P0793the performance of the renal function in the stage ckd 5: a destiny already written?

Abstract Background and Aims There is a large amount of data on the factors and progression of Chronic Kidney Disease (CKD), especially in the early stages. Stages 4 and 5, on the contrary, have always been considered hard to modify in their speed and evolution. Recent observational studies have however shown that, even in these stages, the progression is often non-linear, heterogeneous and with frequent changes of trajectory. We retrospectively evaluated our CKD stage 5 patients (pts) from 1/1/2016 to 12/31/2018, with a view to analyzing their functional evolution. Method We included only patients with longer than 6 months follow-up (Table 1) and at least 4 clinical-laboratory controls that included measured Creatinine Clearance (ClCr) and estimated GFR with CKD-EPI (eGFR). For each patient we analyzed: comparability between eGFR and ClCr, progression rate (Table 2); correlation between ClCr, GFR and some clinical-laboratory parameters (diabetes, blood pressure control, use of ACEi / ARB, ischemic myocardiopathy, peripheral obliterant arteriopathy (POA), proteinuria, Hb, uric acid, PTH, phosphorus). Statistics Linear correlation test for continuous variable analysis, chi-square test for group comparison. Results Average slope of eGFR: -2.98 ± 3.73 ml / min / year, of ClCr: -3.73 ± 5.8 ml / min / year. The slope of the progression rate by eGFR followed a Gaussian distribution (R 16.9%; L 55.9%; S 18.6%; M 8.4%) with a trend not statistically different from the progression assessed with ClCr (R 32.2%, L 45.7%, S 11.8%, M 10.1%) (Figure 1). Measured CrCl and eGFR proved well correlated (r=0.565, p<0.001), especially for GFR values <12ml / min. No correlation was found between eGFR and diabetes, ischemic myocardiopathy, Hb, uric acid, PTH, phosphorus, ACEi / ARB therapy, whereas a significant correlation emerged between the rate of progression and the presence of POA (70% of rapid progression POA, p = 0.035) and pressure control (80% of rapid progression patients do not have adequate pressure control, p = 0.031). Conclusion This analysis confirms what is transpiring from the literature: even in stage CKD5 careful monitoring and precise therapeutic strategies can still modify and slow down functional progression. Less than one third of the patients have a GFR loss> 5 ml / min / year, and this rapid progression seems to correlate with the presence of AOCP and poor blood pressure control. For the remaining 70% of the patients, however, a slow evolution or even the possibility of stabilization or functional improvement is expected. These data on the slope of the renal function progression in CKD5, despite the limits of the sample size, encourage us not to consider CKD stage 5 as an inexorable short journey towards artificial replacement therapy.