney interaction

Cited by 66 publications

References 54 publications

Pulmonary Hypertension in Heart Failure Preserved Ejection Fraction

Pulmonary Hypertension in Heart Failure Preserved Ejection Fraction

Can chronic heart failure induce kidney function damage?

A Patient with Heart Failure and Worsening Kidney Function

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