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Published on: November 7, 2017
Chronic Kidney Disease-Associated Cardiomyopathy: Mechanisms and Therapeutic Strategies
Konstantinos Grigoriou1, Vasileios Lamprou2, Anastasios Chatzichidiroglou3
1Department of Pharmacology, Medical School, University of Athens, 11527 Athens, Greece.
Insights
Chronic kidney disease-associated cardiomyopathy (CKD-CM) involves early heart muscle changes in chronic kidney disease (CKD). Understanding its mechanisms aids early intervention to prevent severe heart disease and reduce mortality in CKD patients.
Area of Science:
- Nephrology
- Cardiology
- Pathophysiology
Background:
- Chronic kidney disease-associated cardiomyopathy (CKD-CM) encompasses myocardial disease developing early in chronic kidney disease (CKD).
- Historically termed uremic cardiomyopathy, it was linked to kidney failure, but injury begins earlier with interstitial fibrosis.
- Fibrosis contributes to heart failure with preserved ejection fraction (HFpEF)-like states, atrial fibrillation, and arrhythmia risk.
Purpose of the Study:
- To review the interacting mechanisms driving CKD-CM.
- To summarize imaging findings across CKD stages.
- To discuss current and novel therapeutic strategies for CKD-CM.
Main Methods:
- Literature review of mechanisms, imaging, and therapeutics for CKD-CM.
- Synthesis of information on abnormal loading, neurohormonal activation, metabolic/inflammatory stress, mineral bone disorder, and microvascular dysfunction.
- Analysis of imaging findings and therapeutic approaches in CKD stages.
Main Results:
- CKD-CM involves complex interactions of multiple factors.
- Interstitial fibrosis precedes overt hypertrophy and reduced ejection fraction.
- HFpEF-like physiology, atrial fibrillation, and arrhythmic risk are driven by fibrosis.
Conclusions:
- Early detection and intervention in CKD-CM are crucial.
- Understanding CKD-CM pathogenesis can reduce severe cardiomyopathy progression.
- Targeting CKD-CM mechanisms may lower cardiovascular mortality in CKD patients.
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.
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