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149 results on '"Schold J.D."'

34. Evaluating Glomerular Filtration Rate Slope as a Surrogate End Point for ESKD in Clinical Trials: An Individual Participant Meta-Analysis of Observational Data

Author

Grams, M.E., Sang, Y., Ballew, Shoshana H., Matsushita, K., Astor, B.C., Carrero, J.J., Chang, A.R., Inker, L.A., Kenealy, T., Kovesdy, C.P., Lee, B.J., Levin, A., Naimark, D., Pena, M.J., Schold, J.D., Shalev, V., Wetzels, J.F.M., Woodward, M., Gansevoort, R.T., Levey, A.S., Coresh, J., Grams, M.E., Sang, Y., Ballew, Shoshana H., Matsushita, K., Astor, B.C., Carrero, J.J., Chang, A.R., Inker, L.A., Kenealy, T., Kovesdy, C.P., Lee, B.J., Levin, A., Naimark, D., Pena, M.J., Schold, J.D., Shalev, V., Wetzels, J.F.M., Woodward, M., Gansevoort, R.T., Levey, A.S., and Coresh, J.

Abstract

Item does not contain fulltext, BACKGROUND: Decline in eGFR is a biologically plausible surrogate end point for the progression of CKD in clinical trials. However, it must first be tested to ensure strong associations with clinical outcomes in diverse populations, including patients with higher eGFR. METHODS: To investigate the association between 1-, 2-, and 3-year changes in eGFR (slope) with clinical outcomes over the long term, we conducted a random effects meta-analysis of 3,758,551 participants with baseline eGFR>/=60 ml/min per 1.73 m(2) and 122,664 participants with eGFR<60 ml/min per 1.73 m(2) from 14 cohorts followed for an average of 4.2 years. RESULTS: Slower eGFR decline by 0.75 ml/min per 1.73 m(2) per year over 2 years was associated with lower risk of ESKD in participants with baseline eGFR>/=60 ml/min per 1.73 m(2) (adjusted hazard ratio, 0.70; 95% CI, 0.68 to 0.72) and eGFR<60 ml/min per 1.73 m(2) (0.71; 95% CI, 0.68 to 0.74). The relationship was stronger with 3-year slope. For a rapidly progressing population with predicted 5-year risk of ESKD of 8.3%, an intervention that reduced eGFR decline by 0.75 ml/min per 1.73 m(2) per year over 2 years would reduce the ESKD risk by 1.6%. For a hypothetical low-risk population with a predicted 5-year ESKD risk of 0.58%, the same intervention would reduce the risk by only 0.13%. CONCLUSIONS: Slower decline in eGFR was associated with lower risk of subsequent ESKD, even in participants with eGFR>/=60 ml/min per 1.73 m(2), but those with the highest risk would be expected to benefit the most.

Published
2019

35. Change in albuminuria and subsequent risk of end-stage kidney disease: an individual participant-level consortium meta-analysis of observational studies.

