scholarly journals Markers of renal function and acute kidney injury in acute heart failure: definitions and impact on outcomes of the cardiorenal syndrome

2010 ◽  
Vol 31 (22) ◽  
pp. 2791-2798 ◽  
Author(s):  
J. P. E. Lassus ◽  
M. S. Nieminen ◽  
K. Peuhkurinen ◽  
K. Pulkki ◽  
K. Siirila-Waris ◽  
...  
2015 ◽  
Vol 21 (5) ◽  
pp. 382-390 ◽  
Author(s):  
Gregory Berra ◽  
Nicolas Garin ◽  
Jérôme Stirnemann ◽  
Anne-Sophie Jannot ◽  
Pierre-Yves Martin ◽  
...  

Nephron ◽  
2020 ◽  
Vol 144 (12) ◽  
pp. 629-633 ◽  
Author(s):  
Yoshio Funahashi ◽  
Sheuli Chowdhury ◽  
Mahaba B. Eiwaz ◽  
Michael P. Hutchens

Cardiorenal syndrome type 1 (CRS-1) is an acute kidney injury (AKI) due to acute worsening of cardiac function. More than 20% of patients with acute heart failure develop AKI, and AKI predicts poor outcome. Although a number of potential pathways have been suggested as heart-kidney connectors which might drive the syndrome, there are significant barriers to investigation, such as a paucity of animal models, a lack of specific biomarkers, and an inconsistent temporal and causal relationship between changes in cardiac flow and development of renal dysfunction. Thus, mechanisms of heart-kidney interaction are still unclear, and there is no specific or effective therapy for CRS-1. This review, therefore, focuses on mitigating these challenges in the investigation of CRS-1. We review the available models and focus on mechanistic insights gained from those models. In particular, we focus on non-flow and endocrine mediators of CRS-1 such as heart-derived messengers which alter renal function and which may represent targetable pathways in this syndrome. As precise connectors of heart-kidney interaction remain unclear, the establishment of animal and relevant cell-culture models and further investigation are required.


Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Jonghanne Park ◽  
Jin Joo Park ◽  
Young-Jin Cho ◽  
Yeon-Yee Yoon ◽  
Il-Young Oh ◽  
...  

Objectives: We investigated the risk factors for contrast-induced acute kidney injury (CIAKI) after coronary angiography (CAG) in patients with acute heart failure (AHF), especially with regard to the volume status. Background: Heart failure is a well-known risk factor for CIAKI after CAG. In HF patients, renal perfusion decreases with systemic congestion. Thus, the standard prevention strategy with isotonic solution infusion may be inappropriate while decongestion may be beneficiary in AHF patients undergoing CAG. Deviation from dry body weight suggests imbalanced volume status. Methods: A total of 199 AHF patients who underwent CAG were eligible for the analysis. Absolute deviation of body weight (


2019 ◽  
Vol 34 (Supplement_1) ◽  
Author(s):  
Davide Catucci ◽  
Caterina Fontana ◽  
Alice Mariotto ◽  
Marco Colucci ◽  
Massimo Torreggiani ◽  
...  

Author(s):  
Dinna N. Cruz ◽  
Anna Giuliani ◽  
Claudio Ronco

Acute kidney injury (AKI) occurring during heart failure (HF) has been labelled cardiorenal syndrome (CRS) type 1. CRS is defined as a group of ‘disorders of the heart and kidneys whereby acute or chronic dysfunction in one organ may induce acute or chronic dysfunction of the other’. This consensus definition was proposed by the Acute Dialysis Quality Initiative, with the aim to standardize those disorders where cardiac and renal diseases coexist. Five subtypes have been proposed, according to which organ is affected first (cardiac vs renal) and whether the dysfunction is acute or chronic. Another subtype which includes systemic conditions leading to both heart and kidney dysfunction is also described.The term ‘worsening renal function’ has been regularly used to describe the acute and/or subacute changes that occur in the kidneys following HF. However, the AKI classification according to the current consensus definition better represents the entire spectrum of AKI in the setting of HF.The pathophysiology of heart–kidney interaction is complex and still poorly understood. Factors beyond the classic haemodynamic mechanisms appear to be involved: neurohormonal activation, venous congestion, and inflammation have all been implicated.Diuretics are still a cornerstone in the management of HF. Intravenous administration by bolus or continuous infusion appears to be equally efficacious. Biomarkers and bioelectrical impedance analysis can be helpful in estimating the real volume overload and may be useful to predict and avoid AKI. The role of ultrafiltration remains controversial, and it is currently recommended only for diuretic-resistant patients as it has not been associated with better outcomes. The occurrence of AKI during HF is associated with substantially greater short- and long-term mortality.


2011 ◽  
Vol 30 (4) ◽  
pp. S180-S181
Author(s):  
M. Rai ◽  
C. Statz ◽  
A. Ras ◽  
J. Rahn ◽  
L. O'Bara ◽  
...  

2014 ◽  
Vol 78 (4) ◽  
pp. 911-921 ◽  
Author(s):  
Akihiro Shirakabe ◽  
Noritake Hata ◽  
Masanori Yamamoto ◽  
Nobuaki Kobayashi ◽  
Takuro Shinada ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document