We successfully developed a patient navigator program and an enhanced personal health record for the CKD population. However, there were no differences in eGFR decline and other outcomes among the study groups. Larger and long-term studies along with cost-effectiveness analyses are needed to evaluate the role of patient navigators and patient education through an enhanced personal health record in those with CKD.

BackgroundChronic Kidney Disease (CKD) is a public health problem and there is a scarcity of type 2 CKD translational research that incorporates educational tools. Patient navigators have been shown to be effective at reducing disparities and improving outcomes in the oncology field. We describe the creation of a CKD Patient Navigator program designed to help coordinate care, address system-barriers, and educate/motivate patients.MethodsThe conceptual framework for the CKD Patient Navigator Program is rooted in the Chronic Care Model that has a main goal of high-quality chronic disease management. Our established multidisciplinary CKD research team enlisted new members from information technology and data management to help create the program. It encompassed three phases: hiring, training, and implementation. For hiring, we wanted a non-medical or lay person with a college degree that possessed strong interpersonal skills and experience in a service-orientated field. For training, there were three key areas: general patient navigator training, CKD education, and electronic health record (EHR) training. For implementation, we defined barriers of care and created EHR templates for which pertinent study data could be extracted.ResultsWe have hired two CKD patient navigators who will be responsible for navigating CKD patients enrolled in a clinical trial. They have undergone training in general patient navigation, specific CKD education through directed readings and clinical shadowing, as well as EHR and other patient related privacy and research training.ConclusionsThe need for novel approaches like our CKD patient navigator program designed to impact CKD care is vital and should utilize team-based care and health information technology given the changing landscape of our health systems.Electronic supplementary materialThe online version of this article (doi:10.1186/s12882-015-0060-2) contains supplementary material, which is available to authorized users.

Background: Sensitive and specific biomarkers for use in progressive multiple sclerosis (MS) have not been established. We investigate neurofilament light (NfL) as a treatment response biomarker in progressive MS. Objective: To evaluate whether ibudilast 100 mg/day alters serum and cerebrospinal fluid (CSF) levels of NfL in progressive MS. Methods: In a protocol-defined exploratory analysis from a 2-year, phase 2 clinical trial of ibudilast in progressive MS (NCT01982942), serum samples were collected from 239 subjects and a subset contributed CSF and assayed using single-molecule assay (SIMOA) immunoassay. A mixed model for repeated measurements yielded log(NfL) as the response variable. Results: The geometric mean baseline serum NfL was 31.9 and 28.8 pg/mL in placebo and ibudilast groups, respectively. The geometric mean baseline CSF NfL was 1150.8 and 1290.3 pg/mL in placebo and ibudilast groups, respectively. Serum and CSF NfL correlations were r = 0.52 and r = 0.78 at weeks 48 and 96, respectively. Over 96 weeks, there was no between-group difference in NfL in either serum ( p = 0.76) or CSF ( p = 0.46). After controlling for factors that may affect NfL, no effect of ibudilast on NfL in either serum or CSF was observed. Conclusion: Ibudilast treatment was not associated with a change in either serum or CSF NfL.

Background: Hyperuricemia is associated with the progression of chronic kidney disease (CKD), but it is not known whether the relationship is causal. We examined the association of hyperuricemia and uric acid lowering therapy (UALT) with progression of CKD in patients with CKD 3 and 4 in the Cleveland Clinic CKD registry. Methods: We included 1,676 patients with CKD stages 3 and 4 from Ohio, who had measured their uric acid (UA) levels a year prior to the recording of the second eGFR <60 mL/min/1.73 m², and follow-up eGFR, between 2005 and 2009. Our primary composite outcome included a 50% drop in eGFR or progression to ESRD. Secondary outcomes included the rate of decline in eGFR, all-cause mortality, progression to ESRD, and a composite measure of progression to ESRD or death. We assessed the association between UA, UALT, and outcomes using Cox models and competing risks regression models. Results: In multivariable models, higher UA was associated with the composite endpoint, but it reached statistical significance only in the 4th quartile (≥8.9 mg/dL). Receipt of UALT was significantly associated with increased risk of the composite outcome. Neither UA nor UALT (considered a time-dependent covariate) was significantly associated with mortality. The inference was similar for UA as high vs. low, quartiles, or continuous. Similarly, neither high UA nor UALT were significantly associated with ESRD, the composite of ESRD and mortality, or eGFR decline. Conclusions: Hyperuricemia is associated with increased risk of progression to ESRD in patients with CKD stages 3 and 4, but UALT does not ameliorate the risk, suggesting that the relationship is not causal.

Background/Aims: contrast-induced nephropathy (CIN) is well described following an administration of intraarterial contrast, but its occurrence after intravenous (IV) contrast is being questioned. We evaluated the incidence of acute kidney injury (AKI), post-contrast AKI (PC-AKI), CIN, dialysis and mortality in patients with chronic kidney disease (CKD) undergoing non-contrast computed tomography (NCCT) or contrast CT (CCT) or coronary angiography (CoA). Methods: We identified individuals who had CoA or CCT or NCCT between 2010 and 2015 in the Cleveland Clinic CKD registry. We used propensity scores to match patients in the 3 groups. We evaluated the proportion of patients that developed AKI and CIN across the groups with chi-square tests. We generated Kaplan-Meier plots comparing mortality and ESRD among patients who developed AKI (in the NCCT group), PC (multifactorial AKI, CIN) AKI and no AKI. Results: Out of 251 eligible patients, 200 who had CoA were matched to each of the other CT scan groups. The incidence of AKI was 27% in CoA, 24% in CCT and 24% in NCCT (p = 0.72). The incidence of CIN AKI was 16.5% in CoA and 12.5% in CCT (p = 0.26). The Kaplan-Meier survival at 2 years was 74.8 (95% CI 63.8–87.7) for those with CIN and 53.2 (95% CI 39.7–71.4) for those with multifactorial AKI and 56.5 (95% CI 43.4–73.6) for those with AKI-NCCT and 71.4 (95% CI 67.2–76.0) for those without AKI. The Kaplan-Meier ESRD-free estimates at 2 years were 89.9 (95% CI 80.8–100) for those with CIN and 89.4 (95% CI 78.7–100) for those with multifactorial AKI and 77.4 (95% CI 63.6–94.3) for those with AKI-NCCT and 94.4 (95% CI 91.9–97.1) for those without AKI. Conclusion: The administration of both IV and intra-arterial contrast is associated with a risk of AKI. Multifactorial AKI was associated with worse outcomes, while CIN was associated with better outcomes.