Eubicarbonatemic Hydrogen Ion Retention and CKD Progression.
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ABSTRACT:
SUBMITTER: Madias NE
PROVIDER: S-EPMC8350821 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:BACKGROUND:In the United States, incidence of ESRD is 1.5 times higher in men than in women, despite men's lower prevalence of CKD. Prior studies, limited by inclusion of small percentages of minorities and other factors, suggested that men have more rapid CKD progression, but this finding has been inconsistent. METHODS:In our prospective investigation of sex differences in CKD progression, we used data from 3939 adults (1778 women and 2161 men) enrolled in the Chronic Renal Insufficiency Cohort Study, a large, diverse CKD cohort. We evaluated associations between sex (women versus men) and outcomes, specifically incident ESRD (defined as undergoing dialysis or a kidney transplant), 50% eGFR decline from baseline, incident CKD stage 5 (eGFR<15 ml/min per 1.73 m2), eGFR slope, and all-cause death. RESULTS:Participants' mean age was 58 years at study entry; 42% were non-Hispanic black, and 13% were Hispanic. During median follow-up of 6.9 years, 844 individuals developed ESRD, and 853 died. In multivariable regression models, compared with men, women had significantly lower risk of ESRD, 50% eGFR decline, progression to CKD stage 5, and death. The mean unadjusted eGFR slope was -1.09 ml/min per 1.73 m2 per year in women and -1.43 ml/min per 1.73 m2 per year in men, but this difference was not significant after multivariable adjustment. CONCLUSIONS:In this CKD cohort, women had lower risk of CKD progression and death compared with men. Additional investigation is needed to identify biologic and psychosocial factors underlying these sex-related differences.
| S-EPMC6317604 | biostudies-literature
Project description:Introduction:High dietary acid load and metabolic acidosis are associated with an accelerated decline in kidney function and may contribute to the observed heterogeneity in end-stage renal disease (ESRD) risk according to APOL1 genotype. Our objective was to examine the associations of metabolic acidosis and dietary acid load with kidney disease progression, according to APOL1 genotype, among individuals with chronic kidney disease (CKD). Methods:We studied 1048 African American participants in the Chronic Renal Insufficiency Cohort. Metabolic acidosis was defined as blood levels of serum bicarbonate less than 22 mEq/L, and dietary acid load was quantified by potential renal acid load (PRAL) using data from the Diet Health Questionnaire. APOL1 status was defined as having 2 risk variants, consisting of either possible combination of the G1 and G2 risk alleles. We tested associations of APOL1 and dietary and metabolic acidosis with CKD progression, defined as time to ESRD or 50% decline in eGFR. Results:During a median follow-up period of 7 years, 379 participants had an incident CKD progression event (6.4 events per 100 person-years). After full adjustment, among participants with 2 APOL1 variants, the analysis failed to detect an association between metabolic acidosis or dietary acid load and CKD progression (hazard ratio [HR], 1.03; 95% confidence interval [CI], 0.96-1.11 per 1 mEq/L higher serum bicarbonate and an HR, 1.03; 95% CI, 0.92-1.15 per 10 mEq/L higher PRAL). Similar associations were noted among participants without the APOL1 high-risk genotype. Conclusion:In a population at high risk of developing ESRD, metabolic acidosis and dietary acid load were not associated with CKD progression.
| S-EPMC6611987 | biostudies-literature
Project description:Stem cells show promise in the treatment of AKI but do not survive long term after injection. However, organ repair has been achieved by extending and attaching the omentum, a fatty tissue lying above the stomach containing stem cells, to various organs. To examine whether fusing the omentum to a subtotally nephrectomized kidney could slow the progression of CKD, we used two groups of rats: an experimental group undergoing 5/6 nephrectomy only and a control group undergoing 5/6 nephrectomy and complete omentectomy. Polydextran gel particles were administered intraperitoneally before suture only in the experimental group to facilitate the fusion of the omentum to the injured kidney. After 12 weeks, experimental rats exhibited omentum fused to the remnant kidney and had lower plasma creatinine and urea nitrogen levels; less glomerulosclerosis, tubulointerstitial injury, and extracellular matrix; and reduced thickening of basement membranes compared with controls. A fusion zone formed between the injured kidney and the omentum contained abundant stem cells expressing stem cell antigen-1, Wilms' tumor 1 (WT-1), and CD34, suggesting active, healing tissue. Furthermore, kidney extracts from experimental rats showed increases in expression levels of growth factors involved in renal repair, the number of proliferating cells, especially at the injured edge, the number of WT-1-positive cells in the glomeruli, and WT-1 gene expression. These results suggest that contact between the omentum and injured kidney slows the progression of CKD in the remnant organ, and this effect appears to be mediated by the presence of omental stem cells and their secretory products.
