Annual change in eGFR in renal hypouricemia: a retrospective pilot study.

IF 2.2 4区医学 Q2 UROLOGY & NEPHROLOGY

Clinical and Experimental Nephrology Pub Date : 2024-10-03 DOI:10.1007/s10157-024-02558-8

Shinobu Sugihara, Yasutaka Yamamoto, Kei Teramoto, Toshiro Hamada, Satoshi Miyazaki, Kazuhide Ogino, Masanari Kuwabara, Akira Ohtahara, Einosuke Mizuta, Kimiyoshi Ichida, Yusuke Endo, Hiroyuki Minato, Haruaki Ninomiya, Masahiko Kato, Kazuhiro Yamamoto, Ichiro Hisatome

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引用次数: 0

Abstract

Background: Extremely low uric acid (UA) levels or increased urinary UA (Uua) excretion might be risk factors for kidney disease in renal hypouricemia (RHU) patients, but their relationship with kidney dysfunction is unclear. This study investigated time-dependent changes in eGFR in RHU patients.

Methods: This multicenter retrospective study assessed UA metabolism and changes in eGFR (median 5.5 years) in 13 RHU patients. We then compared eGFR change in 7 of 13 RHU patients whose eGFR could be measured for 4 years with those in normouricemic group (n = 31). In addition, 7 RHU patients were divided into two groups based on URAT1 gene mutations: homozygote and compound heterozygote mutations (Homo/Com group, n = 3), and wild-type and heterogeneous mutations (WT/Hetero group, n = 4).

Results: In 13 RHU patients, the median and mean serum UA (SUA) were 0.8 (0.4-2.5) and 1.1 ± 0.7 mg/dL. The median and mean Uua were 44.3 (12.7-141.1) and 49.7 ± 36.2 mg/dL. The median and mean urinary urate clearance (Cua/Ccr) were 46.8 (11.3-73.6) and 43.3 ± 19.7%. Over 4 years, eGFR did not change in the RHU group but declined in the normouricemic group. Annual mean eGFR decline and change rate in the RHU group were the same as those in the normouricemic group (- 1.09 ± 1.11 vs. - 1.09 ± 1.92 mL/min/1.73 m²/year, p = 0.996) (- 1.74 ± 1.96 vs. - 1.36 ± 2.10%, p = 0.664). And no significant difference was found in eGFR decline or change rate between Homo/Com and WT/Hetero groups (- 0.33 ± 1.03 vs. - 1.67 ± 0.85 mL/min/1.73 m²/year, p = 0.116) (- 0.61 ± 1.62 vs. - 2.59 ± 1.91%, p = 0.210).

Conclusion: RHU from URAT1 genetic mutation may not show eGFR decline over 4 consecutive years.

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肾功能减退症患者 eGFR 的年度变化：一项回顾性试验研究。

背景：尿酸（UA）水平极低或尿UA（Uua）排泄增加可能是肾性高尿酸血症（RHU）患者发生肾脏疾病的危险因素，但它们与肾功能障碍的关系尚不清楚。本研究调查了 RHU 患者 eGFR 随时间的变化：这项多中心回顾性研究评估了 13 名 RHU 患者的 UA 代谢和 eGFR 变化（中位数为 5.5 年）。然后，我们比较了 13 名 RHU 患者中 7 名的 eGFR 变化情况，这些患者的 eGFR 可以测量 4 年，与正常尿酸血症组（n = 31）的患者进行比较。此外，我们还根据URAT1基因突变情况将7名RHU患者分为两组：同基因突变和复合杂合基因突变组（Homo/Com组，n = 3），以及野生型和杂合型突变组（WT/Hetero组，n = 4）：13 名 RHU 患者的血清 UA（SUA）中位数和平均值分别为 0.8（0.4-2.5）毫克/分升和 1.1 ± 0.7 毫克/分升。尿酸中位数和平均值分别为 44.3（12.7-141.1）毫克/分升和 49.7 ± 36.2 毫克/分升。尿酸盐清除率（Cua/Ccr）的中位数和平均值分别为 46.8 (11.3-73.6) 和 43.3 ± 19.7%。4 年中，RHU 组的 eGFR 没有变化，但正常尿酸血症组的 eGFR 有所下降。RHU 组的年平均 eGFR 下降率和变化率与正常血尿组相同（- 1.09 ± 1.11 vs. - 1.09 ± 1.92 mL/min/1.73 m2/年，p = 0.996）（- 1.74 ± 1.96 vs. - 1.36 ± 2.10%，p = 0.664）。Homo/Com组与WT/Hetero组的eGFR下降或变化率无明显差异（- 0.33 ± 1.03 vs. - 1.67 ± 0.85 mL/min/1.73 m2/年，p = 0.116）（- 0.61 ± 1.62 vs. - 2.59 ± 1.91%，p = 0.210）：结论：URAT1基因突变导致的RHU可能不会出现连续4年的eGFR下降。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Clinical and Experimental Nephrology UROLOGY & NEPHROLOGY-

CiteScore

4.10

自引率

4.30%

发文量

135

审稿时长

4-8 weeks

期刊介绍： Clinical and Experimental Nephrology is a peer-reviewed monthly journal, officially published by the Japanese Society of Nephrology (JSN) to provide an international forum for the discussion of research and issues relating to the study of nephrology. Out of respect for the founders of the JSN, the title of this journal uses the term “nephrology,” a word created and brought into use with the establishment of the JSN (Japanese Journal of Nephrology, Vol. 2, No. 1, 1960). The journal publishes articles on all aspects of nephrology, including basic, experimental, and clinical research, so as to share the latest research findings and ideas not only with members of the JSN, but with all researchers who wish to contribute to a better understanding of recent advances in nephrology. The journal is unique in that it introduces to an international readership original reports from Japan and also the clinical standards discussed and agreed by JSN.