Association of tumor necrosis factor receptors 1 and 2 with kidney volume and function in patients with autosomal dominant polycystic kidney disease.
Аннотация
BACKGROUND
Autosomal dominant polycystic kidney disease (ADPKD) is a prevalent genetic disorder characterized by renal cyst formation, progressive kidney enlargement, and declining kidney function. The pro-inflammatory effects of tumor necrosis factor through its receptors TNFR1 and TNFR2 may have a role in the growth of cysts and kidney volume in ADPKD cases. This study aimed to assess the association between serum TNFR1 and TNFR2 levels, kidney function (estimated glomerular filtration rate (eGFR)), and height-adjusted total kidney volume (HtTKV) in ADPKD patients.
MATERIALS AND
METHODS
We recruited 50 ADPKD and 20 non-ADPKD chronic kidney disease (CKD) patients. Serum TNFR1, TNFR2, and cystatin C levels were measured using enzyme-linked immunosorbent assay. Magnetic resonance imaging was performed to measure kidney volumes, and eGFR was calculated using a serum creatinine-cystatin C-based formula. Correlation analyses and multivariate regression models were utilized to evaluate associations between biomarkers and eGFR.
RESULTS
TNFR1 levels showed a significant negative correlation with eGFR (r = -0.332, p = 0.019) in ADPKD patients, while no such association was observed in CKD patients. No significant correlations were found between HtTKV and either TNFR1 or TNFR2 concentration. Multivariate regression analysis revealed that TNFR1 was independently associated with lower eGFR values (B = -27.114, p = 0.019).
CONCLUSION
High levels of TNFR1 are correlated with lower kidney function in ADPKD patients but are not associated with kidney volume. The absence of linkages with HtTKV may be influenced by the use of tolvaptan in this cohort. Further longitudinal studies are warranted to explore the causal roles of TNFRs in ADPKD progression.
Предметные рубрики MeSH
Подготовка и перевод публикации
Обработка статьи · этапы, ошибки и управление
Ошибки и ограничения
История · было → стало
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