Left Ventricular Hypertrophy in Chronic Kidney Disease Patients: From Pathophysiology to Treatment

Abstract

Cardiovascular diseases represent the main causes of morbidity and mortality in patients with chronic kidney disease (CKD). According to a well-established classification, cardiovascular involvement in CKD can be set in the context of cardiorenal syndrome type 4. Left ventricular hypertrophy (LVH) represents a key feature to provide an accurate picture of systolic-diastolic left heart involvement in CKD patients. Cardiovascular involvement is present in about 80% of prevalent hemodialysis patients, and it is evident in CKD patients since stage IIIb-IV renal disease (according to the K/DOQI CKD classification). According to the definition of cardiorenal syndrome type 4, kidney disease is detected before the development of heart failure, although timing of the diagnosis is not always possible. The evaluation of LVH is a bit heterogeneous, and few standard imaging methods can provide the accuracy of either CT- or MRI-derived left ventricular mass. Key principles in the treatment of LVH in CKD patients are mainly based on anemia and blood pressure control, together with the management of secondary hyperparathyroidism and sudden cardiac death prevention. This review is mainly focused on the clinical aspects of CKD-related LVH to provide practical guidelines both for cardiologists and nephrologists in the daily clinical approach to CKD patients.

LCZ696 (Sacubitril/Valsartan), an Angiotensin-Receptor Neprilysin Inhibitor, Attenuates Cardiac Hypertrophy, Fibrosis, and Vasculopathy in a Rat Model of Chronic Kidney Disease

“…Many diverse mechanisms contribute to the development CVD in CKD which manifest mainly as LV hypertrophy, cardiovascular fibrosis, arteriosclerosis and atherosclerosis. 16 These mechanisms include oxidative stress, inflammation, fluid and electrolyte disorders, retained uremic metabolites and mitochondrial dysfunction. In this regard, studies have documented oxidative stress and inflammation in the cardiac tissue of animals with experimental CKD.…”

“…21 Partly as a result of the above-mentioned mechanisms, CKD results in significant myocardial hypertrophy and activation of cellular apoptotic signals which trigger activation of extracellular matrix production pathways leading to fibrosis. 16,22 In fact CKD induced by subtotal nephrectomy leads to increased cross-sectional area of cardiomyocytes and increased abundance of protein markers of hypertrophy such as α-SM actin. 23 In addition, cardiac tissue from CKD animals had increased matrix and TGF-β abundance and reduced matrix metalloproteinase-1.…”

The Relationship Between Pulse Pressure, the Estimated Glomerular Filtration Rate, and Urine Microalbumin/Creatinine Ratio in Korean Adults

“…PP is a powerful predictor of arterial stiffness. Increased arterial stiffness leads to left ventricular hypertrophy [30], and left ventricular hypertrophy is associated with mortality risk and cardiovascular events in patient with CKD and ESRD as demonstrated by higher rates of sudden cardiac death in these patients [31]. Therefore, Fernandez-Fresnedo et al .…”

Cardiac hypertrophy in chronic kidney disease—role of Aldosterone and FGF23

“…Cardiac hypertrophy is a critical complication that is frequently observed in CKD [106,107]. Cardiac hypertrophy develops beginning at early stages of CKD and is quite common in patients on dialysis therapy.…”