The Hemodynamic and Nonhemodynamic Crosstalk in Cardiorenal Syndrome Type 1

There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

Abstract

The organ crosstalk can be defined as the complex biological communication and feedback between distant organs mediated via cellular, molecular, neural, endocrine and paracrine factors. In the normal state, this crosstalk helps to maintain homeostasis and optimal functioning of the human body. However, during disease states this very crosstalk can carry over the influence of the diseased organ to initiate and perpetuate structural and functional dysfunction in the other organs. Heart performance and kidney function are intimately interconnected, and the communication between these organs occurs through a variety of bidirectional pathways. The cardiorenal syndrome (CRS) is defined as a complex pathophysiological disorder of the heart and the kidneys whereby acute or chronic dysfunction in one organ may induce acute or chronic dysfunction in the other organ. In particular, CRS type 1 is characterized by a rapid worsening of the cardiac function leading to acute kidney injury. This clinical condition requires a more complex management given its more complicated hospital course and higher mortality. A lot of research has emerged in the last years trying to explain the pathophysiology of CRS type 1 which remains in part poorly understood. This review primarily focuses on the hemodynamic and nonhemodynamic mechanisms involved in this syndrome.

Related collections

Most cited references 51

Record: found
Abstract: found
Article: not found

Cardiorenal syndrome.

Claudio Ronco, Mikko Haapio, Andrew House … (2008)

The term cardiorenal syndrome (CRS) increasingly has been used without a consistent or well-accepted definition. To include the vast array of interrelated derangements, and to stress the bidirectional nature of heart-kidney interactions, we present a new classification of the CRS with 5 subtypes that reflect the pathophysiology, the time-frame, and the nature of concomitant cardiac and renal dysfunction. CRS can be generally defined as a pathophysiologic disorder of the heart and kidneys whereby acute or chronic dysfunction of 1 organ may induce acute or chronic dysfunction of the other. Type 1 CRS reflects an abrupt worsening of cardiac function (e.g., acute cardiogenic shock or decompensated congestive heart failure) leading to acute kidney injury. Type 2 CRS comprises chronic abnormalities in cardiac function (e.g., chronic congestive heart failure) causing progressive chronic kidney disease. Type 3 CRS consists of an abrupt worsening of renal function (e.g., acute kidney ischemia or glomerulonephritis) causing acute cardiac dysfunction (e.g., heart failure, arrhythmia, ischemia). Type 4 CRS describes a state of chronic kidney disease (e.g., chronic glomerular disease) contributing to decreased cardiac function, cardiac hypertrophy, and/or increased risk of adverse cardiovascular events. Type 5 CRS reflects a systemic condition (e.g., sepsis) causing both cardiac and renal dysfunction. Biomarkers can contribute to an early diagnosis of CRS and to a timely therapeutic intervention. The use of this classification can help physicians characterize groups of patients, provides the rationale for specific management strategies, and allows the design of future clinical trials with more accurate selection and stratification of the population under investigation.

0 comments Cited 306 times – based on 0 reviews      Review now

Bookmark

Record: found
Abstract: found
Article: not found

Apoptosis in neurodegenerative disorders.

M Mattson (2000)

Neuronal death underlies the symptoms of many human neurological disorders, including Alzheimer's, Parkinson's and Huntington's diseases, stroke, and amyotrophic lateral sclerosis. The identification of specific genetic and environmental factors responsible for these diseases has bolstered evidence for a shared pathway of neuronal death--apoptosis--involving oxidative stress, perturbed calcium homeostasis, mitochondrial dysfunction and activation of cysteine proteases called caspases. These death cascades are counteracted by survival signals, which suppress oxyradicals and stabilize calcium homeostasis and mitochondrial function. With the identification of mechanisms that either promote or prevent neuronal apoptosis come new approaches for preventing and treating neurodegenerative disorders.

0 comments Cited 221 times – based on 0 reviews      Review now

Bookmark

Record: found
Abstract: found
Article: not found

Contrast-induced acute kidney injury.

Peter A. McCullough (2008)

Cardiac angiography and coronary/vascular interventions depend on iodinated contrast media and consequently pose the risk of contrast-induced acute kidney injury (AKI). This is an important complication that accounts for a significant number of cases of hospital-acquired renal failure, with adverse effects on prognosis and health care costs. The epidemiology and pathogenesis of contrast-induced AKI, baseline renal function measurement, risk assessment, identification of high-risk patients, contrast medium use, and preventive strategies are discussed in this report. An advanced algorithm is suggested for the risk stratification and management of contrast-induced AKI as it relates to patients undergoing cardiovascular procedures. Contrast-induced AKI is likely to remain a significant challenge for cardiologists in the future because the patient population is aging and chronic kidney disease and diabetes are becoming more common.

0 comments Cited 179 times – based on 0 reviews      Review now

Bookmark

All references

Author and article information

Journal

Journal ID (publisher-id): CRM

Journal ID (nlm-ta): Cardiorenal Med

Journal ID (doi): 10.1159/issn.1664-5502

Title: Cardiorenal Medicine

Publisher: S. Karger AG

ISSN (Print): 1664-3828

ISSN (Electronic): 1664-5502

Publication date Subscription-year: 2014

Publication date (Print): August 2014

Publication date (Electronic): 14 May 2014

Volume: 4

Issue: 2

Pages: 103-112

Affiliations

Departments of ^aNephrology, Dialysis and Transplantation and ^bInternal Medicine, San Bortolo Hospital, and ^cIRRIV-International Renal Research Institute, Vicenza, ^dClinical Genetics Unit, Department of Women's and Children's Health, University of Padua, Padua, and ^eDepartment of Nephrology and Dialysis, San Giovanni Di Dio, Agrigento, Italy

Author notes

*Dr.ssa Grazia Maria Virzì, Department of Nephrology, Dialysis and Transplantation, International Renal Research Institute Vicenza (IRRIV), San Bortolo Hospital, Via Rodolfi 37, IT-36100 Vicenza (Italy), E-Mail graziamaria.virzi@gmail.com

Article

Publisher ID: 362650 Pmcid ID: PMC4164059 Other ID: Cardiorenal Med 2014;4:103-112

DOI: 10.1159/000362650

PMC ID: PMC4164059

PubMed ID: 25254032

License:

Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.