The cardiovascular–dialysis nexus: the transition to dialysis is a treacherous time for the heart

Abstract

Chronic kidney disease (CKD) patients require dialysis to manage the progressive complications of uraemia. Yet, many physicians and patients do not recognize that dialysis initiation, although often necessary, subjects patients to substantial risk for cardiovascular (CV) death. While most recognize CV mortality risk approximately doubles with CKD the new data presented here show that this risk spikes to >20 times higher than the US population average at the initiation of chronic renal replacement therapy, and this elevated CV risk continues through the first 4 months of dialysis. Moreover, this peak reflects how dialysis itself changes the pathophysiology of CV disease and transforms its presentation, progression, and prognosis. This article reviews how dialysis initiation modifies the interpretation of circulating biomarkers, alters the accuracy of CV imaging, and worsens prognosis. We advocate a multidisciplinary approach and outline the issues practitioners should consider to optimize CV care for this unique and vulnerable population during a perilous passage.

Inflammation and Cardiovascular Disease Associated With Hemodialysis for End-Stage Renal Disease

“…B-type natriuretic peptide (BNP) and NT-proBNP are elevated due to reduced renal clearance, fluid retention, and abnormal left ventricular function. In particular, NT-proBNP is filtered through the kidneys and regulated by dialysis resulting in large fluctuations in patients with advanced kidney disease, making it impossible to define a threshold value to assess the patient's cardiac function (Chan et al, 2021). sST2 soluble suppression of tumorigenicity (sST2) has received much attention in recent years as a new biomarker for risk stratification in acute and chronic heart failure, for therapeutic assessment, and for predicting patient prognosis (Gaggin and Januzzi, 2013;Januzzi et al, 2015;Dalal et al, 2018;Mirna et al, 2020).…”

“…This is due to the rapid exchange of fluid through the dialysis membrane, which reduces coronary perfusion and thus induces obstruction or microvascular damage. Troponin is metabolized by the kidneys, which may further elevate the peak troponin levels seen in dialysis-induced coronary artery disease ( Chan et al, 2021 ). This elevated troponin level cannot be explained by ischaemic myocardial necrosis, even if the patient has concomitant coronary artery disease.…”

“…B-type natriuretic peptide (BNP) and NT-proBNP are elevated due to reduced renal clearance, fluid retention, and abnormal left ventricular function. In particular, NT-proBNP is filtered through the kidneys and regulated by dialysis resulting in large fluctuations in patients with advanced kidney disease, making it impossible to define a threshold value to assess the patient’s cardiac function ( Chan et al, 2021 ).…”

Kidney dysfunction requiring dialysis is a heterogeneous syndrome: we should treat it like one

“…Healthcare expenditures for patients on chronic dialytic therapy mount up to $35.9 billion, accounting for 7.2% of the overall Medicare-paid claims in the fee-for-service system event though they constitute 1% of the Medicare population [4]. Notably, the mortality rates in patients treated with dialysis, while modestly improved over the last decade, are alarmingly high, rating at 15-30% in the first 4 months after commencing dialysis and 10-20% annually, exceeding by 20-fold that of age-matched individuals in the general United States population [3,5,6]. Five-year and 10 year-survival probabilities for patients on maintenance hemodialysis are worse than for patients with breast cancer, prostate cancer, and colorectal cancer [7 investments in oncology research, relative to nephrology research, have driven the development of precision and immune-oncology therapies, offering hope to millions of patients with cancer [8,9].…”

Initiation of Dialysis Is Associated With Impaired Cardiovascular Functional Capacity

“… 1 The transition to dialysis dependency introduces additional stressors, such as rapid fluid and electrolyte shifts, repetitive myocardial ischemia secondary to coronary microvascular dysfunction and intradialytic hypotension, increased inflammation attributable to blood contact with the dialysis membrane and catheters, and increased myocardial oxygen demand attributable to access‐associated augmentation in cardiac output. 2 , 3 , 4 Accordingly, cardiovascular mortality rate in patients with ESKD is at its highest during the first year of dialysis, and ≈80% of cardiovascular deaths in patients on dialysis are secondary to primary arrythmia or sudden cardiac death. 5 , 6 …”