**1. Introduction**

Cardiorenal syndrome (CRS) refers to the "vicious circle" of interrelated damage of the heart and kidneys, in which dysfunction of one organ complicates the dysfunction of the other, with gradual development of the cardiorenal decompensation.

C. Ronco distinguished 5 clinical types of CRS [1]:

Type 1: Acute worsening of heart function leading to kidney injury and/or dysfunction.

Type 2: Chronic abnormalities in heart function leading to kidney injury or dysfunction. This subtype refers to a more chronic state of kidney disease complicating chronic heart disease, the so-called chronic kidney disease (CKD).

Type 3: Acute worsening of kidney function leading to heart injury and/or dysfunction (acute heart failure).

Type 4: Chronic kidney disease causing cardiac overload, leading to progressive chronic cardiac dysfunction.

Type 5: Systemic condition (e.g., sepsis, vasculitis) leading to simultaneous injury and/or dysfunction of heart and kidney.

We can see the interplay of decreased glomerular filtration rate and impaired cardiac contractile function early in chronic kidney disease (CKD) worsening as renal failure increases. However, the existing classification of CRS does not consider the population of patients on renal replacement therapy (RRT), where the effect of dialysis treatment itself engages additional mechanisms of pathogenesis of cardiac pathology. Thus, the progression of cardiac dysfunction with decreasing ejection fraction reduces the effectiveness of hemodialysis (HD), while reducing the intensity of dialysis regimen and gradual loss of residual renal function speeds up the atherosclerosis and cardiomyopathy progression.

Thus, one can consider the cardiorenal relationships in patients on RRT, reflecting progression and myocardial damage in dialysis patients, as a separate type of CRS where the renal component implies end stage renal disease (ESRD) with complicating metabolic and endocrine disorders, complete loss of residual renal function, and dialysis therapy.

The features of cardiac dysfunction in patients on RRT include its widespread prevalence and severity [2]. The incidence of left ventricular myocardial hypertrophy (LVH) increases with increasing stage of CKD, reaching 90% in stages 4–5 [3]. Prevalence and severity of cardiac pathology, both coronary and non-coronary, increases rapidly in the dialysis stage of renal failure, correlating with dialysis experience. In 75–80% of patients with CKD stage 5D, secondary cardiomyopathy develops predisposing to congestive heart failure (CHF), acute coronary syndrome, or complex rhythm and conduction abnormalities. In patients on RRT, progressive atherosclerosis is associated with activation of inflammatory reactions and high frequency of protein-energy malnutrition (PEM) [4]. Thus, PEM is diagnosed in 20–50% of patients with pre-dialysis stages of CKD, increasing to 50–80% in patients on regular HD and permanent PD.

The cardiac function in patients on RRT deteriorates progressively under several pathogenetic mechanisms. These include bio-incompatibility of dialysis membranes and solutions, ineffective dialysis, PEM, dialysis hypotension, rapid decline and subsequent complete loss of residual renal function, vascular calcification, excessive shunt from arterio-venous hemodialysis fistula (AVF).
