Kidney Function Decline in Patients with CKD and Untreated Hepatitis C Infection.
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ABSTRACT:
SUBMITTER: Tartof SY
PROVIDER: S-EPMC6218821 | biostudies-other | 2018 Oct
REPOSITORIES: biostudies-other
Publications
Kidney Function Decline in Patients with CKD and Untreated Hepatitis C Infection.
Tartof Sara Yee SY Hsu Jin-Wen JW Wei Rong R Rubenstein Kevin B KB Hu Haihong H Arduino Jean Marie JM Horberg Michael M Derose Stephen F SF Qian Lei L Rodriguez Carla V CV
Clinical journal of the American Society of Nephrology : CJASN 20180921 10
<h4>Background and objectives</h4>Studies evaluating the role of hepatitis C viral (HCV) infection on the progression of CKD are few and conflicting. Therefore, we evaluated the association of untreated HCV on kidney function decline in patients with stage 3-5 CKD.<h4>Design, setting, participants, & measurements</h4>This retrospective cohort study included members of Kaiser Permanente Southern California and Kaiser Permanente Mid-Atlantic States aged ≥18 years, with incident HCV and CKD diagnos ...[more]
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Project description:BACKGROUND AND OBJECTIVES:In the Systolic Blood Pressure Intervention Trial (SPRINT), intensive systolic BP treatment (target <120 mm Hg) was associated with fewer cardiovascular events and higher incidence of kidney function decline compared with standard treatment (target <140 mm Hg). We evaluated the association between mean arterial pressure reduction, kidney function decline, and cardiovascular events in patients without CKD. DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS:We categorized patients in the intensive treatment group of the SPRINT according to mean arterial pressure reduction throughout follow-up: <20, 20 to <40, and ?40 mm Hg. We defined the primary outcome as kidney function decline (?30% reduction in eGFR to <60 ml/min per 1.73 m2 on two consecutive determinations at 3-month intervals), and we defined the secondary outcome as cardiovascular events. In a propensity score analysis, patients in each mean arterial pressure reduction category from the intensive treatment group were matched with patients from the standard treatment group to calculate the number needed to treat regarding cardiovascular events and the number needed to harm regarding kidney function decline. RESULTS:In the intensive treatment group, 1138 (34%) patients attained mean arterial pressure reduction <20 mm Hg, 1857 (56%) attained 20 to <40 mm Hg, and 309 (9%) attained ?40 mm Hg. Adjusted hazard ratios for kidney function decline were 2.10 (95% confidence interval, 1.22 to 3.59) for mean arterial pressure reduction between 20 and 40 mm Hg and 6.22 (95% confidence interval, 2.75 to 14.08) for mean arterial pressure reduction ?40 mm Hg. In propensity score analysis, mean arterial pressure reduction <20 mm Hg presented a number needed to treat of 44 and a number needed to harm of 65, reduction between 20 and <40 mm Hg presented a number needed to treat of 42 and a number needed to harm of 35, and reduction ?40 mm Hg presented a number needed to treat of 95 and a number needed to harm of 16. CONCLUSIONS:In the intensive treatment group of SPRINT, larger declines in mean arterial pressure were associated with higher incidence of kidney function decline. Intensive treatment seemed to be less favorable when a larger reduction in mean arterial pressure was needed to attain the BP target.
| S-EPMC5753311 | biostudies-other
Project description:Hepatitis C virus (HCV) infection is common and can accelerate chronic kidney disease (CKD) progression. Direct-acting antiviral (DAA) therapies against hepatitis C have consistently shown rates of sustained viral remission. However, the effect on kidney function is unknown. In a retrospective observational cohort study of HCV-infected patients receiving DAA therapies from 2013 to 2017, the slopes of estimated glomerular filtration rate (eGFR) decline were compared in the three years before DAA therapy to the slope after therapy. Pre- and post-treatment albuminuria values were also compared. In all, 1,178 patients were included; mean age of 56, 64% male, 71% white, 21% were diabetic, and 42% with cirrhosis. In patients with eGFR less than 60ml/min per 1.73m2, the annual decline in eGFR in the three years prior to treatment was -5.98 ml/min per year (95% confidence interval -7.30 to -4.67) and improved to -1.32 ml/min per year (95% confidence interval -4.50 to 1.88) after DAA therapy. In patients with eGFR greater than 60ml/min per 1.73m2 the annual decline in eGFR in the three years prior to treatment was -1.43 ml/min per year (95% confidence interval -1.78 to -1.08) and after DAA therapy was -2.32 ml/min per year (95% confidence interval -3.36 to -1.03). Albuminuria improved significantly in patients without diabetes, but not in those with diabetes. Predictors of eGFR improvement included having CKD at baseline and being non-diabetic. Events of acute kidney injury were rare, occurring in 29 patients, and unrelated to antiviral therapy in 76% of cases. Thus, DAA therapy for HCVs infection may slow CKD progression.
