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Development and validation of a risk score for the prediction of cardiovascular disease in living donor kidney transplant recipients
Author(s) -
Kenji Ueki,
Akihiro Tsuchimoto,
Yuta Matsukuma,
Kaneyasu Nakagawa,
Hiroaki Tsujikawa,
Kosuke Masutani,
Shigeru Tanaka,
Keizo Kaku,
Hiroshi Noguchi,
Yasuhiro Okabe,
Kohei Unagami,
Yoichi Kakuta,
Masayoshi Okumi,
Masafumi Nakamura,
Kazuhiko Tsuruya,
Toshiaki Nakano,
Kazunari Tanabe,
Takanari Kitazono
Publication year - 2020
Publication title -
nephrology dialysis transplantation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.654
H-Index - 168
eISSN - 1460-2385
pISSN - 0931-0509
DOI - 10.1093/ndt/gfaa275
Subject(s) - medicine , cohort , goodness of fit , proportional hazards model , statistic , framingham risk score , dialysis , retrospective cohort study , disease , statistics , mathematics
Background Cardiovascular disease (CVD) is a major cause of death in kidney transplant (KT) recipients. To improve their long-term survival, it is clinically important to estimate the risk of CVD after living donor KT via adequate pre-transplant CVD screening. Methods A derivation cohort containing 331 KT recipients underwent living donor KT at Kyushu University Hospital from January 2006 to December 2012. A prediction model was retrospectively developed and risk scores were investigated via a Cox proportional hazards regression model. The discrimination and calibration capacities of the prediction model were estimated via the c-statistic and the Hosmer–Lemeshow goodness of fit test. External validation was estimated via the same statistical methods by applying the model to a validation cohort of 300 KT recipients who underwent living donor KT at Tokyo Women’s Medical University Hospital. Results In the derivation cohort, 28 patients (8.5%) had CVD events during the observation period. Recipient age, CVD history, diabetic nephropathy, dialysis vintage, serum albumin and proteinuria at 12 months after KT were significant predictors of CVD. A prediction model consisting of integer risk scores demonstrated good discrimination (c-statistic 0.88) and goodness of fit (Hosmer–Lemeshow test P = 0.18). In a validation cohort, the model demonstrated moderate discrimination (c-statistic 0.77) and goodness of fit (Hosmer–Lemeshow test P = 0.15), suggesting external validity. Conclusions The above-described simple model for predicting CVD after living donor KT was accurate and useful in clinical situations.

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