Heart failure and kidney dysfunction: epidemiology, mechanisms and management
Abstract
Heart failure (HF) is a major health-care problem and the prognosis of affected patients is poor. HF often coexists with a number of comorbidities of which declining renal function is of particular importance. A loss of glomerular filtration rate, as in acute kidney injury (AKI) or chronic kidney disease (CKD), independently predicts mortality and accelerates the overall progression of cardiovascular disease and HF. Importantly, cardiac and renal diseases interact in a complex bidirectional and interdependent manner in both acute and chronic settings. From a pathophysiological perspective, cardiac and renal diseases share a number of common pathways, including inflammatory and direct, cellular immune-mediated mechanisms; stress-mediated and (neuro)hormonal responses; metabolic and nutritional changes including bone and mineral disorder, altered haemodynamic and acid-base or fluid status; and the development of anaemia. In an effort to better understand the important crosstalk between the two organs, classifications such as the cardio-renal syndromes were developed. This classification might lead to a more precise understanding of the complex interdependent pathophysiology of cardiac and renal diseases. In light of exceptionally high mortality associated with coexisting HF and kidney disease, this Review describes important crosstalk between the heart and kidney, with a focus on HF and kidney disease in the acute and chronic settings. Underlying molecular and cellular pathomechanisms in HF, AKI and CKD are discussed in addition to current and future therapeutic approaches.
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Heightened TMAO levels correlate with adverse diastolic indices such as increased left atrial volume index.
“The most intriguing aspect of this association was that heightened TMAO levels correlate with adverse diastolic indices such as increased left atrial volume index, suggesting that perhaps an accumulation of this metabolite may affect tissue mechanics.”
From Dietary metabolism, the gut microbiome, and heart failure (2019) · cites this paper as [182]
Similar findings were observed in chronic systolic heart failure patients.
“In a separate study, we observed similar findings in chronic systolic heart failure patients182.”
From Dietary metabolism, the gut microbiome, and heart failure (2019) · cites this paper as [182]
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- Authors
- Schefold, J. C., Filippatos, G., Hasenfuss, G., Anker, S. D., & von Haehling, S.
- Affiliations
- University Hospital of Bern (CH)
- National and Kapodistrian University of Athens (GR)
- Universitätsmedizin Göttingen (DE)
- Corresponding author
- Anker, Stefan D.
- Venue
- Nature Reviews Nephrology
- Published
- 2016-08-30
- Volume
- 12
- Issue
- 10
- Pages
- 610-623
- ISSN
- 1745-8323 (ISSN-L)
- 1759-5061
- 1759-507X
- OpenAlex
- W2513245700
- Cited by
- 671
- References
- 208
- Citations by year
- 2026: 49 · 2025: 94 · 2024: 100 · 2023: 105 · 2022: 94 · 2021: 75 · 2020: 53 · 2019: 42 · 2018: 34 · 2017: 21 · 2016: 3 · 2015: 1
- FWCI
- 5.82
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Reviews Nephrology (publishedVersion)
- PubMed (publishedVersion)
- BORIS (University Library Bern) (submittedVersion)
- GRO (submittedVersion)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Heart Failure Treatment and Management
- Health Sciences › Medicine › Nephrology › Chronic Kidney Disease and Diabetes
- Health Sciences › Medicine › Nephrology › Acute Kidney Injury Research
- Keywords
- heart failure, renal dysfunction, acute kidney injury, chronic kidney disease, cardiorenal syndrome, glomerular filtration rate decline, mortality, pathophysiology, anemia, neurohormonal response, inflammation, hemodynamics, volume status, acid-base balance, treatment options
- MeSH terms
- Animals, Heart, Heart Failure, Hemodynamics, Humans, Kidney, Neurotransmitter Agents, Renal Insufficiency, Chronic, Acute Kidney Injury, Cardio-Renal Syndrome
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