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527 results on '"Parving, H H"'

3. Irbesartan treatment does not influence plasma levels of the dicarbonyls methylglyoxal, glyoxal and 3-deoxyglucosone in participants with type 2 diabetes and microalbuminuria:An IRMA2 sub-study

Author

Piazza, M., Hanssen, N. M.J., Persson, F., Scheijen, J. L., van de Waarenburg, M. P.H., van Greevenbroek, M. M.J., Rossing, P., Hovind, P., Stehouwer, C. D.A., Parving, H. H., Schalkwijk, C. G., Piazza, M., Hanssen, N. M.J., Persson, F., Scheijen, J. L., van de Waarenburg, M. P.H., van Greevenbroek, M. M.J., Rossing, P., Hovind, P., Stehouwer, C. D.A., Parving, H. H., and Schalkwijk, C. G.

Abstract

Aim: Angiotensin receptor blockers (ARBs) reduce vascular complications in diabetes independently of blood pressure. Experimental studies suggested that ARBs may restore the detoxifying enzyme glyoxalase 1, thereby lowering dicarbonyls such as methylglyoxal. Human data on the effects of ARBs on plasma dicarbonyl levels are lacking. We investigated, in individuals with type 2 diabetes, whether irbesartan lowered plasma levels of the dicarbonyls methylglyoxal, glyoxal, 3-deoxyglucosone and their derived advanced glycation end products (AGEs), and increased d-lactate, reflecting greater methylglyoxal flux. Methods: We analysed a subset of the Irbesartan in Patients with T2D and Microalbuminuria (IRMA2) study. We measured plasma dicarbonyls methylglyoxal, glyoxal and 3-deoxyglucosone, free AGEs and d-lactate using ultra-performance liquid chromatography tandem mass-spectrometry (UPLC-MS/MS) in the treatment arm receiving 300 mg irbesartan (n = 121) and a placebo group (n = 101) at baseline and after 1 and 2 years. Effect of treatment was analysed with repeated measurements ANOVA. Results: There was a slight, but significant difference in baseline median methylglyoxal levels [placebo 1119 (907–1509) nmol/l vs. irbesartan 300 mg 1053 (820–1427) nmol/l], but no significant changes were observed in any of the plasma dicarbonyls over time in either group and there was no effect of irbesartan treatment on plasma free AGEs or d-lactate levels at either 1 or 2 years. Conclusion: Irbesartan treatment does not change plasma levels of the dicarbonyls methylglyoxal, glyoxal and 3-deoxyglucosone, free AGEs or d-lactate in type 2 diabetes. This indicates that increased dicarbonyls in type 2 diabetes are not targetable by ARBs, and other approaches to lower systemic dicarbonyls are needed in type 2 diabetes. (Clinical Trial Registry No: #NCT00317915).

Published
2021

21. COMPARISON OF INSULIN DEGLUDEC AND GLARGINE U100 IN PATIENTS WITH TYPE 1 DIABETES PRONE TO SEVERE NOCTURNAL HYPOGLYCAEMIA

Author

Agesen, R., Alibegovic, A., Andersen, H., Beck-Nielsen, H., Gustenhoff, P., Hansen, T., Hedetoft, C., Jensen, T., Juhl, C., Kryger, A., Lerche, S., Norgaard, K., Parving, H. -H., Sørensen, A., Tarnow, L., Thorsteinsson, B., Pedersen-Bjergaard, U., Agesen, R., Alibegovic, A., Andersen, H., Beck-Nielsen, H., Gustenhoff, P., Hansen, T., Hedetoft, C., Jensen, T., Juhl, C., Kryger, A., Lerche, S., Norgaard, K., Parving, H. -H., Sørensen, A., Tarnow, L., Thorsteinsson, B., and Pedersen-Bjergaard, U.

Published
2020

48. 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

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