*Review* **Cardiac Remodeling in Chronic Kidney Disease**

### **Nadine Kaesler 1,**†**, Anne Babler 1,**†**, Jürgen Floege 1 and Rafael Kramann 1,2,\***


† These authors contributed equally.

Received: 17 February 2020; Accepted: 3 March 2020; Published: 5 March 2020

**Abstract:** Cardiac remodeling occurs frequently in chronic kidney disease patients and a ffects quality of life and survival. Current treatment options are highly inadequate. As kidney function declines, numerous metabolic pathways are disturbed. Kidney and heart functions are highly connected by organ crosstalk. Among others, altered volume and pressure status, ischemia, accelerated atherosclerosis and arteriosclerosis, disturbed mineral metabolism, renal anemia, activation of the renin-angiotensin system, uremic toxins, oxidative stress and upregulation of cytokines stress the sensitive interplay between di fferent cardiac cell types. The fatal consequences are left-ventricular hypertrophy, fibrosis and capillary rarefaction, which lead to systolic and/or diastolic left-ventricular failure. Furthermore, fibrosis triggers electric instability and sudden cardiac death. This review focuses on established and potential pathophysiological cardiorenal crosstalk mechanisms that drive uremia-induced senescence and disease progression, including potential known targets and animal models that might help us to better understand the disease and to identify novel therapeutics.

**Keywords:** uremia; uremic cardiomyopathy; organ crosstalk; cardiorenal syndrome; chronic kidney disease; left-ventricular hypertrophy; heart failure; cardiac fibrosis

**Key Contribution:** Here, we provide a most recent overview on the proposed mechanisms in organ crosstalk from kidney disease to myocardium, underlying cellular mechanisms and available mouse models. We thereby aim to o ffer potential therapeutic target sites in this understudied disease condition.
