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终末期多囊肾病的代谢紊乱与其他原发性肾脏疾病有何不同?

Do metabolic derangements in end-stage polycystic kidney disease differ versus other primary kidney diseases?

作者信息

Jankowska Magdalena, Qureshi Abdul Rashid, Barany Peter, Heimburger Olof, Stenvinkel Peter, Lindholm Bengt

机构信息

Division of Renal Medicine and Baxter Novum, Karolinska Institutet, Stockholm, Sweden.

Department of Nephrology, Transplantology and Internal Medicine, Medical University of Gdansk, Poland.

出版信息

Nephrology (Carlton). 2018 Jan;23(1):31-36. doi: 10.1111/nep.12927.

DOI:10.1111/nep.12927
PMID:27653449
Abstract

AIM

Autosomal dominant polycystic kidney disease (ADPKD), a systemic disorder caused by mutation in genes encoding polycystins, has been reported to lead to metabolic derangements including new-onset diabetes mellitus after kidney transplantation. We analyzed markers of insulin resistance (IR), inflammation, nutritional status and insulin-like growth factor-1 (IGF-1) in end-stage renal disease (ESRD) patients with ADPKD and ESRD patients with other primary kidney diseases.

METHODS

In a post hoc cross-sectional analysis in 254 non-diabetic CKD 5 patients starting on dialysis, glucose metabolism (insulin, IGF-1, homeostasis model assessment of IR, HOMA-IR), inflammation (high sensitivity C-reactive protein, interleukin-6, and tumour necrosis factor), nutritional status, and bone mineral density (BMD), were assessed. Survival was recorded for median time of 28 months (IQR 15-48 months).

RESULTS

Neither indices of IR, nor IGF-1, inflammatory status, nutritional status, or BMD were different in patients with ADPKD as compared to other aetiologies of ESRD. Kaplan-Meier curves showed better survival among the ADPKD group versus other aetiologies, even after an exclusion of diabetic patients.

CONCLUSIONS

The ESRD phenotype did not differ in ADPKD versus other primary kidney diseases in terms of markers of IR, inflammation, and nutritional status. This argues against the proposition that ADPKD patients are more prone to develop metabolic derangements beyond those generally observed in advanced CKD. However, additional studies are warranted to further elucidate systemic metabolic aspects of ADPKD.

摘要

目的

常染色体显性遗传性多囊肾病(ADPKD)是一种由编码多囊蛋白的基因突变引起的全身性疾病,据报道可导致代谢紊乱,包括肾移植后新发糖尿病。我们分析了晚期肾病(ESRD)合并ADPKD患者以及ESRD合并其他原发性肾病患者的胰岛素抵抗(IR)、炎症、营养状况和胰岛素样生长因子-1(IGF-1)指标。

方法

在一项对254例开始透析的非糖尿病CKD 5期患者的事后横断面分析中,评估了葡萄糖代谢(胰岛素、IGF-1、IR的稳态模型评估,HOMA-IR)、炎症(高敏C反应蛋白、白细胞介素-6和肿瘤坏死因子)、营养状况和骨密度(BMD)。记录了28个月(四分位间距15 - 48个月)的中位生存时间。

结果

与ESRD的其他病因相比,ADPKD患者的IR指标、IGF-1、炎症状态、营养状况或BMD均无差异。Kaplan-Meier曲线显示,即使排除糖尿病患者,ADPKD组的生存率也高于其他病因组。

结论

在IR、炎症和营养状况指标方面,ADPKD患者的ESRD表型与其他原发性肾病患者并无差异。这与ADPKD患者比晚期CKD患者更容易发生代谢紊乱的观点相悖。然而,仍需要进一步的研究来进一步阐明ADPKD的全身代谢情况。

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