Congenital Heart Disease in Pregnancy
Afshan B. Hameed, Diana S. Wolfe in Cardio-Obstetrics, 2020
Severe pulmonary arterial hypertension in the presence of an intra- or extracardiac shunt results in cyanosis due to right-to-left shunting, right ventricular hypertrophy and diastolic dysfunction, and variable right ventricular systolic dysfunction. However, Eisenmenger syndrome is also a multi-organ disease. Patients have a bleeding diathesis due to low platelets and dysfunction of von Willebrand factor but may also have in situ thrombosis in the pulmonary arteries and are predisposed to thromboembolic events such as strokes due to paradoxical embolism across the shunt. The right-to-left shunt also increases risk for infection, particularly endocarditis and brain abscesses from septic emboli. Renal dysfunction can occur due to a nephrotic syndrome, or due to cardiorenal syndrome.
Diagnostic Approach to Acute Kidney Injury in the Critical Care Unit
Cheston B. Cunha, Burke A. Cunha in Infectious Diseases and Antimicrobial Stewardship in Critical Care Medicine, 2020
The presence of numerous connectors between the kidney and heart predisposes patients with heart disease to developing AKI. Common risk factors for development of AKI in cardiovascular patients include advanced age, myocardial infarction, stroke, heart failure, hypertension, diabetes mellitus, advanced New York Heart Association heart failure functional class, and previous hospitalizations for heart failure [10]. Acute kidney injury in the setting of acute decompensated heart failure, a form of Type 1 cardiorenal syndrome, is characterized by a hemodynamically mediated decrease in RBF, compounded by increased sympathetic output, renin-angiotensin system activation, and increased release of inflammatory mediators among various mechanisms [11,12]. Cardiac interventions themselves may predispose to AKI through mechanisms, including exposure to iodinated radiocontrast. Patients undergoing such procedures often have pre-existing comorbidities, including diabetes, hypertension, and use of medications such as diuretics that may make them especially vulnerable to contrast induced AKI. Acute kidney injury has been reported to occur in about 10% of patients after percutaneous coronary angiography and has been associated with increased cardiovascular morbidity and mortality [13].
Roles of Melatonin in Maintaining Mitochondrial Welfare
Shamim I. Ahmad in Handbook of Mitochondrial Dysfunction, 2019
In close association with the previously mentioned relationship with NO and renal protection, more recently it was shown in a model of hypertension that melatonin exerts a renoprotective effect associated with NO bioavailability. The low NO levels occur during CKD, where NO depletion increases the kidney damage. However, melatonin treatment produced renal protection due to a reduction of oxidative stress and restored NO production in the kidney116. Also, melatonin attenuated urine protein excretion, serum creatinine and reduced oxidative stress in renal tissues. The kidney improvements were correlated with the increases in the inducible nitric oxide synthase (iNOS) and intercellular adhesion molecule 1 (ICAM‑1) expression117. According, melatonin associated with exendin-4 was more efficient in reducing renal function in cardiorenal syndrome. Notably, the combined treatment produced, at the renal level, a reduction of protein expression of inflammation (TNF-α/NF-κB/MMP-9/iNOS/RANTES), oxidative stress (NOX-1/NOX-2/NOX-4/oxidized protein), apoptosis (cleaved caspase-3/cleaved PARP/Bax), DNA-damaged markers (γ-H2AX) and fibrosis (p-mad3/TFG-β)118.
Protein biomarkers for cardiorenal syndrome
Published in Expert Review of Proteomics, 2019
Eleni Petra, Jerome Zoidakis, Antonia Vlahou
Under normal conditions, heart and kidney interact to maintain homeostasis. It is well known that the kidney normally controls salt and water content of the body, erythropoietin synthesis, electrolytes and vitamin D activation while the heart regulates the oxygen-rich fluids, blood flow and pressure; hence cardiovascular (CV) function depends directly on the kidney and vice versa [1].The pathological conditions in which heart dysfunction induces or stimulates acute or chronic dysfunction to the kidney and vice versa are described as cardiorenal syndrome (CRS) [2]. CRS is complex, very heterogeneous and patients with renal or heart failure have an increased risk of developing cardiovascular disease (CVD)/heart failure (HF) or acute kidney injury (AKI)/chronic kidney disease (CKD) respectively with high morbidity and mortality [3,4]. The molecular mechanisms which are related to the complex pathophysiology of CRS are partly understood.
