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1.  Correction: Determinants of the creatinine clearance to glomerular filtration rate ratio in patients with chronic kidney disease: a cross-sectional study 
BMC Nephrology  2014;15:85.
After the publication of our paper Lin et al. “Determinants of the creatinine clearance to glomerular filtration rate ratio in patients with chronic kidney disease: a cross-sectional study” BMC Nephrology 2013, 14:268, we became aware of errors in the manuscript arising from to a misunderstanding of serum creatinine calibration in the released Chronic Renal Insufficiency Cohort (CRIC) study data obtained from the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) Data Repository. Specifically further multiplication by 0.95 was actually not necessary to arrive at the standardized creatinine values.
Here we present the revised results of the re-analyses along with revisions of the relevant tables. Mean CrCl/iGFR ratio should be 1.13 ± 0.46 instead of 1.19 ± 0.48. The main conclusion of the paper remain unchanged: “Contrary to what had been suggested by prior smaller studies, CrCl/GFR ratio does not vary with degree of proteinuria or race/ethnicity. The ratio is also closer to 1.0 than reported by several frequently cited reports in the literature.”
PMCID: PMC4061100
2.  Determinants of the creatinine clearance to glomerular filtration rate ratio in patients with chronic kidney disease: a cross-sectional study 
BMC Nephrology  2013;14:268.
Creatinine secretion, as quantified by the ratio of creatinine clearance (CrCl) to glomerular filtration rate (GFR), may introduce another source of error when using serum creatinine concentration to estimate GFR. Few studies have examined determinants of the CrCl/GFR ratio. We sought to study whether higher levels of albuminuria would be associated with higher, and being non-Hispanic black with lower, CrCl/GFR ratio.
We did a cross-sectional analysis of 1342 patients with chronic kidney disease from the Chronic Renal Insufficiency Cohort (CRIC) who had baseline measure of iothalamate GFR (iGFR) and 24-hour urine collections. Our predictors included urine albumin as determined from 24-hour urine collections (categorized as: <30, 30-299, 300-2999 and ≥3000 mg), and race/ethnicity (non-Hispanic white, non-Hispanic black, Hispanic). Our outcome was CrCl/iGFR ratio, a measure of creatinine secretion.
Mean iGFR was 48.0 ± 19.9 mL/min/1.73 m2, median albuminuria was 84 mg per day, and 36.8% of the study participants were non-Hispanic black. Mean CrCl/iGFR ratio was 1.19 ± 0.48. There was no association between the CrCl/iGFR ratio and urine albumin (coefficient 0.11 [95% CI−0.01-0.22] for higest verus lowest levels of albuminuria, p = 0.07). Also, there was no association between race/ethnicity and CrCl/iGFR ratio (coefficient for non-Hispanic blacks was−0.03 [95% CI−0.09-0.03] compared with whites, p = 0.38).
Contrary to what had been suggested by prior smaller studies, CrCl/GFR ratio does not vary with degree of proteinuria or race/ethnicity. The ratio is also closer to 1.0 than reported by several frequently cited reports in the literature.
PMCID: PMC3924195  PMID: 24305166
Albuminuria; Chronic kidney disease; Glomerular filtration rate; Race/Ethnicity
3.  Timing of preemptive vascular access placement: do we understand the natural history of advanced CKD?: an observational study 
BMC Nephrology  2013;14:115.
Little is known about the targets and expectations of practicing nephrologists with regard to timing of preemptive AV access surgery and how these relate to actual observed practice patterns in clinical care.
We administered a 8-question survey to assess nephrologists’ expectations for preemptive vascular access placement to 53 practicing nephrologists in California. We performed a retrospective chart review of 116 patients who underwent preemptive vascular access placement at a large academic medical center and examined progression to ESRD.
According to our survey of nephrologists, most aimed to have preemptive vascular access created about 6 months prior to start of ESRD or when the chances of ESRD within the next year is two-thirds or greater. The estimated GFR level at which they believe match these conditions is approximately 18 ml/min/1.73 m2. Among the 116 patients with CKD who underwent preemptive vascular access creation, the mean estimated GFR at the time of access creation was 16.1 (6.8) ml/min/1.73 m2. Only 57 out of the 116 patients (49.1%) patients initiated maintenance HD within 1 year after surgery.
In our study, most nephrologists aim for preemptive vascular access surgery approximately 6 months prior to the start of HD. However in fact, only approximately 50% of patients who underwent preemptive vascular access surgery started HD within 1 year. Better tools are needed to predict the natural history of advanced CKD.
PMCID: PMC3671964  PMID: 23714195
Advanced CKD; AVF; Dialysis; ESRD; Progression
4.  Potential role of differential medication use in explaining excess risk of cardiovascular events and death associated with chronic kidney disease: A cohort study 
BMC Nephrology  2011;12:44.