| S-EPMC7094798 | biostudies-literature
Project description:Rationale & objectiveThe direct and indirect effects of the coronavirus disease 2019 (COVID-19) pandemic on kidney function in the chronic kidney disease (CKD) population are not well understood.Study designCohort study.Setting & participantsRetrospective study of kidney function trajectories using deidentified administrative claims and laboratory data for Medicare Advantage and commercially insured enrollees with CKD stages G3-4 between 2018 and 2021.PredictorsCOVID-19 infection.OutcomeRapid kidney function decline defined as annual estimated glomerular filtration rate (eGFR) decline of ≥40%.Analytical approachPropensity score matching was used to identify individuals without COVID-19 infection matched 1:1 to a COVID-19 infected cohort and indexed on the date of diagnosing COVID-19 infection, age, sex, race or ethnicity, and Charlson comorbidity index score. Outpatient kidney function was compared during the prepandemic period (January 1, 2018, to February 29, 2020) with the pandemic period (March 1, 2020, to August 31, 2021). Two creatinine measurements, after the infection date and ≥60 days apart, were required to reduce correlation with acute infection.ResultsOf 97,203 enrollees with CKD G3-4, 9% experienced a COVID-19 infection. Characteristics of 8,901 propensity matched enrollees include mean age 74 years, 58% women, 67% White, and 63% CKD G3a, 28% CKD G3b, and 9% CKD G4. Median overall annual eGFR change was -2.65 ml/min/1.73m2, with 76% of the cohort experiencing worsened eGFR in the pandemic period. Rapid kidney function decline was observed in 1.9% and 2.0% of enrollees in the prepandemic and pandemic periods, respectively. Rapid kidney function decline was observed in 2.5% of those with COVID-19 infection and 1.5% of those without COVID-19 infection (P < 0.05). Factors associated with increased odds of rapid kidney function decline during pandemic included Asian race, higher Charlson comorbidity index, advancing CKD stage, prepandemic rapid kidney function decline, and COVID-19 infection.LimitationsRetrospective study design with potential bias.ConclusionsCOVID-19 infection increased odds of rapid kidney function decline during the pandemic. The downstream impact of pandemic-related eGFR decline on health outcomes, such as kidney failure or mortality, requires further study.Plain-language summaryWe used a cohort of insured individuals with moderate-to-severe chronic kidney disease (CKD) to compare the rates of rapid kidney function decline in prepandemic and pandemic periods and to evaluate the impact of the coronavirus disease 19 (COVID-19) on kidney function decline. We found that overall rates of rapid kidney function decline did not change during the prepandemic and pandemic periods but were significantly higher in both periods among individuals with a COVID-19 infection. As CKD severity increased, rates of both rapid kidney function decline and COVID-19 increased. Advancing CKD, higher comorbid condition, Asian race, prepandemic rapid kidney function decline, and COVID-19 were all associated with higher odds of rapid kidney function decline in the pandemic. These findings suggest close monitoring is warranted for individuals with CKD and COVID-19.