| S-EPMC4033364 | biostudies-literature
Project description:CKD is a global public health problem with significant mortality and morbidity.We examined the multivariable association of plasma levels of IL-1, IL-1 receptor antagonist, IL-6, TNF-?, TGF-?, high-sensitivity C-reactive protein, fibrinogen, and serum albumin with progression of CKD in 3430 Chronic Renal Insufficiency Cohort study participants.Over a median follow-up time of 6.3 years, 899 participants reached the composite end point of ?50% decline in eGFR from baseline or onset of ESRD. Elevated plasma levels of fibrinogen, IL-6, and TNF-? and lower serum albumin were associated with a greater decline in eGFR over time. After adjusting for demographics, BP, laboratory variables, medication use, and baseline eGFR, hazard ratios for the composite outcome were greater for the patients in the highest quartile of fibrinogen (hazard ratio, 2.05; 95% confidence interval, 1.64 to 2.55; P<0.001), IL-6 (hazard ratio, 1.44; 95% confidence interval, 1.17 to 1.77; P<0.01), and TNF-? (hazard ratio, 1.94; 95% confidence interval, 1.52 to 2.47; P<0.001) compared with those in the respective lowest quartiles. The hazard ratio was 3.48 (95% confidence interval, 2.88 to 4.21; P<0.001) for patients in the lowest serum albumin quartile relative to those in the highest quartile. When also adjusted for albuminuria, the associations of fibrinogen (hazard ratio, 1.49; 95% confidence interval, 1.20 to 1.86; P<0.001), serum albumin (hazard ratio, 1.52; 95% confidence interval, 1.24 to 1.87; P<0.001), and TNF-? (hazard ratio, 1.42; 95% confidence interval, 1.11 to 1.81; P<0.001) with outcome were attenuated but remained significant.Elevated plasma levels of fibrinogen and TNF-? and decreased serum albumin are associated with rapid loss of kidney function in patients with CKD.
| S-EPMC5012490 | biostudies-other
Project description:IntroductionMedial arterial calcification is common in chronic kidney disease (CKD) and portends poor clinical outcomes, but its progression relative to the severity of CKD and the role of other risk factors is unknown because of the lack of reliable quantification.MethodsCalcification of breast arteries detected by mammography, which is exclusively medial and correlates with medial calcification in peripheral arteries and with cardiovascular outcomes, was used to measure the progression of medial arterial calcification in women with CKD and end-stage renal disease (ESRD). Measurements showed intra- and interobserver correlations of 0.98, an interstudy variability of 8% to 11%, and a correlation with computed tomographic measurements of 0.92.ResultsProgression of calcification was measured in 60 control subjects (estimated glomerular filtration rate (eGFR) ? 90 ml/min per 1.73 m2) and 137 subjects with CKD (eGFR < 90 ml/min per 1.73 m2). Progression in control subjects was linear over time and independent of age. The rate of progression was increased in CKD but only at eGFR < 40 ml/min per 1.73 m2 (median, 8.1 vs. 3.9 mm/breast/yr in controls; P = 0.006). Progression accelerated markedly in subjects with ESRD (median, 20 mm/breast/yr; n = 36), but did not differ from controls after kidney transplantation (n = 25). Diabetes significantly augmented progression in subjects with CKD and ESRD but not in controls.ConclusionMammography is a convenient and reliable method to measure the progression of medial arterial calcification. Progression does not increase until advanced stages of CKD, accelerates markedly in ESRD, and returns to control rates after kidney transplantation. Diabetes significantly increases progression in CKD and ESRD.
