**4. Influence of residual kidney function reduction on progression of cardiovascular pathology in patients on RRT**

Preservation of residual kidney function in dialysis patients improves their survival and prognosis. For example, Dutch joint NECOSAD study [40] in 740 patients on HD showed an increase in residual kidney function (Kt/V by 1 unit) associated with a 66% reduction in the relative risk of death. Prospective analysis by W. Van der Wal et al., which included 1800 dialysis patients (1191 patients were on HD and 609 on PD), found a 1.5-fold death risk increase after loss of residual renal function compared to patients with preserved residual renal function [41]. Y. Obi et al. found that higher and more stable residual renal function (GFR) was associated with better patient survival one year after initiation of regular HD. Mortality related inversely with residual renal function measured by urea clearance and daily urine output [42]. In several other multicenter studies [43, 44] residual function has been an independent predictor of survival in patients on PD. The Canadian-American Study (CANUSA) [45] showed on 601 patients on PD that residual renal function rather than peritoneal creatinine clearance and peritoneal ultrafiltration (UF) correlate with patient survival. A study of residual renal function in PD patients showed a 36% reduction in the relative risk of death with an increase in daily urine output by 250 mL.

Preservation of residual renal function provides better control of hyperhydration, dyselectrolytemia, inflammatory activity, and clearance of protein-bound low molecular weight toxins and medium-molecular-weight molecules. Even a small amount of residual function reduces the level of plasma dissolved uremic toxins and β2-microglobulin [46–48].

The residual renal function allows to reduce cardiac mortality and progression of cardiovascular disease in dialysis patients primarily through better hydration control. Both on regular and continuous PD, CKD patients with uncorrected hyperhydration are at high risk of developing cardiovascular complications: volume/sodium-dependent hypertension, left ventricular hypertrophy, arrhythmias, and congestive heart failure [49–51]. The expansion of intravascular volume leads to elongation of myocardial cells, and eccentric or asymmetrical left ventricular remodeling [52].

In patients on intermittent HD, UF causes post-ischemic impairment of myocardial contractile function (myocardial stunning) even in the absence of angiographically significant coronary disease [53]. Recurrent UF-induced ischemia provokes chronic left ventricular dysfunction, a cause of CHF progression in patients on HD [54]. Preserved residual renal function in patients on regular PD allows to reduce UF volumes during dialysis session, thus reducing risk of recurrent myocardial ischemia or systolic pressure drop during the session (hemodialysis-induced hypotension) [54–57]. In patients on PD, maintenance of residual renal function and significant diuresis attenuates the damaging effects of dextrose on the peritoneal membrane and reduces hyperglycemia and the risk of obesity and diabetes.

The residual renal function not only increases survival but also improves hormonal, mineral-bone, and nutritional disorders and the quality of life in patients on HD and PD, as confirmed by the CHOICE study [58]. Higher quality of life in patients with diuresis over 250 ml per day is also associated with a less restriction in diet and fluid intake, and better nutritional status [59] and control of hyperphosphatemia, renal osteodystrophy, and anemia. The latter depend on a renal synthesis of erythropoietin and active forms of vitamin D3 in kidneys [60, 61]. Several data have shown an association between the preserved residual

renal function and decreased production of inflammatory markers: C-reactive protein and interleukin-6 [62, 63].