| S-EPMC10462879 | biostudies-literature
Project description:Background and objectivesHepatitis C virus infection is common in patients with CKD and leads to accelerated progression to ESRD. Sofosbuvir is a potent direct-acting antiviral therapy against hepatitis C virus; however, there are concerns about its safety in patients with CKD. The objective of our study was to determine the safety and efficacy of sofosbuvir in patients with CKD.Design, setting, participants, & measurementsWe studied a retrospective observational cohort of patients with CKD defined by eGFR<60 ml/min per 1.73 m2, ?30 mg albuminuria per 1 g creatinine, or ?200 mg proteinuria per 1 g creatinine who received sofosbuvir-based therapy in a large health care system. Regression models were constructed to predict likelihood of sustained virologic response, detect adverse events, and examine changes in eGFR from baseline to follow-up.ResultsNinety-eight patients with CKD (42% stage 1 or 2 CKD and 58% stage 3 CKD) were included. Mean age was 62 years old, 78% were men, and 65% were white. Additionally, 49% of patients had diabetes, 38% of patients had cirrhosis, and 33% of patients had prior solid organ transplant. Overall sustained virologic response was 81% and varied by regimen used and viral genotype. Average baseline eGFR was equivalent to average on-treatment eGFR, but seven patients experienced a rise in creatinine ?1.5 times baseline while taking sofosbuvir; all but one recovered. In patients with eGFR<60 ml/min per 1.73 m2 at baseline (stage 3 CKD), regression models showed that hepatitis C cure was associated with a 9.3 (95% confidence interval, 0.44 to 18) ml/min per 1.73 m2 improvement in eGFR during the 6-month post-treatment follow-up period. Adverse events were common (81%), but serious adverse events (17%) and treatment discontinuations (8%) were uncommon.ConclusionsSofosbuvir-based direct-acting antiviral therapy is safe and effective in a cohort of patients with CKD infected with hepatitis C.
| S-EPMC5628711 | biostudies-literature
Project description:Background and objectivesRisk of hospitalizations is increased in patients with CKD. We sought to examine the association between rate of kidney function decline and risk of hospitalization in a cohort of patients with early CKD.Design, settings, participants, & measurementsWe built a cohort of 247,888 United States veterans who had at least one eGFR measurement between October 1999 and September 2003 and an additional eGFR between October 2003 and September 2004. We selected patients whose initial eGFR was between 45 and 59 ml/min per 1.73 m2. Rate of eGFR change (in milliliters per minute per 1.73 m2 per year) was categorized as no decline (>0), mild (0 to -1, and served as the referent group), moderate (-1 to -5), or severe (>-5) eGFR decline. We built survival models to examine the association between the rate of kidney function decline and the risk of hospitalization and readmission and linear regression to estimate length of hospital stay.ResultsOver a median observation of 9 years (interquartile range, 5.28-9.00), patients with moderate and severe eGFR decline exhibited a higher risk of hospitalizations (hazard ratio [HR], 1.22; 95% confidence interval [95% CI], 1.19 to 1.26; and HR, 1.33; 95% CI, 1.28 to 1.39, respectively). Among patients with moderate and severe eGFR decline, the association between the rate of decline and the risk of hospitalizations was more pronounced with an increased number of hospitalizations (P<0.01). Patients with moderate and severe eGFR decline had a higher risk of readmission (HR, 1.19; 95% CI, 1.13 to 1.26; and HR, 1.53; 95% CI, 1.43 to 1.63, respectively). Among patients with severe eGFR decline, the association between the rate of kidney function decline and the risk of readmission was stronger with an increased number of readmissions (P<0.01). Patients with moderate and severe eGFR decline experienced an additional length of stay of 1.40 (95% CI, 0.88 to 1.92) and 5.00 days per year (95% CI, 4.34 to 5.66), respectively.ConclusionsThe rate of kidney function decline is associated with a higher risk of hospitalizations, readmissions, and prolonged length of hospital stay.
| S-EPMC4633789 | biostudies-literature
Project description:IntroductionNormally, blood pressure (BP) declines by at least 10% from daytime to nighttime. In adults, blunted nocturnal dipping has been associated with more rapid decline in kidney function. Nondipping is prevalent in children with chronic kidney disease (CKD). We sought to determine whether nondipping is associated with proteinuria and progression to kidney failure in children with CKD.MethodsIn the prospective CKD in children (CKiD) cohort, Cox proportional hazards models were used to evaluate the relationship between baseline nondipping and progression to kidney failure. Linear mixed effects models were used to evaluate the relationship between nondipping and changes in iohexol glomerular filtration rate (GFR) and urine protein-to-creatinine ratio (log-UPCR, mg/mg) over time.ResultsAmong 620 participants, mean age was 11 (± 4) years, mean iohexol GFR was 52 (± 22) ml/min per 1.73 m2, and 40% were nondippers at baseline. There were 169 kidney failure events during 2.9 years (median) of follow-up. Dipping status was not significantly associated with kidney failure overall (hazard ratio [HR] 1.08; 95% confidence interval [CI] 0.77, 1.51) or in those with (HR 1.21; 95% CI 0.53, 2.77) or without (HR 1.05; 95% CI 0.71, 1.55) glomerular disease. Dipping status did not modify the relationship between time and change in iohexol GFR or log (UPCR) from baseline (interaction P values = 0.20 and 0.054, respectively).ConclusionNondipping is not associated with end-stage kidney disease, GFR decline, or change in proteinuria within the CKiD cohort.
