Evidence map›Paper›PMID 29635733›Full record

ArticleJournal of diabetes investigation2019

Renal impairment markers in type 2 diabetes patients with different types of hyperuricemia.

Zhongai Gao, Minxia Zuo, Fei Han, Xinxin Yuan, Mengdi Sun, Xiaochen Li, Ran Liu, Wenhui Jiang, Liyi Zhang, Baocheng Chang and 1 more

Abstract read
In one paragraph

Article in Journal of diabetes investigation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 3 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

16 citing papers in PubMed, 3 syntheses or guidelines pooled it.

  1. Pooled it
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors.

Zhongai GaoKey Laboratory of Hormones and Development (Ministry of Health), Tianjin Key Laboratory of Metabolic Diseases, Tianjin Metabolic Diseases Hospital & Tianjin Institute of Endocrinology, Tianjin Medical University, Tianjin, China.ORCID http://orcid.org/0000-0002-0091-6057
Minxia ZuoKey Laboratory of Hormones and Development (Ministry of Health), Tianjin Key Laboratory of Metabolic Diseases, Tianjin Metabolic Diseases Hospital & Tianjin Institute of Endocrinology, Tianjin Medical University, Tianjin, China.
Fei HanKey Laboratory of Hormones and Development (Ministry of Health), Tianjin Key Laboratory of Metabolic Diseases, Tianjin Metabolic Diseases Hospital & Tianjin Institute of Endocrinology, Tianjin Medical University, Tianjin, China.
Xinxin YuanKey Laboratory of Hormones and Development (Ministry of Health), Tianjin Key Laboratory of Metabolic Diseases, Tianjin Metabolic Diseases Hospital & Tianjin Institute of Endocrinology, Tianjin Medical University, Tianjin, China.
Mengdi SunKey Laboratory of Hormones and Development (Ministry of Health), Tianjin Key Laboratory of Metabolic Diseases, Tianjin Metabolic Diseases Hospital & Tianjin Institute of Endocrinology, Tianjin Medical University, Tianjin, China.
Xiaochen LiKey Laboratory of Hormones and Development (Ministry of Health), Tianjin Key Laboratory of Metabolic Diseases, Tianjin Metabolic Diseases Hospital & Tianjin Institute of Endocrinology, Tianjin Medical University, Tianjin, China.
Ran LiuKey Laboratory of Hormones and Development (Ministry of Health), Tianjin Key Laboratory of Metabolic Diseases, Tianjin Metabolic Diseases Hospital & Tianjin Institute of Endocrinology, Tianjin Medical University, Tianjin, China.
Wenhui JiangKey Laboratory of Hormones and Development (Ministry of Health), Tianjin Key Laboratory of Metabolic Diseases, Tianjin Metabolic Diseases Hospital & Tianjin Institute of Endocrinology, Tianjin Medical University, Tianjin, China.
Liyi ZhangKey Laboratory of Hormones and Development (Ministry of Health), Tianjin Key Laboratory of Metabolic Diseases, Tianjin Metabolic Diseases Hospital & Tianjin Institute of Endocrinology, Tianjin Medical University, Tianjin, China.
Baocheng ChangKey Laboratory of Hormones and Development (Ministry of Health), Tianjin Key Laboratory of Metabolic Diseases, Tianjin Metabolic Diseases Hospital & Tianjin Institute of Endocrinology, Tianjin Medical University, Tianjin, China.
Juhong YangKey Laboratory of Hormones and Development (Ministry of Health), Tianjin Key Laboratory of Metabolic Diseases, Tianjin Metabolic Diseases Hospital & Tianjin Institute of Endocrinology, Tianjin Medical University, Tianjin, China.

Funding

National Natural Science Foundation of China 81373864National Natural Science Foundation of China 81473472National Natural Science Foundation of China 81603461Tianjin Natural Science Foundation 17JCZDJC34700
6 · The paper itself

Abstract

AIMS/

introductionHyperuricemia (HUA) occurs because of decreased excretion of uric acid, increased synthesis of uric acid or a combination of both mechanisms. The proportions of these three types of HUA in type 2 diabetes patients are not known. In the mean time, we assume that different types of HUA might manifest with different renal damage, even in patients with normal renal filtration function. MATERIALS AND

methodsWe included 435 inpatients with type 2 diabetes at the Metabolic Disease Hospital of Tianjin Medical University from 2015 to 2016. Based on the clearance of uric acid, 90 patients with HUA were divided into three types: synthesis-increased HUA, excretion-decreased HUA and mixed type of HUA.

resultsPatients with the mixed type of HUA had the severest kidney injury manifested by a high level of 24 h urinary microalbumin, urinary immunoglobulin G, transferrin, α-galactosidase and β2-microglobulin compared with the normal uric acid group. Urinary immunoglobulin G, transferrin and α-galactosidase were also increased in patients with synthesis-increased HUA compared with the normal uric acid group. Patients with excretion-decreased HUA did not have an increased level of renal impairment markers; however, these patients had an increased body mass index, which might cause dysfunction of kidney excretion.

conclusionsExcretion-decreased HUA is a more common type of HUA in type 2 diabetes patients that might be caused by dysfunction of tubular excretion instead of structural damage. The mixed type of HUA patients had the severest kidney glomerular and tubular damage compared with the normal uric acid group. Clinically, different types of hyperuricemia should be given individualized treatment according to their own characteristics.

Indexed as

BiomarkersDiabetes Mellitus, Type 2FemaleHumansHyperuricemiaKidney DiseasesMaleMiddle AgedRisk FactorsBiomarkersHyperuricemiaRenal impairmentType 2 diabetes mellitus

Identifiers

PMID29635733
PMCPMC6319488

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.