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Heart Attack and Kidney Attack: Evolution of Lay and Clinical Terms for Spontaneous, Acute Organ Injury Syndromes | OMICS International
ISSN-2155-9929
Journal of Molecular Biomarkers & Diagnosis

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Heart Attack and Kidney Attack: Evolution of Lay and Clinical Terms for Spontaneous, Acute Organ Injury Syndromes

Claudio Ronco1, Peter A. McCullough2, Pupalan Iyngkaran3* and Lakhmir S Chawla4

1Department of Nephrology Dialysis & Transplantation, International Renal Research Institute, Italy

2Baylor Healthcare System, Baylor Heart and Vascular Institute, TX, USA

3Department of Cardiology, Royal Darwin Hospital and Flinders University, Northern Territory, Australia

4Department of Anesthesiology and Critical Care Medicine, George Washington University Medical Center, USA

*Corresponding Author:
Claudio Ronco
Department of Nephrology Dialysis & Transplantation
International Renal Research Institute, Italy
E-mail: [email protected]

Received Date: November 23, 2013; Accepted Date: January 29, 2014; Published Date: January 31, 2014

Citation: Ronco C, McCullough PA, Iyngkaran P, Chawla LS (2014) Heart Attack and Kidney Attack: Evolution of Lay and Clinical Terms for Spontaneous, Acute Organ Injury Syndromes. J Mol Biomark Diagn 5:164. doi:10.4172/2155-9929.1000164

Copyright: © 2014 Ronco C, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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Dear Sir,

The term ‘heart attack’, inclusive of Acute Coronary Syndromes (ACS) and myocardial infarction (MI) is based on symptoms, Electrocardiographic (ECG) abnormalities and biomarkers. In an attempt to engage laypeople and non-experts, the term ‘kidney attack’ has been introduced to refer to Acute Kidney Injury (AKI) [1]. Acute kidney injury is a clinical syndrome associated with increased morbidity and mortality making early recognition critical in patient management. The consensus definition of AKI is based on changes in serum Creatinine (sCr) or urine output (UO) [2]. However, it has been long recognized that perturbations in sCr and UO can be induced by pathophysiologic processes that do not cause injury (e.g. volume depletion); just as cardiac output can be decreased by pathophysiologic process unrelated to cardiac ischemia (e.g. bradycardia or volume depletion). Similar to the approach used to differentiate ST-segment elevation myocardial infarction (STEMI) from non-ST-segment elevation myocardial infarction (NSTEMI), a new classification schema of AKI has been proposed. With the advent of robust novel AKI biomarkers, subclinical AKI (a rise in novel AKI biomarkers alone) is analogous to an NSTEMI, while clinical AKI (a rise in AKI biomarkers and significant perturbation in SCr or UO) is analogous to STEMI [3,4].

In patients with ACS, cardiac angina is a symptom complex that prompts care, is well codified, and helps clinicians assess pre-test probability for integration into diagnostic testing (i.e. a supportive history for ACS). Because AKI does not cause visceral discomfort, the concept of Renal Angina (RA) or pathophysiologic stress on the kidneys, the parallel of cardiac angina, has been introduced in order to provide a similar construct to help direct the use and interpretation of AKI diagnostics [5]. Renal angina is currently undergoing validation in prospective studies of adults and children.

Thus, a new nomenclature for ‘kidney attack’ and AKI related syndromes with a wider spectrum of clinical criteria (clinical AKI, subclinical AKI, and renal angina) could be used for classification purposes (Figure 1 and Figure 2) [6-12]. The parallels between the terminology used in ACS and AKI is intentional, as we hope to use these familiar and accessible terms to help teach the non-experts how to appropriately integrate these new terms into the clinical vernacular. The public health burden of AKI is substantial. The population incidence of AKI is approximately 2,100 per million population and the case fatality rate is 25-50% [6]. Given the population of the developed world (USA, Canada, Western Europe, Japan, and Australia) of approximately 1 billion, there will be over 2 million cases of AKI this year, with 500,000 associated deaths and an expected 1.5 million AKI survivors. Of these patients, approximately 15-20% will progress to advanced stage CKD within 24 months, resulting in 300,000 cases of advanced CKD per year. With the increasing incidence of AKI in the aging population, the projected incidence of CKD associated with AKI is expected to increase [7,8].

molecular-biomarkers-diagnosis-Proposed-umbrella

Figure 1: Proposed umbrella lay terms ‘heart attack’ and ‘kidney attack’ with parallel clinical syndromes.

molecular-biomarkers-diagnosis-Established-chest

Figure 2: Established chest pain pathway for ‘heart attack’ and proposed kidney injury pathway for ‘kidney attack’.

In conclusion, the advances in consensus definitions and diagnostic biomarkers in AKI have led to an evolution in the nomenclature of the syndrome. Similar to the progress made in ACS and the lay term ‘heart attack’, AKI and ‘kidney attack’ hold promise. We believe that an educational campaign for awareness and alertness should be undertaken to prevent and improve early recognition of ‘kidney attack’ with use of novel, approved biomarkers and careful assessment of urine output. We think that the new terminology centered around ‘kidney attack’ will provide uniformity in the public health approach to AKI, and help to reveal what has been neglected and underestimated for too long simply because it was not clinically detectable.

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