| S-EPMC9751682 | biostudies-literature
Project description:OBJECTIVE:To examine the impact of sustained virologic response (SVR) and illicit (injection and noninjection) drug use on kidney function among hepatitis C virus (HCV) and HIV co-infected individuals. DESIGN:Longitudinal observational cohort study of HCV-HIV co-infected patients. METHODS:Data from 1631 patients enrolled in the Canadian Co-Infection Cohort between 2003 and 2016 were analyzed. Patients who achieved SVR were matched 1?:?2 with chronically infected patients using time-dependent propensity scores. Linear regression with generalized estimating equations was used to model differences in estimated glomerular filtration rates (eGFR) between chronic HCV-infected patients and those achieving SVR. The relationship between illicit drug use and eGFR was explored in patients who achieved SVR. RESULTS:We identified 384 co-infected patients who achieved SVR (53% treated with interferon-free antiviral regimens) and 768 propensity-score matched patients with chronic HCV infection. Most patients were men (78%) and white (87%), with a median age of 51 years (interquartile range: 45-56). During 1767 person-years of follow-up, 4041 eGFR measurements were available for analysis. Annual rates of decline in eGFR were similar between patients with SVR [-1.32?(ml/min per 1.73?m)/year, 95% confidence interval (CI) -1.75 to -0.90] and chronic infection [-1.19?(ml/min per 1.73?m) per year, 95% CI -1.55 to -0.84]. Among SVR patients, recent injection cocaine use was associated with rapid eGFR decline [-2.16?(ml/min per 1.73 m)/year, 95% CI -4.17 to -0.16]. CONCLUSION:SVR did not reduce the rate of kidney function decline among HCV-HIV co-infected patients. Increased risk of chronic kidney disease in co-infection may not be related to persistent HCV replication but to ongoing injection cocaine use.
| S-EPMC5895129 | biostudies-literature
Project description:Background and objectiveseGFR and albuminuria primarily reflect glomerular function and injury, whereas tubule cell atrophy and interstitial fibrosis on kidney biopsy are important risk markers for CKD progression. Kidney tubule injury markers have primarily been studied in hospitalized AKI. Here, we examined the association between urinary kidney tubule injury markers at baseline with subsequent loss of kidney function in persons with nondiabetic CKD who participated in the Systolic Blood Pressure Intervention Trial (SPRINT).Design, setting, participants, & measurementsAmong 2428 SPRINT participants with CKD (eGFR<60 ml/min per 1.73 m2) at baseline, we measured urine markers of tubule injury (IL-18, kidney injury molecule-1 [KIM-1], neutrophil gelatinase-associated lipocalin [NGAL]), inflammation (monocyte chemoattractant protein-1 [MCP-1]), and repair (human cartilage glycoprotein-40 [YKL-40]). Cox proportional hazards models evaluated associations of these markers with the kidney composite outcome of 50% eGFR decline or ESKD requiring dialysis or kidney transplantation, and linear mixed models evaluated annualized change in eGFR.ResultsMean participant age was 73±9 (SD) years, 60% were men, 66% were white, and mean baseline eGFR was 46±11 ml/min per 1.73 m2. There were 87 kidney composite outcome events during a median follow-up of 3.8 years. Relative to the respective lowest quartiles, the highest quartiles of urinary KIM-1 (hazard ratio, 2.84; 95% confidence interval [95% CI], 1.31 to 6.17), MCP-1 (hazard ratio, 2.43; 95% CI, 1.13 to 5.23), and YKL-40 (hazard ratio, 1.95; 95% CI, 1.08 to 3.51) were associated with higher risk of the kidney composite outcome in fully adjusted models including baseline eGFR and urine albumin. In linear analysis, urinary IL-18 was the only marker associated with eGFR decline (-0.91 ml/min per 1.73 m2 per year for highest versus lowest quartile; 95% CI, -1.44 to -0.38), a finding that was stronger in the standard arm of SPRINT.ConclusionsUrine markers of tubule cell injury provide information about risk of subsequent loss of kidney function, beyond the eGFR and urine albumin.
