Background
Early arteriovenous fistula (AVF) creation is necessary to curb the use of central venous catheters (CVCs) and reduce their complications. We sought to examine patient characteristics that may influence persistent CVC use 90 days after dialysis therapy initiation among patients using a CVC.
Methods
Data from the 1999 to 2003 Clinical Performance Measures Project was linked to the Centers for Medicare & Medicaid Services Medical Evidence (2728) form.
Results
Most patients (59.4%) starting dialysis with a CVC failed to transition to permanent access within 90 days, whereas 25.4% received a graft and only 15.2% received an AVF. Older patients (>75 years) were more than 2-fold more likely to remain CVC dependent at 90 days (P = 0.0.001) compared with those younger than 50 years. In addition, race and sex were highly predictive of CVC dependence at 90 days; black females, white females, and black males were 75% (P < 0.001), 61% (P < 0.001), and 35% (P = 0.023) more likely than white males to maintain CVC use, whereas patients with ischemic heart disease and peripheral vascular disease were 35% (P = 0.023) and 39% (P = 0.007) more likely to remain CVC dependent at 90 days, respectively.
Conclusion
Prolonged CVC dependence is more likely to occur among patients of older age, females, blacks, and those with cardiovascular comorbidity, suggesting inadequate or late access referral or greater primary access failure. Our findings suggest possible missed opportunities for early conversion of patients to permanent vascular access that may vary by race and sex.
by
Michael V. Rocco;
Kaycee M. Sink;
Laura C. Lovato;
Dawn F. Wolfgram;
Thomas B. Wiegmann;
Barry M. Wall;
Kausik Umanath;
Frederic Rahbari Oskoui;
Anna C. Porter;
Roberto Pisoni;
Cora E. Lewis;
Julia B. Lewis;
James P. Lash;
Lois A. Katz;
Amret T. Hawfield;
William E. Haley;
Barry I. Freedman;
Jamie P. Dwyer;
Paul E. Drawz;
Mirela Dobre;
Alfred K. Cheung;
Ruth C. Campbell;
Udayan Bhatt;
Srinivasan Beddhu;
Paul L. Kimmel;
David M. Reboussin;
Glenn M. Chertow
Background: Treating to a lower blood pressure (BP) may increase acute kidney injury (AKI) events. Study Design: Data for AKI resulting in or during hospitalization or emergency department visits were collected as part of the serious adverse events reporting process of the Systolic Blood Pressure Intervention Trial (SPRINT). Setting & Participants: 9,361 participants 50 years or older with 1 or more risk factors for cardiovascular disease. Interventions: Participants were randomly assigned to a systolic BP target of <120 (intensive arm) or <140 mm Hg (standard arm). Outcomes & Measurements: Primary outcome was the number of adjudicated AKI events. Secondary outcomes included severity of AKI and degree of recovery of kidney function after an AKI event. Baseline creatinine concentration was defined as the most recent SPRINT outpatient creatinine value before the date of the AKI event. Results: There were 179 participants with AKI events in the intensive arm and 109 in the standard arm (3.8% vs 2.3%; HR, 1.64; 95% CI, 1.30-2.10; P < 0.001). Of 288 participants with an AKI event, 248 (86.1%) had a single AKI event during the trial. Based on modified KDIGO (Kidney Disease: Improving Global Outcomes) criteria for severity of AKI, the number of AKI events in the intensive versus standard arm by KDIGO stage was 128 (58.5%) versus 81 (62.8%) for AKI stage 1, 42 (19.2%) versus 18 (14.0%) for AKI stage 2, and 42 (19.2%) versus 25 (19.4%) for AKI stage 3 (P = 0.5). For participants with sufficient data, complete or partial resolution of AKI was seen for 169 (90.4%) and 9 (4.8%) of 187 AKI events in the intensive arm and 86 (86.9%) and 4 (4.0%) of 99 AKI events in the standard arm, respectively. Limitations: Trial results are not generalizable to patients with diabetes mellitus or without risk factors for cardiovascular disease. Conclusions: More intensive BP lowering resulted in more frequent episodes of AKI. Most cases were mild and most participants had complete recovery of kidney function. Trial Registration: Registered at ClinicalTrials.gov with study number NCT01206062.
Background: Few studies have examined the association between obesity and markers of kidney injury in a chronic kidney disease population. We hypothesized that obesity is independently associated with proteinuria, a marker of chronic kidney disease progression. Study Design: Observational cross-sectional analysis. Setting & Participants: Post hoc analysis of baseline data for 652 participants in the African American Study of Kidney Disease (AASK). Predictors: Obesity, determined using body mass index (BMI). Measurements & Outcomes: Urine total proteincreatinine ratio and albumin-creatinine ratio measured in 24-hour urine collections. Results: AASK participants had a mean age of 60.2 ± 10.2 years and serum creatinine level of 2.3 ± 1.5 mg/dL; 61.3% were men. Mean BMI was 31.4 ± 7.0 kg/m2. Approximately 70% of participants had a daily urine total protein excretion rate <300 mg/d. In linear regression analyses adjusted for sex, each 2-kg/m 2 increase in BMI was associated with a 6.7% (95% CI, 3.2-10.4) and 9.4% (95% CI, 4.9-14.1) increase in urine total proteincreatinine and urine albumin-creatinine ratios, respectively. In multivariable models adjusting for age, sex, systolic blood pressure, serum glucose level, uric acid level, and creatinine level, each 2-kg/m2 increase in BMI was associated with a 3.5% (95% CI, 0.4-6.7) and 5.6% (95% CI, 1.5-9.9) increase in proteinuria and albuminuria, respectively. The interaction between older age and BMI was statistically significant, indicating that this relationship was driven by younger AASK participants. Limitations: May not generalize to other populations; cross-sectional analysis precludes statements regarding causality. Conclusions: BMI is associated independently with urine total protein and albumin excretion in African Americans with hypertensive nephrosclerosis, particularly in younger patients.
