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Publications

Journal Article Review Ppublish

PubMed: 42528432 DOI: 10.31083/BJHM51534

Chronic Kidney Disease-Associated Cardiomyopathy: Mechanisms and Therapeutic Strategies.

Br J Hosp Med (Lond) 87(7):51534

Authors: Konstantinos Grigoriou, Vasileios Lamprou, Anastasios Chatzichidiroglou, Panagiotis Theofilis, Panagiotis Iliakis, Anastasios Apostolos, Nikolaos Ktenopoulos, Efstratios Karagiannidis, Antonios P Antoniadis, Nikolaos Fragakis, Dimitrios Patoulias, Paschalis Karakasis

Affiliations

  • Department of Pharmacology, Medical School, University of Athens, 11527 Athens, Greece.
  • Manchester Heart Centre, Manchester Royal Infirmary, Manchester University NHS Foundation Trust, M13 9WL Manchester, UK.
  • Department of Internal Medicine, International Hellenic University, 57001 Thermi, Greece.
  • First Cardiology Department, School of Medicine, Hippokration General Hospital, National and Kapodistrian University of Athens, 11527 Athens, Greece.
  • Department of Cardiology, Harefield Hospital, Guy's and St Thomas' NHS Foundation Trust, UB9 6JH London, UK.
  • Emergency Department, AHEPA University General Hospital of Thessaloniki, 54636 Thessaloniki, Greece.
  • Second Department of Cardiology, Hippokration General Hospital, Aristotle University of Thessaloniki, 54642 Thessaloniki, Greece.
  • Second Propedeutic Department of Internal Medicine, Faculty of Health Sciences, Aristotle University of Thessaloniki, 54642 Thessaloniki, Greece.

Abstract

Chronic kidney disease-associated cardiomyopathy (CKD-CM) is a term that captures the spectrum of myocardial disease that begins early in chronic kidney disease (CKD) and progresses as kidney function declines. Historically described as uremic cardiomyopathy, the condition was associated with severe left ventricular hypertrophy and fibrosis in patients with kidney failure. However, functional abnormalities and myocardial injury have been shown to begin much earlier, with diffuse interstitial fibrosis preceding overt hypertrophy or reduced ejection fraction. Fibrosis drives heart failure with preserved ejection fraction (HFpEF)-like physiology and atrial fibrillation and increases arrhythmic risk. In this review, we describe the multiple interacting mechanisms, including abnormal loading, neurohormonal activation, metabolic and inflammatory stress, mineral bone disorder, and microvascular dysfunction. We summarize imaging findings across CKD stages and describe established and emerging therapeutic strategies. A better understanding of CKD-CM pathogenesis is likely to enable early intervention and prevention, with successful outcomes measured by reduced progression to severe cardiomyopathy and lower cardiovascular mortality in CKD.

MeSH

Kidney Diseases, Hypertrophy, Left Ventricular, Fibrosis, Heart Failure, Heart Failure, Diastolic, Hypertrophy, Kidney, Atrial Fibrillation, Therapeutics, Cardiomyopathies