| S-EPMC6224661 | biostudies-literature
Project description:The prevalence of chronic kidney disease (CKD) in Taiwan is 11.9%, and the incidence and prevalence of end-stage renal disease (ESRD) is ranked first in the world. The severity of CKD progression to ESRD is dependent on glomerular filtration rate and proteinuria. However, the risk factors for ESRD also include diabetes, hypertension, hyperlipidemia, age, sex, and so on, and predicting CKD progression using few variables is insufficient. Currently, there are no models with high accuracy and high explanatory power that could predict the risk of progression to dialysis in CKD patients in Taiwan. Our aim was to establish an optimal prediction model for CKD progression in patientsThis study was a retrospective cohort study, which reviewed data from the "Public health insurance Pre-ESRD preventive program and patient health education program" that was implemented by the National Health Insurance Administration, Ministry of Health and Welfare. From 2006 to 2013, data of CKD patients from the Tri-Service General Hospital in Neihu District, Taipei City was examined. The data collected in this study included demographic variables, past medical history, and blood biochemical values. After exclusion of variables with >30% missing data, the remaining variables were interpolated using multiple imputations and inputted into the prediction model for analysis. The Cox proportion hazard model was used to investigate the influence of CKD risk factors on progression to dialysis. The strengths of various models were evaluated using likelihood ratios (LR), in order to identify a model which uses the least factors but has the strongest explanatory power.The study results included 1549 CKD patients, of whom 1017 eventually had dialysis. This study found that in the prediction model with the best explanatory power, the influencing factors and hazard ratios (HR) were: age 0.95 (0.91-0.99), creatinine 1.03 (1.02-1.05), urea nitrogen 1.18 (1.14-1.23), and comorbid systemic diabetes 1.65 (1.45-1.88).A prediction model was developed in this study, which could be used to carry out predictions based on blood biochemical values from patients, in order to accurately predict the risk of CKD progression to dialysis.
| S-EPMC6617424 | biostudies-literature
Project description:Background and objectivesCKD is a global public health problem. Some cross-sectional studies have associated environmental melamine exposure with kidney diseases, but evidence is limited.Design, setting, participants, & measurementsWe conducted this prospective cohort study to enroll patients with eGFR≥30 ml/min per 1.73 m2 in 2006-2010. Urinary corrected melamine levels (ratio of urinary melamine to urinary creatinine) were measured by liquid chromatography/tandem mass spectrometry at enrollment. Kidney outcomes included doubling of serum creatinine levels, eGFR decline >3 ml/min per 1.73 m2 per year, and 30% decline in eGFR in the first 2 years. Subjects were followed until targeted kidney outcomes, cancer, death, last contact, or the end of observation in December 2016.ResultsIn a total of 293 subjects, the median urinary corrected melamine level was 0.97 (interquartile range, 0.43-2.08) μg/mmol. Over a median follow-up period of 7.0 years, serum creatinine levels doubled in 80 subjects (27%). Subjects in the highest tertile of urinary melamine level 12.70 μg/mmol) had a 2.30 (95% confidence interval, 1.25 to 4.23; P<0.01) hazard risk for doubling of serum creatinine compared with those in the lowest tertile (0.02-0.58 μg/mmol). Similar significant dose-response results were found in eGFR decline >3 ml/min per 1.73 m2 per year and 30% decline in eGFR in the first 2 years.ConclusionsUrinary melamine level is significantly associated with kidney function deterioration in patients with early-stage CKD.
| S-EPMC6682811 | biostudies-literature
Project description:IntroductionIn the general population, medication nonadherence contributes to poorer outcomes. However, little is known about medication adherence among adults with chronic kidney disease (CKD). We evaluated the association of self-reported medication adherence with CKD progression and all-cause death in patients with CKD.MethodsIn this prospective observational study of 3305 adults with mild-to-moderate CKD enrolled in the Chronic Renal Insufficiency Cohort (CRIC) Study, the baseline self-reported medication adherence was assessed by responses to 3 questions and categorized as high, medium, and low. CKD progression (50% decline in eGFR or incident end-stage renal disease) and all-cause death were measured using multivariable Cox proportional hazards.ResultsOf the patients, 68% were categorized as high adherence, 17% medium adherence, and 15% low adherence. Over a median follow-up of 6 years, there were 969 CKD progression events and 675 deaths. Compared with the high-adherence group, the low-adherence group experienced increased risk for CKD progression (hazard ratio = 1.27, 95% confidence interval = 1.05, 1.54) after adjustment for sociodemographic and clinical factors, cardiovascular medications, number of medication types, and depressive symptoms. A similar association existed between low adherence and all-cause death, but did not reach standard statistical significance (hazard ratio = 1.14 95% confidence interval = 0.88, 1.47).ConclusionBaseline self-reported low medication adherence was associated with an increased risk for CKD progression. Future work is needed to better understand the mechanisms underlying this association and to develop interventions to improve adherence.