Background Life-Space Assessment captures community mobility and social participation and quantifies the distance, frequency, and independence obtained as an older adult moves through his or her environment. Reduced estimated glomerular filtration rate (eGFR) is associated with decline in activities of daily living among older adults, but less is known about the association of eGFR with restrictions in mobility. Study Design Prospective observational cohort study. Setting & Participants Community-dwelling Medicare beneficiaries from the University of Alabama at Birmingham Study of Aging who had serum creatinine measured during a baseline in-home study visit and completed at least one telephone follow-up (N = 390). Predictor eGFR ≥ 60, 45-59, and <45 mL/min/1.73 m2. Outcome Life-space mobility trajectory. Measurements Life-space mobility was evaluated by telephone every 6 months for up to 4.5 years using the previously validated Life-Space Assessment. Scores using this tool range from 0-120 (higher scores indicate greater mobility). Results Mean age of the 390 participants was 77.6 ± 5.8 (SD) years, 41% were African American, 50.5% were women; 30.0% had eGFR of 45-59 mL/min/1.73 m2, and 20.2% had eGFR < 45 mL/min/1.73 m2. Age-, race-, and sex-adjusted mean baseline life-space mobility scores were 64.8 (95% CI, 62.0-67.6), 63.8 (95% CI, 60.3-67.4), and 58.3 (95% CI, 53.8-62.7) among those with eGFR categories ≥ 60, 45-59, and <45 mL/min/1.73 m2, respectively. Compared with those with eGFRs ≥ 60 mL/min/1.73 m2, a more rapid decline in life-space mobility was found among those with eGFRs < 45 mL/min/1.73 m2, though this did not reach statistical significance (P = 0.06); a similar effect was not seen among those with eGFRs of 45-59 mL/min/1.73 m2 (P = 0.3). Limitations Urinary albumin or longitudinal measures of eGFR were not available. Conclusions eGFR < 45 mL/min/1.73 m2 was associated with a trend toward a more rapid decline in life-space mobility among community-dwelling older adults. Findings should be confirmed in a larger population.
by
Adebowale Adeyemo;
Christopher Esezobor;
Adaobi Solarin;
Asiri Abeyagunawardena;
Jameela A. Kari;
Sherif El Desoky;
Larry Greenbaum;
Margret Kamel;
Mahmoud Kallash;
Cynthia Silva;
Alex Young;
Tracey E. Hunley;
Nilka de Jesus-Gonzalez;
Tarak Srivastava;
Rasheed Gbadegesin
Background: Few data exist for the genetic variants underlying the risk for steroid-sensitive nephrotic syndrome (SSNS) in children. The objectives of this study were to evaluate HLA-DQA1 and APOL1 variants as risk factors for SSNS in African American children and use classic HLA antigen types and amino acid inference to refine the HLA-DQA1 association. Study Design: Case-control study. Setting & Participants: African American children with SSNS or steroid-resistant nephrotic syndrome (SRNS) were enrolled from Duke University and centers participating in the Midwest Pediatric Nephrology Consortium. Factor: Genetic variants in HLA-DQA1 (C34Y [rs1129740]; F41S [rs1071630]) and APOL1 high-risk alleles. Outcomes: SSNS and SRNS. Measurements: Direct sequencing for the HLA-DQA1 and APOL1 variants in 115 African American children (65 with SSNS and 50 with SRNS). Imputation of classic HLA alleles and amino acids was done in 363 South Asian children. Results: The 2 HLA-DQA1 variants were significantly associated with SSNS in African American children (C34Y: P = 5.7 × 10 -11 ; OR, 3.53; 95% CI, 2.33-5.42; F41S: P = 1.2 × 10 -13 ; OR, 4.08; 95% CI, 2.70-6.28), but not with SRNS (C34Y: P = 0.6; F41S: P = 0.2). APOL1 high-risk variants were not associated with SSNS (P = 0.5) but showed significant associations with SRNS (P = 1.04 × 10 -7 ; OR, 4.17; 95% CI, 2.23-7.64). HLA-DQA1*0201, HLA-DQB1*0201, and HLA-DRB1*0701 were the classic HLA alleles with the most significant associations with SSNS risk. The most significantly associated amino acid positions were HLA-DQα1 56 and 76 (both P = 2.8 × 10 -7 ). Conditional analysis revealed that these variants most likely account for the observed association. Limitations: Modest sample size and limited statistical power to detect small to moderate effect sizes. Children studied may not be representative of all African American children in the United States. Conclusions: HLA-DQA1 is a risk locus for SSNS, but not SRNS, in African American children, consistent with its role in SSNS risk in children of European, Asian, and African ancestries. There is little evidence of a significant role for the APOL1 high-risk alleles in childhood SSNS in African American children. Refinement of the HLA-DQA1 association identified the critical classic HLA antigen types and amino acids of the HLA-DQ α1 molecule.