Cardiorenal syndrome: Resistant to diuretics, sensitive to ultraflitration

Aundhakar, Swati C; Mahajan, Sanket K; Mane, Makarand; Lakhotia, Akshay Navalkishor; Mahajani, Vikrant

doi:10.4103/0975-3583.95379

Cited by 3 publications

(2 citation statements)

References 8 publications

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“…RAS activation has also been implicated in the development of cardiac fibrosis in CKD and ESRD patients 74 – 78 . Evidence from multiple randomized clinical trials supports the notion that inhibiting the RAS improves all causes of mortality and reduces adverse cardiovascular events and strokes, which is not commonly seen with other antihypertensive medications 64 , 79 – 81 . RAS inhibition has been widely utilized in managing patients with CVD, especially with co-morbidities of CKD or diabetes mellitus 82 – 87 .…”

Section: Discussionmentioning

confidence: 89%

Pathological cardiac remodeling occurs early in CKD mice from unilateral urinary obstruction, and is attenuated by Enalapril

Ham

Jin

Lei

et al. 2018

Sci Rep

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Cardiovascular disease constitutes the leading cause of mortality in patients with chronic kidney disease (CKD) and end-stage renal disease. Despite increasing recognition of a close interplay between kidney dysfunction and cardiovascular disease, termed cardiorenal syndrome (CRS), the underlying mechanisms of CRS remain poorly understood. Here we report the development of pathological cardiac hypertrophy and fibrosis in early stage non-uremic CKD. Moderate kidney failure was induced three weeks after unilateral urinary obstruction (UUO) in mice. We observed pathological cardiac hypertrophy and increased fibrosis in UUO-induced CKD (UUO/CKD) animals. Further analysis indicated that this cardiac fibrosis was associated with increased expression of transforming growth factor β (TGF-β) along with significant upregulation of Smad 2/3 signaling in the heart. Moreover early treatment of UUO/CKD animals with an angiotensin-converting-enzyme inhibitor (ACE I), Enalapril, significantly attenuated cardiac fibrosis. Enalapril antagonized activation of the TGF-β signaling pathway in the UUO/CKD heart. In summary our study demonstrates the presence of pathological cardiac hypertrophy and fibrosis in mice early in UUO-induced CKD, in association with early activation of the TGF-β/Smad signaling pathway. We also demonstrate the beneficial effect of ACE I in alleviating this early fibrogenic process in the heart in UUO/CKD animals.

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Section: Discussionmentioning

confidence: 89%

Pathological cardiac remodeling occurs early in CKD mice from unilateral urinary obstruction, and is attenuated by Enalapril

Ham

Jin

Lei

et al. 2018

Sci Rep

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“…A recently published study conducted on surgical patients undergoing congenital heart disease surgery on cardiac bypass; revealed 28% of patients developing AKI, both children and adult population were included in this study (7). When search made for other regional studies; a case report found from India reporting diuretic resistance and later developing CRS was found (8). Another original Naqvi article from India highlighting predictors of CRS type 1 in patients with acute right ventricular dysfunction indicated diabetes and presentation in state of shock as poor prognostic markers in their series (9).…”

Section: Discussionmentioning

confidence: 98%

Acute kidney injury with cardiorenal syndrome; experience from a tertiary care renal unit in Pakistan

Naqvi

2020

J Renal Inj Prev

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Introduction: Acute kidney injury (AKI) is a commonly recognized clinical problem after many morbid conditions related to heart like congenital heart disease surgery, acute or chronic congestive heart failure, acute myocardial infarction, infective endocarditis or cardiomyopathies. Cardio-renal syndrome (CRS) includes a spectrum of disorders involving both the heart and kidneys simultaneously; here acute or chronic dysfunction in one organ may induce acute or chronic dysfunction in the other. Objectives: To report here, case series of patients with AKI developing in association with CRS. We aim to report different causes of CRS and outcome of patients in this group of patients. Patients and Methods: Subjects for the study reported here comprised a cohort of 34 patients coming to this institution with AKI in association of CRS. AKI was defined according to KDIGO guidelines and CRS based on consensus conference of ADQI in 2012. Type 1or type2 CRS are included in the study. All patients had normal size kidneys on ultrasonography. Results: Thirty-four patients with AKI and CRS were brought to this institute from January 1990 to December 2014; this was contributing 1% to medical causes of total AKI. Among these 25 were males and 9 females; mean age of these patients was 54.06±14.106 years. Causes of CRS were acute myocardial infarction (ST elevated), congestive cardiac failure, infective endocarditis and dilated cardiomyopathy. More than two third of patients were either oliguric or anuric on presentation. Fluid replacement and/or inotropic support required in 79%. Renal replacement therapy in form of hemodialysis was conducted in 64.7% and intermittent peritoneal dialysis in one patient. Complete renal recovery was observed in 19 (56%) patients, while 12 (35%) died during acute phase of illness. CKD-V developed in one patient, 2 patients lost long term follow up, but became dialysis free and renal functions were in improving trends, they were labeled as partial recovery. Secondary insults like hypotension, aggressive diuresis, and volume loss from gastro-intestinal tract or infection were evaluated for any co-relation with outcome but statistically no significant difference was found. Conclusion: CRS can be severe life-threatening condition especially when patients present with circulatory collapse. Diuretics must be used cautiously in patients with congestive cardiac failure. Infective endocarditis with acute right heart failure can lead to CRS.

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Strategies for the Management of Cardiorenal Syndrome in the Acute Hospital Setting

Chandramohan,

Simhadri,

Jena

et al. 2024

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Cardiorenal syndrome (CRS) is a life-threatening disorder that involves a complex interplay between the two organs. Managing this multifaceted syndrome is challenging in the hospital and requires a multidisciplinary approach to tackle the many manifestations and complications. There is no universally accepted algorithm to treat patients, and therapeutic options vary from one patient to another. The mainstays of therapy involve the stabilization of hemodynamics, decongestion using diuretics or renal replacement therapy, improvement of cardiac output with inotropes, and goal-directed medical treatment with renin–angiotensin–aldosterone system inhibitors, beta-blockers, and other medications. Mechanical circulatory support is another viable option in the armamentarium of agents that improve symptoms in select patients.

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Cardiorenal syndrome: Resistant to diuretics, sensitive to ultraflitration

Cited by 3 publications

References 8 publications

Pathological cardiac remodeling occurs early in CKD mice from unilateral urinary obstruction, and is attenuated by Enalapril

Pathological cardiac remodeling occurs early in CKD mice from unilateral urinary obstruction, and is attenuated by Enalapril

Acute kidney injury with cardiorenal syndrome; experience from a tertiary care renal unit in Pakistan

Strategies for the Management of Cardiorenal Syndrome in the Acute Hospital Setting

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