Patients with chronic kidney disease (CKD) are less likely to receive cardiovascular medications. It is unclear whether differential cardiovascular drug use explains, in part, the excess risk of cardiovascular events and death in patients with CKD and coronary heart disease (CHD).
The ADVANCE Study enrolled patients with new onset CHD (2001-2003) who did (N = 159) or did not have (N = 1088) CKD at entry. The MDRD equation was used to estimate glomerular filtration rate (eGFR) using calibrated serum creatinine measurements. Patient characteristics, medication use, cardiovascular events and death were ascertained from self-report and health plan electronic databases through December 2008.
Post-CHD event ACE inhibitor use was lower (medication possession ratio 0.50 vs. 0.58, P = 0.03) and calcium channel blocker use higher (0.47 vs. 0.38, P = 0.06) in CKD vs. non-CKD patients, respectively. Incidence of cardiovascular events and death was higher in CKD vs. non-CKD patients (13.9 vs. 11.5 per 100 person-years, P < 0.001, respectively). After adjustment for patient characteristics, the rate of cardiovascular events and death was increased for eGFR 45-59 ml/min/1.73 m2 (hazard ratio [HR] 1.47, 95% CI: 1.10 to 2.02) and eGFR < 45 ml/min/1.73 m2 (HR 1.58, 95% CI: 1.00 to 2.50). After further adjustment for statins, β-blocker, calcium channel blocker, ACE inhibitor/ARB use, the association was no longer significant for eGFR 45-59 ml/min/1.73 m2 (HR 0.82, 95% CI: 0.25 to 2.66) or for eGFR < 45 ml/min/1.73 m2 (HR 1.19, 95% CI: 0.25 to 5.58).
In adults with CHD, differential use of cardiovascular medications may contribute to the higher risk of cardiovascular events and death in patients with CKD.
PMCID: PMC3180367  PMID: 21917174
5.  End-stage renal disease preceded by rapid declines in kidney function: a case series 
BMC Nephrology  2011;12:5.
Few studies have defined alternate pathways by which chronic kidney disease (CKD) patients transition into end-stage renal disease (ESRD).
We studied all consecutive patients initiated on maintenance hemodialysis or peritoneal dialysis over several years at two dialysis units in Northern California. Rapid decline in kidney function was considered to have occurred if a patient was documented to have estimated GFR > 30 ml/min/1.73 m2 within three months prior to the initiation of chronic dialysis.
We found that 8 out of 105 incident chronic dialysis patients one dialysis unit (7.6%; 95% confidence interval 3.4-14.5%) and 9 out of 71 incident patients at another (12.7%, 95% CI 6.0%-22.7%) suffered rapid decline in kidney function that was the immediate precipitant for the need for permanent renal replacement therapy. All these patients started hemodialysis and all relied on catheters for vascular access. Documentation submitted to United States Renal Data System did not fully reflect the health status of these patients during their "pre-ESRD" period.
A sizeable minority of ESRD cases are preceded by rapid declines in kidney function. The importance of these periods of rapid decline may have been under-appreciated in prior studies of the natural history of CKD and ESRD.
PMCID: PMC3042936  PMID: 21284877
6.  The assessment, serial evaluation, and subsequent sequelae of acute kidney injury (ASSESS-AKI) study: design and methods 
BMC Nephrology  2010;11:22.
The incidence of acute kidney injury (AKI) has been increasing over time and is associated with a high risk of short-term death. Previous studies on hospital-acquired AKI have important methodological limitations, especially their retrospective study designs and limited ability to control for potential confounding factors.
The Assessment, Serial Evaluation, and Subsequent Sequelae of Acute Kidney Injury (ASSESS-AKI) Study was established to examine how a hospitalized episode of AKI independently affects the risk of chronic kidney disease development and progression, cardiovascular events, death, and other important patient-centered outcomes. This prospective study will enroll a cohort of 1100 adult participants with a broad range of AKI and matched hospitalized participants without AKI at three Clinical Research Centers, as well as 100 children undergoing cardiac surgery at three Clinical Research Centers. Participants will be followed for up to four years, and will undergo serial evaluation during the index hospitalization, at three months post-hospitalization, and at annual clinic visits, with telephone interviews occurring during the intervening six-month intervals. Biospecimens will be collected at each visit, along with information on lifestyle behaviors, quality of life and functional status, cognitive function, receipt of therapies, interim renal and cardiovascular events, electrocardiography and urinalysis.
ASSESS-AKI will characterize the short-term and long-term natural history of AKI, evaluate the incremental utility of novel blood and urine biomarkers to refine the diagnosis and prognosis of AKI, and identify a subset of high-risk patients who could be targeted for future clinical trials to improve outcomes after AKI.
PMCID: PMC2944247  PMID: 20799966

Results 1-6 (6)