Article in Renal failure, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper, 1 of them a synthesis that pooled it.
0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed, 1 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
1 citing paper in PubMed, 1 synthesis or guideline pooled it.
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
7 authors.
Shujun WangDepartment of Nephrology, National Clinical Key Specialty Construction Program (2023); Institute of Nephrology; Guangdong Provincial Key Laboratory of Autophagy and Major Chronic Non-communicable Diseases; Key Laboratory of Prevention and Management of Chronic Kidney Disease of Zhanjiang City, Affiliated Hospital of Guangdong Medical University, Zhanjiang, China.
Lawei YangDepartment of Nephrology, National Clinical Key Specialty Construction Program (2023); Institute of Nephrology; Guangdong Provincial Key Laboratory of Autophagy and Major Chronic Non-communicable Diseases; Key Laboratory of Prevention and Management of Chronic Kidney Disease of Zhanjiang City, Affiliated Hospital of Guangdong Medical University, Zhanjiang, China.
Peijia HuangDepartment of Nephrology, National Clinical Key Specialty Construction Program (2023); Institute of Nephrology; Guangdong Provincial Key Laboratory of Autophagy and Major Chronic Non-communicable Diseases; Key Laboratory of Prevention and Management of Chronic Kidney Disease of Zhanjiang City, Affiliated Hospital of Guangdong Medical University, Zhanjiang, China.
Jingjing ZhengDepartment of Nephrology, National Clinical Key Specialty Construction Program (2023); Institute of Nephrology; Guangdong Provincial Key Laboratory of Autophagy and Major Chronic Non-communicable Diseases; Key Laboratory of Prevention and Management of Chronic Kidney Disease of Zhanjiang City, Affiliated Hospital of Guangdong Medical University, Zhanjiang, China.
Qian WangDepartment of Nephrology, National Clinical Key Specialty Construction Program (2023); Institute of Nephrology; Guangdong Provincial Key Laboratory of Autophagy and Major Chronic Non-communicable Diseases; Key Laboratory of Prevention and Management of Chronic Kidney Disease of Zhanjiang City, Affiliated Hospital of Guangdong Medical University, Zhanjiang, China.
Hua-Feng LiuDepartment of Nephrology, National Clinical Key Specialty Construction Program (2023); Institute of Nephrology; Guangdong Provincial Key Laboratory of Autophagy and Major Chronic Non-communicable Diseases; Key Laboratory of Prevention and Management of Chronic Kidney Disease of Zhanjiang City, Affiliated Hospital of Guangdong Medical University, Zhanjiang, China.ORCID 0000-0001-6547-212X
Yongzhi XuDepartment of Nephrology, National Clinical Key Specialty Construction Program (2023); Institute of Nephrology; Guangdong Provincial Key Laboratory of Autophagy and Major Chronic Non-communicable Diseases; Key Laboratory of Prevention and Management of Chronic Kidney Disease of Zhanjiang City, Affiliated Hospital of Guangdong Medical University, Zhanjiang, China.
Funding
No grant is acknowledged in the PubMed record.
6 · The paper itself
Abstract
Sodium-glucose cotransporter 2 inhibitors reduced proteinuria in patients with IgA nephropathy; however, their efficacy in patients at high risk of progression receiving immunosuppressive agents and renin angiotensin-aldosterone system inhibitors remains unclear. After 3 months of low-dose steroid alone or combined with mycophenolate mofetil, as well as renin angiotensin-aldosterone system inhibitors treatment, 105 biopsy-proven IgA nephropathy patients with proteinuria greater than 0.5 g/d were included in this study. The changes in proteinuria and renal function were analyzed at 3 and 6 months after initiating dapagliflozin. Among 105 patients, the MEST-C lesions of M1, E1, S1, C1, C2 and T1 were more frequent and accounted for 74.3%, 61.0%, 80.0%, 50.5%, 8.6% and 40%, respectively. Baseline characteristics were similar between 49 patients in the dapagliflozin groups and 56 patients in the control groups. After 6 months of therapy, the total remission rate in the dapagliflozin group was higher than that in the control group (55.1% vs. 33.9%,
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.
Dapagliflozin reduces proteinuria in IgA nephropathy patients receiving immunosuppressive therapy. · full record | OpenQuestion