| S-EPMC5976857 | biostudies-literature
Project description:Background and objectivesData on whether low or high urinary potassium excretion is associated with poor kidney outcome have been conflicting. The aim of this study was to clarify the association between urinary potassium excretion and CKD progression.Design, setting, participants, & measurementsWe investigated the relationship between lower urinary potassium excretion and CKD progression and compared three urinary potassium indices among 1821 patients from the Korean Cohort Study for Outcome in Patients with CKD. Urinary potassium excretion was determined using spot urinary potassium-to-creatinine ratio, spot urinary potassium concentration, and 24-hour urinary potassium excretion. Patients were categorized into four groups according to quartiles of each urinary potassium excretion metric. The study end point was a composite of a ≥50% decrease in eGFR from baseline values and ESKD.ResultsDuring 5326 person-years of follow-up, the primary outcome occurred in 392 (22%) patients. In a multivariable cause-specific hazard model, lower urinary potassium-to-creatinine ratio was associated with higher risk of CKD progression (adjusted hazard ratio, 1.47; 95% confidence interval, 1.01 to 2.12) comparing the lowest quartile with the highest quartile. Sensitivity analyses with other potassium metrics also showed consistent results in 855 patients who completed 24-hour urinary collections: adjusted hazard ratios comparing the lowest quartile with the highest quartile were 3.05 (95% confidence interval, 1.54 to 6.04) for 24-hour urinary potassium excretion, 1.95 (95% confidence interval, 1.05 to 3.62) for spot urinary potassium-to-creatinine ratio, and 3.79 (95% confidence interval, 1.51 to 9.51) for spot urinary potassium concentration.ConclusionsLow urinary potassium excretion is associated with progression of CKD.
| S-EPMC6419276 | biostudies-literature
Project description:Introduction:Cardiac biomarkers soluble ST2 (sST2) and galectin-3 may reflect cardiac inflammation and fibrosis. It is plausible that these mechanisms may also contribute to the progression of kidney disease. We examined associations of sST2 and galectin-3 with kidney function decline in participants with chronic kidney disease (CKD). Methods:This was a pooled analysis of 2 longitudinal cohorts of participants with CKD: the Clinical Phenotyping and Resource Biobank (C-PROBE) study and the Seattle Kidney Study (SKS). We measured circulating concentrations of sST2 and galectin-3 at baseline. Our primary outcome was progression to estimated glomerular filtration rate (eGFR) <15 ml/min per 1.73 m2 or end-stage renal disease (ESRD). We used competing risk Cox regression models to study the association of sST2 and galectin-3 with CKD progression, adjusting for demographics, kidney function, and comorbidity. Results:Among the 841 participants in the pooled cohort, baseline eGFR was 51 ± 27 ml/min per 1.73 m2 and median urine albumin-to-creatinine ratio (UACR) was 141 (interquartile range = 15-736) mg/g. Participants with higher sST2 and galectin-3 were more likely to be older, to have heart failure and diabetes, and to have lower eGFR. Adjusting for demographics, kidney function, and comorbidity, every doubling of sST2 was not associated with progression to eGFR <15 ml/min per 1.73 m2 or ESRD (adjusted hazard ratio 1.02, 95% confidence interval = 0.76-1.38). Every doubling of galectin-3 was significantly associated with a 38% (adjusted hazard ratio = 1.35, 95% confidence interval = 1.01-1.80) increased risk of progression to eGFR <15 ml/min per 1.73 m2 or ESRD. Conclusion:Higher concentrations of the cardiac biomarker galectin-3 may be associated with progression of CKD, highlighting potential novel mechanisms that may contribute to the progression of kidney disease.
| S-EPMC6308819 | biostudies-other