Dialysis-Induced Cardiovascular and Multiorgan Morbidity

Abstract

Hemodialysis has saved many lives, albeit with significant residual mortality. Although poor outcomes may reflect advanced age and comorbid conditions, hemodialysis per se may harm patients, contributing to morbidity and perhaps mortality. Systemic circulatory "stress" resulting from hemodialysis treatment schedule may act as a disease modifier, resulting in a multiorgan injury superimposed on preexistent comorbidities. New functional intradialytic imaging (i.e., echocardiography, cardiac magnetic resonance imaging [MRI]) and kinetic of specific cardiac biomarkers (i.e., Troponin I) have clearly documented this additional source of end-organ damage. In this context, several factors resulting from patienthemodialysis interaction and/or patient management have been identified. Intradialytic hypovolemia, hypotensive episodes, hypoxemia, solutes, and electrolyte fluxes as well as cardiac arrhythmias are among the contributing factors to systemic circulatory stress that are induced by hemodialysis. Additionally, these factors contribute to patients' symptom burden, impair cognitive function, and finally have a negative impact on patients' perception and quality of life. In this review, we summarize the adverse systemic effects of current intermittent hemodialysis therapy, their pathophysiologic consequences, review the evidence for interventions that are cardioprotective, and explore new approaches that may further reduce the systemic burden of hemodialysis. These include improved biocompatible materials, smart dialysis machines that automatically may control the fluxes of solutes and electrolytes, volume and hemodynamic control, health trackers, and potentially disruptive technologies facilitating a more personalized medicine approach.

Minimizing Myocardial Ischemic Injury by Cool Dialysate in Maintenance Hemodialysis Patients: A Randomized Controlled Trial

“…As shown in figure (1), We initially evaluated (138) Maintenance HD patients for enrollment in the study, (38) were ruled out (18 were ineligible and 20 were not interested in the study), (50) patients were randomized to each treatment arm. (6) patients from each arm were reallocated to the other treatment arm based on the decision of the treating physician.…”

“…Cardiovascular disease (CVD) is the leading cause of morbidity and mortality among End-Stage Renal Disease (ESRD) patients on Hemodialysis (HD) (1) . Early in the course of Chronic Kidney Disease (CKD) with 75% of patients having preexisting CVD, patients are more likely to experience Major Adverse Cardiovascular Events (MACE) than to progress to ESRD.…”

The Pathogenesis of End-Stage Renal Disease from the Standpoint of the Theory of General Pathological Processes of Inflammation

“…To begin with, the development of systemic proinflammatory tissue stress is promoted by the presence of ESRD and PH due to multiple sources of inflammatory stimuli, such as oxidative stress, acidosis, and fluid overload, increased comorbidity, including infections, dialysis procedure, production, and inadequate removal (insufficient clearance) of proinflammatory cytokines [ 112 ]. These changes in PH are associated with insufficiently effective filtration of cytokines and other molecules weighing 15–45 kDa, activation of leukocytes and plasma systems of hemostasis, complement, and kallikrein-kinins during the interaction of blood with dialysis membranes, cyclical fluctuations in blood volume and electrolyte levels, and osmotic shifts [ 113 , 114 , 115 ]. Uremia, as a common link in the pathophysiology of ESRD, causes tissue stress in adipose tissue and skeletal muscles, increasing insulin resistance and leading to the development of SIR in facultatively glycosylating organs [ 116 ].…”

Blood-incompatibility in haemodialysis: alleviating inflammation and effects of coagulation

“…Several untoward clinical consequences have been associated with extracorporeal procedures. The ‘residual syndrome’ and ‘dialysis-induced systemic stress’ are two explanations of the additional disturbances HD creates [ 4 , 5 ]. Together with the partial correction of the uraemic syndrome by dialysis, these effects perhaps explain why further improvements of patient outcomes have been so difficult to achieve.…”