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1. 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

2. 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

3. 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

4. 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

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