Author

Ichikawa K., Collins J.F., Drury P.L., Ellis S.G., Nadukuru R., Metzger M., Flamant M., Houillier P., Haymann J.-P., Froissart M., Kenealy T., Elley R.C., Cuddeback J.K., Ciemins E.L., Stempniewicz R., Nelson R.G., Knowler W.C., Bakker S.J., Major R.W., Medcalf J.F., Shepherd D., Barrett-Connor E., Bergstrom J., Ix J.H., Molnar M.Z., Maciulaitis R., Manley T., Smith K., Stockbridge N., Thompson A., Vetter T., Willis K., Zhang L., Coresh J., Heerspink H.J.L., Sang Y., Matsushita K., Arnlov J., Astor B.C., Black C., Brunskill N.J., Carrero J.-J., Feldman H.I., Fox C.S., Inker L.A., Ishani A., Ito S., Jassal S., Konta T., Polkinghorne K., Romundstad S., Solbu M.D., Stempniewicz N., Stengel B., Tonelli M., Umesawa M., Waikar S.S., Wen C.-P., Wetzels J.F.M., Woodward M., Grams M.E., Kovesdy C.P., Levey A.S., Gansevoort R.T., Appel L.J., Greene T., Chen T.K., Chalmers J., Arima H., Perkovic V., Levin A., Djurdjev O., Tang M., Nally J., Navaneethan S.D., Schold J.D., Weldegiorgis M., Herrington W.G., Smith M., Hsu C.Y., Hwang S.-J., Chang A.R., Kirchner H.L., Green J.A., Ho K., Marks A., Prescott G., Clark L.E., Fluck N., Shalev V., Chodick G., Blankestijn P.J., Van Zuilen A., Van den Brand J.A., Sarnak M.J., Bottinger E., Nadkarni G.N., Sumida K., de Zeeuw D., Brenner B., Qureshi A.R., Elinder C.-G., Runesson B., Evans M., Segelmark M., Stendahl M., Schon S., Naimark D.M., Tangri N., Sud M., Hirayama A., Bilo H.J., Landman G.W., Van Hateren K.J., Kleefstra N., Hallan S.I., Ballew S.H., Chen J., Kwak L., Surapaneni A., Parving H.-H., Rodby R.A., Rohde R.D., Lewis J.B., Lewis E., Perrone R.D., Abebe K.Z., Hou F.F., Xie D., Hunsicker L.G., Imai E., Kobayashi F., Makino H., Remuzzi G., Ruggenenti P., Eckardt K.-U., Gudmundsdottir H., Ichikawa K., Collins J.F., Drury P.L., Ellis S.G., Nadukuru R., Metzger M., Flamant M., Houillier P., Haymann J.-P., Froissart M., Kenealy T., Elley R.C., Cuddeback J.K., Ciemins E.L., Stempniewicz R., Nelson R.G., Knowler W.C., Bakker S.J., Major R.W., Medcalf J.F., Shepherd D., Barrett-Connor E., Bergstrom J., Ix J.H., Molnar M.Z., Maciulaitis R., Manley T., Smith K., Stockbridge N., Thompson A., Vetter T., Willis K., Zhang L., Coresh J., Heerspink H.J.L., Sang Y., Matsushita K., Arnlov J., Astor B.C., Black C., Brunskill N.J., Carrero J.-J., Feldman H.I., Fox C.S., Inker L.A., Ishani A., Ito S., Jassal S., Konta T., Polkinghorne K., Romundstad S., Solbu M.D., Stempniewicz N., Stengel B., Tonelli M., Umesawa M., Waikar S.S., Wen C.-P., Wetzels J.F.M., Woodward M., Grams M.E., Kovesdy C.P., Levey A.S., Gansevoort R.T., Appel L.J., Greene T., Chen T.K., Chalmers J., Arima H., Perkovic V., Levin A., Djurdjev O., Tang M., Nally J., Navaneethan S.D., Schold J.D., Weldegiorgis M., Herrington W.G., Smith M., Hsu C.Y., Hwang S.-J., Chang A.R., Kirchner H.L., Green J.A., Ho K., Marks A., Prescott G., Clark L.E., Fluck N., Shalev V., Chodick G., Blankestijn P.J., Van Zuilen A., Van den Brand J.A., Sarnak M.J., Bottinger E., Nadkarni G.N., Sumida K., de Zeeuw D., Brenner B., Qureshi A.R., Elinder C.-G., Runesson B., Evans M., Segelmark M., Stendahl M., Schon S., Naimark D.M., Tangri N., Sud M., Hirayama A., Bilo H.J., Landman G.W., Van Hateren K.J., Kleefstra N., Hallan S.I., Ballew S.H., Chen J., Kwak L., Surapaneni A., Parving H.-H., Rodby R.A., Rohde R.D., Lewis J.B., Lewis E., Perrone R.D., Abebe K.Z., Hou F.F., Xie D., Hunsicker L.G., Imai E., Kobayashi F., Makino H., Remuzzi G., Ruggenenti P., Eckardt K.-U., and Gudmundsdottir H.

