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      The Prevalence of Metabolic Acidosis in Patients with Different Stages of Chronic Kidney Disease: Single-Centre Study

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          Background: Metabolic acidosis (MA) is one of the most common consequences of CKD. MA is also a risk factor of CKD progression and increased mortality in these patients. Aim: The aim of this retrospective, cross-sectional study was to assess the prevalence of MA in different stages of CKD and renal replacement therapy (RRT) modalities – haemodialysis (HD) and peritoneal dialysis (PD). Additionally, the relationship between the prevalence of MA and aetiology of kidney disease was analysed. Methods: One thousand five patients in different stages of CKD, or modalities of RRT were enrolled into this single-centre cross-sectional study. Forty-one patients were ruled out because of oral bicarbonate supplementation. In the remaining 964 patients (698 CKD stages 1–5, 226 HD, 40 PD), venous blood HCO<sub>3</sub><sup>−</sup> concentration, as well as serum Cr and urea concentrations were assessed. MA was diagnosed when blood HCO<sub>3</sub><sup>−</sup> concentration was below 22 mmol/L. Results: The prevalence of MA increased among all stages of CKD. Patients on HD had lower prevalence of MA in comparison with CKD 5 patients with no RRT (38.5 vs. 56.0%; p = 0.02) In PD patients, the prevalence of MA was significantly lower than in HD patients (2.5 vs. 38.5%; p < 0.001). In the whole study group, there were no significant differences in the prevalence of MA between different aetiologies of CKD (glomerulonephritis 24%, hypertension 23%, diabetes 25%, and tubule-interstitial diseases 24%). Also, when only patients in stages CKD 3–5 were compared, no significant differences in the prevalence of acidosis were found (glomerulonephritis 28%, hypertension 22%, diabetes 24%, and tubule-interstitial 21%). Conclusions: (1) MA is more frequent in patients with more advanced stages of CKD. (2) RRT reduces the prevalence of MA. (3) In PD patients, MA is rare. (4) Aetiology of CKD seems not to have a significant impact on MA prevalence.

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          Most cited references 33

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          Bicarbonate supplementation slows progression of CKD and improves nutritional status.

          Bicarbonate supplementation preserves renal function in experimental chronic kidney disease (CKD), but whether the same benefit occurs in humans is unknown. Here, we randomly assigned 134 adult patients with CKD (creatinine clearance [CrCl] 15 to 30 ml/min per 1.73 m(2)) and serum bicarbonate 16 to 20 mmol/L to either supplementation with oral sodium bicarbonate or standard care for 2 yr. The primary end points were rate of CrCl decline, the proportion of patients with rapid decline of CrCl (>3 ml/min per 1.73 m(2)/yr), and ESRD (CrCl <10 ml/min). Secondary end points were dietary protein intake, normalized protein nitrogen appearance, serum albumin, and mid-arm muscle circumference. Compared with the control group, decline in CrCl was slower with bicarbonate supplementation (5.93 versus 1.88 ml/min 1.73 m(2); P < 0.0001). Patients supplemented with bicarbonate were significantly less likely to experience rapid progression (9 versus 45%; relative risk 0.15; 95% confidence interval 0.06 to 0.40; P < 0.0001). Similarly, fewer patients supplemented with bicarbonate developed ESRD (6.5 versus 33%; relative risk 0.13; 95% confidence interval 0.04 to 0.40; P < 0.001). Nutritional parameters improved significantly with bicarbonate supplementation, which was well tolerated. This study demonstrates that bicarbonate supplementation slows the rate of progression of renal failure to ESRD and improves nutritional status among patients with CKD.
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            Amelioration of metabolic acidosis in patients with low GFR reduced kidney endothelin production and kidney injury, and better preserved GFR.

            Metabolic acidosis often accompanies low glomerular filtration rate and induces secretion of endothelin, which in turn might mediate kidney injury. Here we tested whether treatment of metabolic acidosis in patients with low glomerular filtration rate reduced the progression of kidney disease. Fifty-nine patients with hypertensive nephropathy and metabolic acidosis had their blood pressure reduced with regimens that included angiotensin-converting enzyme inhibition. Thirty patients were then prescribed sodium citrate, and the remaining 29, unable or unwilling to take sodium citrate, served as controls. All were followed for 24 months with maintenance of their blood pressure reduction. Urine endothelin-1 excretion, a surrogate of kidney endothelin production, and N-acetyl-beta-D-glucosaminidase, a marker of kidney tubulointerstitial injury, were each significantly lower, while the rate of estimated glomerular filtration rate decline was significantly slower. The estimated glomerular filtration rate was statistically higher after 24 months of sodium citrate treatment compared to the control group. Hence it appears that sodium citrate is an effective kidney-protective adjunct to blood pressure reduction and angiotensin-converting enzyme inhibition.
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              Insulin resistance in patients with chronic kidney disease.

              It has been reported that insulin resistance appears at an earlier stage of chronic kidney disease (CKD). However, few data are available concerning what factors of metabolic abnormalities, such as apolipoprotein (Apo) profile or acidosis, might be associated with insulin resistance in patients with CKD. We used the hyperinsulinemic euglycemic glucose clamp technique to examine insulin sensitivity in patients without diabetes (n = 29) with different stages of renal function. Results were compared with those in healthy subjects (n = 10) and related to various affecting variables. In healthy subjects, the glucose disposal rate (GDR) was 9.93 +/- 1.33 mg/kg/min. The GDR of patients with CKD (6.91 +/- 2.46 mg/kg/min) was significantly less than that of healthy subjects ( P < 0.01), which shows diminished insulin sensitivity in patients with CKD. There was a negative correlation between GDR and serum creatinine level ( r = -0.449; P < 0.05) and positive correlations between GDR and creatinine clearance ( r = 0.549; P < 0.01) and Apo A-1/B levels ( r = 0.396; P < 0.05). Of particular relevance is the observed close correlation between GDR and bicarbonate level, with an extremely high predictive value for degree of acidosis ( r = 0.611; P < 0.0005). Stepwise multivariate regression analysis selected bicarbonate (F = 13.28) and Apo A-1/B levels (F = 6.58) as independent contributing variables. We found that insulin resistance correlated linearly with decline in renal function. Independent variables related to insulin resistance were bicarbonate and Apo A-1/B levels in patients with CKD.

                Author and article information

                Kidney Blood Press Res
                Kidney and Blood Pressure Research
                S. Karger AG
                December 2020
                16 October 2020
                : 45
                : 6
                : 863-872
                Department of Nephrology, Transplantation and Internal Medicine, Medical University of Silesia, Katowice, Poland
                Author notes
                *Andrzej Wiecek, Department of Nephrology, Transplantation and Internal Medicine, Medical University of Silesia, Francuska 20/24 Street, PL–40-027 Katowice (Poland),
                508980 Kidney Blood Press Res 2020;45:863–872
                © 2020 The Author(s). Published by S. Karger AG, Basel

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                Page count
                Figures: 2, Tables: 5, Pages: 10
                Research Article

                Cardiovascular Medicine, Nephrology

                Metabolic acidosis, Chronic kidney disease


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