China
Africa
Explore chapters and articles related to this topic
Diagnostic Approach to Acute Kidney Injury in the Critical Care Unit
Published in Cheston B. Cunha, Burke A. Cunha, Infectious Diseases and Antimicrobial Stewardship in Critical Care Medicine, 2020
Sonali Gupta, Divyansh Bajaj, Sana Idrees, Joseph Mattana
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].
Congenital Heart Disease in Pregnancy
Published in Afshan B. Hameed, Diana S. Wolfe, 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.
Cardiovascular system
Published in Brian J Pollard, Gareth Kitchen, Handbook of Clinical Anaesthesia, 2017
Redmond P Tully, Robert Turner
If present, arrythmias may be symptomatic with palpations, dizziness or syncopal episodes. If HF is secondary or in the presence of coexisting CAD, the patient may report angina episodes. Signs of gout may be present and signs of chronic renal failure in the presence of cardiorenal syndrome.
The impact of preoperative kidney replacement therapy on kidney outcome and survival in patients with left ventricular assist device
Published in Renal Failure, 2023
Hojin Jeon, Junseok Jeon, Kyungho Lee, Darae Kim, Yang Hyun Cho, Jung Eun Lee, Jin-Oh Choi, Wooseong Huh, Yoon-Goo Kim, Eun-Seok Jeon, Hye Ryoun Jang
Cardiorenal syndrome (CRS) is defined as a spectrum of disorders involving both heart and kidneys in which acute or chronic dysfunction in one organ induces acute or chronic dysfunction in the other organ [6]. Therefore, kidney dysfunction is very common in patients with HF. More than half of patients with HF usually have some degree of kidney impairment, and approximately 30% of HF patients have moderate to severe kidney impairment [7]. Kidney dysfunction may be associated with poor survival in HF patients including the patients undergoing HT [8]. On the other hand, the incidence of cardiovascular events has been shown to be significantly higher in patients with advanced CKD [9]. In considering the importance of heart–kidney crosstalk defined as CRS, combined heart–kidney transplantation was recommended for irreversible severe kidney dysfunction (GFR < 30 mL/min/1.73 m2) [10].
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].