Abstract

Background: Change in albuminuria as a surrogate endpoint for progression of chronic kidney disease is strongly supported by biological plausibility, but empirical evidence to support its validity in epidemiological studies is lacking. We aimed to assess the consistency of the association between change in albuminuria and risk of end-stage kidney disease in a large individual participant-level meta-analysis of observational studies. Method(s): In this meta-analysis, we collected individual-level data from eligible cohorts in the Chronic Kidney Disease Prognosis Consortium (CKD-PC) with data on serum creatinine and change in albuminuria and more than 50 events on outcomes of interest. Cohort data were eligible if participants were aged 18 years or older, they had a repeated measure of albuminuria during an elapsed period of 8 months to 4 years, subsequent end-stage kidney disease or mortality follow-up data, and the cohort was active during this consortium phase. We extracted participant-level data and quantified percentage change in albuminuria, measured as change in urine albumin-to-creatinine ratio (ACR) or urine protein-to-creatinine ratio (PCR), during baseline periods of 1, 2, and 3 years. Our primary outcome of interest was development of end-stage kidney disease after a baseline period of 2 years. We defined an end-stage kidney disease event as initiation of kidney replacement therapy. We quantified associations of percentage change in albuminuria with subsequent end-stage kidney disease using Cox regression in each cohort, followed by random-effects meta-analysis. We further adjusted for regression dilution to account for imprecision in the estimation of albuminuria at the participant level. We did multiple subgroup analyses, and also repeated our analyses using participant-level data from 14 clinical trials, including nine clinical trials not in CKD-PC. Finding(s): Between July, 2015, and June, 2018, we transferred and analysed data from 28 cohorts in the C

Published
2019

37. Mood, body image, fear of kidney failure, life satisfaction, and decisional stability following living kidney donation: Findings from the KDOC study

Author

Rodrigue, J.R., primary, Schold, J.D., additional, Morrissey, P., additional, Whiting, J., additional, Vella, J., additional, Kayler, L.K., additional, Katz, D., additional, Jones, J., additional, Kaplan, B., additional, Fleishman, A., additional, Pavlakis, M., additional, and Mandelbrot, D.A., additional

Published
2018
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38. Supplementary Material for: National Impact of Maintenance Dialysis or Renal Transplantation on Outcomes Following ST Elevation Myocardial Infarction

Author

Sakhuja, A., Wright, R.S., Schold, J.D., McCarthy, J.T., Williams, A.W., Amer, H., and Albright, R.C.

Subjects
surgical procedures, operative
Abstract

Background: Though cardiovascular disease is an important cause of mortality in patients with end-stage renal disease, epidemiology of ST-elevation myocardial infarction (STEMI) is less well described in this population. Methods: This study included STEMI hospitalizations in patients aged ≥20 using Nationwide Inpatient Sample Database from 2006 to 2010. Primary outcomes were incidence and trends of STEMI hospitalizations based on renal function status. We also looked at utilization of revascularization procedures, all-cause-hospital mortality and predictors of mortality. Results: Of the estimated 882,447 STEMI hospitalizations, 11,383 were on maintenance dialysis and 1,076 had renal transplants. The incidence of STEMI was over 7 times in patients on maintenance dialysis and 1.73 times in renal transplant recipients compared to the general population. This incidence has however declined in those on maintenance dialysis (p for trend Conclusions: STEMI hospitalizations are more common in patients on maintenance dialysis and with renal transplants. The utilization of revascularizations procedures remains low and mortality high in these patients.

Published
2016
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48. Integrating APOL1Gene Variants Into Renal Transplantation: Considerations Arising From the American Society of Transplantation Expert Conference

Author

Newell, K.A., Formica, R.N., Gill, J.S., Schold, J.D., Allan, J.S., Covington, S.H., Wiseman, A.C., and Chandraker, A.

Abstract

Thirteen percent of individuals of African ancestry express two variant copies of the gene encoding apolipoprotein 1 (APOL1) that has been associated with an increased risk of end-stage renal disease (ESRD) in the general population. Limited studies suggest that the survival of transplanted kidneys from donors expressing two APOL1risk alleles is inferior to that of kidneys from donors with zero or one risk allele. In living kidney donation, two case reports describe donors expressing two APOL1risk alleles who developed ESRD. Given the potential impact of APOL1variants on the utility and safety of kidney transplantation and living kidney donation, the American Society of Transplantation convened a meeting with the goals of summarizing the current state of knowledge with respect to transplantation and APOL1, identifying knowledge gaps and studies to address these gaps, and considering approaches to integrating APOL1into clinical practice. The authors recognize that current data are not sufficient to support traditional evidence-based guidelines but also recognize that it may require several years to generate the necessary data. Thus, approaches as to how APOL1might currently be integrated into the clinical decision-making process were considered. This report summarizes the group’s deliberations.

Published
2017
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