| S-EPMC7057300 | biostudies-literature
Project description:Although anthropometric measures of body fat are associated with development of CKD, they may not be able to distinguish between various forms of fat and therefore may be less accurate than computed tomography (CT) measures. We compared the association of CT and anthropometric measures of obesity with kidney outcomes in the Health Aging and Body Composition Study.Participants were recruited from March of 1997 through July of 1998. CT measures included visceral abdominal fat (VAT), subcutaneous adipose tissue (SAT), and intermuscular fat area (IMAT), whereas anthropometric measures included waist circumference (WC) and body mass index (BMI). Kidney outcomes included kidney function (KF) decline (30% decrease in eGFRcysC in follow-up at either year 3 or 10) or incident CKD (follow-up eGFRcysC?60 ml/min per 1.73 m2 in individuals with baseline GFR>60 ml/min per 1.73 m2). Multivariable logistic regression models and Poisson regression models were used to evaluate the association with decline in KF and incident kidney disease, respectively. We also assessed for the independent associations among the exposure measures by including them in the same model.Two-thousand four-hundred and eighty-nine individuals were included. Mean age was 74±3 years, 49% were men, 39% were black, 59% were hypertensive, and 15% were diabetic. KF decline occurred in 17% of the population, whereas incident CKD also occurred in 17% of those at risk. In continuous models, SAT, VAT, IMAT, BMI, and WC (per SD increase) were all significantly associated with KF decline. There was a significant interaction between VAT and CKD with regard to KF decline (P=0.01). Only VAT, BMI, and WC were associated with incident CKD. Only VAT remained a significant risk factor for incident CKD when other exposure variables were included in the same model. There was no association between any measure of obesity and kidney outcomes when creatinine values at years 3 and 10 were used to estimate changes in eGFR.Anthropometric measures of body fat appear to provide as consistent estimates of KF decline risk as CT measures in elders.
| S-EPMC5460706 | biostudies-literature
Project description:BackgroundInvestigation of circulating metabolites associated with kidney function and chronic kidney disease (CKD) risk could enhance our understanding of underlying pathways and identify new biomarkers for kidney function.MethodsWe selected participants from the population-based Rotterdam Study with data on circulating metabolites and estimated glomerular filtration rate based on serum creatinine (eGFRcreat) available at the same time point. Data on eGFR based on serum cystatin C (eGFRcys) and urine albumin-to-creatinine ratio (ACR) were also included. CKD was defined as eGFRcreat <60 ml/min per 1.73 m2. Data on circulating metabolites (ntotal = 1381) was obtained from the Nightingale and Metabolon platform. Linear regression, linear mixed, and Cox proportional-hazards regression analyses were conducted to study the associations between metabolites and kidney function. We performed bidirectional two-sample Mendelian randomization analyses to investigate causality of the identified associations.ResultsWe included 3337 and 1540 participants with data from Nightingale and Metabolon, respectively. A total of 1381 metabolites (243 from Nightingale and 1138 from Metabolon) were included in the analyses. A large number of metabolites were significantly associated with eGFRcreat, eGFRcys, ACR, and CKD, including 16 metabolites that were associated with all four outcomes. Among these, C-glycosyltryptophan (HR 1.50, 95%CI 1.31;1.71) and X-12026 (HR 1.46, 95%CI 1.26;1.68) were most strongly associated with CKD risk. We revealed sex differences in the associations of 11-ketoetiocholanolone glucuronide and 11-beta-glucuronide with the kidney function assessments. No causal associations between the identified metabolites and kidney function were observed.ConclusionOur study indicates that several circulating metabolites are associated with kidney function which are likely to have potential as biomarkers, rather than as molecules involved in the pathophysiology of kidney function decline.
| S-EPMC10783258 | biostudies-literature