Search Results For Kshmr (9) ((HOT))
The results of this study support the hypothesis proposed by Nath et al.14 >25 yr ago in which it was suggested that compensatory changes such as increased ammonia production and the resultant complement cascade activation in remnant tubules in the declining renal mass is injurious to the tubulointerstitium. We did not investigate the mechanistic pathways but can speculate, in light of our findings of dissociation between lack of change of proteinuria and preservation of renal function, that prevention of maladaptive compensatory changes in the tubular function may be the most plausible explanation for our study results. In this regard, a small short-term study demonstrated that sodium bicarbonate supplementation reduced tubular peptide hypercatabolism and total urinary ammonia excretion in 11 patients with moderate renal impairment even in the absence of MA.20
Search results for kshmr (9)
The results of this study are also in complete agreement with our previously reported study.21 In this pilot observational study, we were able to demonstrate that during a 2-yr follow-up period, patients with stage 4 CKD and persistent uncorrected low bicarbonate levels between 16 and 21 mmol/L experienced an annual decline in their estimated GFR of >3 ml/min compared with 1 ml/min in those with bicarbonate levels >22 mmol/L. In this randomized study, bicarbonate supplementation was associated with slower rate of decline of CrCl similar to the level seen in nonacidotic patients with CKD in the observational study.
This study has several strengths. The sample size of 134 patients is substantial for a single-center study and is the first report of its kind in this area of research. Duration of follow-up was sufficiently long to observe clinically meaningful outcomes. Moreover, the study was conducted from a busy predialysis clinic and was close to a real-life setting. The patients were heterogeneous with respect to underlying disease, race and ethnic group, and duration of disease, making it likely that the findings can be translated to other populations with CKD. Clearly, it cannot apply to those with associated morbid obesity, cognitive impairment, chronic sepsis, overt congestive heart failure, and uncontrolled hypertension because these comorbidities were the exclusion criteria for this study. Nutritional parameters were assessed blindly by a single dietitian, and, as expected from a single-center study, data collection was complete. Compliance in the study was satisfactory as evident by consistent elevation of bicarbonate levels and urinary sodium excretion, and the end points were rigorous and clinically meaningful; however, this study can be criticized for a lack of placebo use and absence of a double-blind design. Like any other single-center study, reproducibility and generalizability of this report will require further validation by a double-blind, placebo-controlled, multicenter trial.
M.M.Y., chief investigator, designed and wrote the research protocol for this study. I.d.B.-A., principal investigator, carried out the study, monitored nutritional status progress, and collected data. M.M.Y. and I.d.B.-A. had full access to all of the data in the study, and both take responsibility for the integrity of the data and the accuracy of the data analysis. I.d.B.-A. also drafted the manuscript that was revised and edited by all authors. M.V. carried out the statistical analysis but had no other part in the study and was blind to research questions and group allocation. 041b061a72