ArticleKidney medicine2026
Kidney Transplantation-Induced Reduction in Myocardial Fibrosis and Modulation of Plasma Proteome: Results of a Pilot Study.
Article in Kidney medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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14 authors.
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Abstract
Rationale & Objective: Kidney transplantation (KT) improves cardiovascular outcomes in patients with kidney failure, yet the biological mechanisms underlying post-KT myocardial recovery remain unclear. Study Design: Prospective observational cohort study with matched controls. Setting & Participants: Fifty participants were enrolled at 2 transplant centers: 28 received a living KT, and a cardiac magnetic resonance imaging (CMRI) scan assessment of interstitial myocardial fibrosis with T1 maps before and nine months post-KT; 22 matched waitlisted controls had baseline and 9-month CMRI scans. The groups were matched using baseline characteristics and T1 values. Exposure: Receipt of kidney transplantation. Outcome: Change in native T1 mapping CMRI scan, a surrogate marker of interstitial myocardial fibrosis. Analytical Approach: Regression models were used to estimate the effect of KT versus no KT (the waitlisted control group) on interstitial myocardial fibrosis, adjusted for demographic characteristics, comorbidities, blood pressure, and medications. Plasma collected at baseline was analyzed using SomaScan v.4.1 (6,472 unique proteins). Regression models were used to identify proteins associated with baseline and longitudinal changes in T1, adjusted for clinical covariates and corrected for multiple testing. Results: KT recipients had reduced interstitial myocardial fibrosis compared with waitlisted controls (-47.49 ± 81.63 vs +13.77 ± 62.13 ms, Limitations: A modest sample size and a single time-point proteomic assessment. External validation is needed. Conclusions: KT leads to regression of interstitial myocardial fibrosis within 9 months, supporting a structural cardiac benefit of transplantation. Pretransplant proteomic signatures, particularly macrophage colony-stimulating factor, reflect underlying fibrotic burden and may serve as a predictive biomarker to monitor post-KT cardiac recovery.
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