Emerging sodium-glucose cotransporter-2 inhibitor therapies for managing heart failure in patients with chronic kidney disease
Published in Expert Opinion on Pharmacotherapy, 2023
Jeffrey Shi Kai Chan, Francesco Perone, Yasmin Bayatpoor, Gary Tse, Amer Harky
Although SGLT2 inhibitors have established roles in the separate treatments of CKD and HF, relatively little guidance is available for patients with both CKD and HF, i.e. those with type 2, 4, or 5 cardiorenal syndrome. First formally defined in 2004, cardiorenal syndrome is a heterogeneous condition that is classified into five subtypes according to the temporal relationship between the occurrence of HF and renal impairment, as well as whether HF and renal impairment were due to other systemic conditions [28]. In type 2 cardiorenal syndrome, chronic HF results in CKD, while in type 4 cardiorenal syndrome, the reverse occurs [28]. Meanwhile, other systemic conditions result in both HF and CKD (or acute renal failure) in type 5 cardiorenal syndrome [28]. Although cardiorenal syndrome was not specifically mentioned in the 2021 European Society of Cardiology guidelines for the diagnosis and treatment of acute and chronic heart failure [26], and the incidence and prevalence of cardiorenal syndrome varied considerably between reports, it is the general consensus that chronic HF and CKD commonly coexist which is associated with poor prognosis [29–31]. As little specific guidance exists for the management of these patients, this article sought to review the mechanisms, clinical evidence, real-world consideration, and future research directions in the use of SGLT2 inhibitors for treating patients with both HF and CKD.
Secretory activity of the coronary artery endothelial cells in conditions of the peritoneal dialysis
Published in Renal Failure, 2022
Monika Misian, Ewa Baum, Andrzej Bręborowicz
Cardiorenal syndrome is a frequent cause of death in a group of patients with end-stage renal failure. Uremia causes dysfunction of the endothelium which is an important factor predisposing patients to the development of cardiorenal syndrome [1]. Renal replacement therapy removes molecules that are toxic toward the endothelial cells but at the same time initiates the development of their inflammatory phenotype [2,3]. One can assume that hemodialysis is more damaging than peritoneal dialysis, to the endothelial cells, because of the direct contact of blood with the dialysis membrane, which may induce intravascular inflammation. Hemodialysis performed with a cellulosic cuprophane membrane, contrary to a synthetic polysulfone membrane, more strongly impaired the endothelium-dependent flow-mediated dilation of the brachial artery [4]. In renal patients treated with hemodialysis, higher than in patients treated with peritoneal dialysis, levels of CD14+ and CD16+ monocytes and apoptotic endothelial microparticles were found [5]. On the other hand, in children treated with hemodialysis, stronger destruction of the endothelium was observed than during treatment with peritoneal dialysis [6]. However, both in patients treated with hemodialysis and peritoneal dialysis, significant damage to the endothelial glycocalyx was observed, which may disturb the function of the endothelium [7]. Endothelial dysfunction strongly correlates with cardiovascular complications in peritoneal dialysis patients [8]. In patients treated with peritoneal dialysis, dysfunction of the endothelium is also linked with the loss of residual renal function [9].
Related Knowledge Centers
- Acute Kidney Injury
- Chronic Kidney Disease
- Diuretic
- Reactive Oxygen Species
- Troponin
- Sympathetic Nervous System
- Nitric Oxide
- Hypovolemia
- Heart Failure
- New York Heart Association Functional Classification