ReviewKidney international2012
The kallikrein-kinin system in diabetic nephropathy.
Review in Kidney international, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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.
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.
Who cites it
31 citing papers in PubMed, 52 citations in OpenAlex.
- KNG-1, HSPG and Robo4 reflect hypertension-driven subclinical renal alterations and provide incremental diagnostic value in type 2 diabetic nephropathy.Scientific reports · 2026Article
- Article
- Kallikrein-kinin system as a potential target for the treatment of intervertebral disc degeneration.European journal of medical research · 2025Review
- Factor XII signaling via uPAR-integrin β1 axis promotes tubular senescence in diabetic kidney disease.Nature communications · 2024Article
- Screening candidate diagnostic biomarkers for diabetic kidney disease.Journal of clinical laboratory analysis · 2024Article
- Reduced hepatic bradykinin degradation accounts for cold-induced BAT thermogenesis and WAT browning in male mice.Nature communications · 2023Article
- Human plasma kallikrein: roles in coagulation, fibrinolysis, inflammation pathways, and beyond.Frontiers in physiology · 2023Review
- Proteomic Analysis of Serum Lysine Acetylation in Uyghur Patients With T2DM.Frontiers in molecular biosciences · 2022Article
- Molecular basis for kinin selectivity and activation of the human bradykinin receptors.Nature structural & molecular biology · 2021Article
- Recent Advancements in the Medical Treatment of Diabetic Retinal Disease.International journal of molecular sciences · 2021Review
- Review
- Decreased plasma kallikrein activity is associated with reduced kidney function in individuals with type 1 diabetes.Diabetologia · 2020Article
- Diabetes-induced upregulation of kallistatin levels exacerbates diabetic nephropathy via RAS activation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Article
- Impact of a Complement Factor H Gene Variant on Renal Dysfunction, Cardiovascular Events, and Response to ACE Inhibitor Therapy in Type 2 Diabetes.Frontiers in genetics · 2019Article
- Chronic kidney disease: a review of proteomic and metabolomic approaches to membranous glomerulonephritis, focal segmental glomerulosclerosis, and IgA nephropathy biomarkers.Proteome science · 2019Review
- Role of Kidney Biopsies for Biomarker Discovery in Diabetic Kidney Disease.Advances in chronic kidney disease · 2018Review
- A Network Pharmacology Approach to Uncover the Mechanisms of Shen-Qi-Di-Huang Decoction against Diabetic Nephropathy.Evidence-based complementary and alternative medicine : eCAM · 2018Article
- The Gut-Kidney Axis: Putative Interconnections Between Gastrointestinal and Renal Disorders.Frontiers in endocrinology · 2018Review
- Early urinary biomarkers of diabetic nephropathy in type 1 diabetes mellitus show involvement of kallikrein-kinin system.BMC nephrology · 2017Observational
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Diabetic nephropathy is the major cause of end-stage renal disease worldwide. Although the renin-angiotensin system has been implicated in the pathogenesis of diabetic nephropathy, angiotensin I-converting enzyme inhibitors have a beneficial effect on diabetic nephropathy independently of their effects on blood pressure and plasma angiotensin II levels. This suggests that the kallikrein-kinin system (KKS) is also involved in the disease. To study the role of the KKS in diabetic nephropathy, mice lacking either the bradykinin B1 receptor (B1R) or the bradykinin B2 receptor (B2R) have been commonly used. However, because absence of either receptor causes enhanced expression of the other, it is difficult to determine the precise functions of each receptor. This difficulty has recently been overcome by comparing mice lacking both receptors with mice lacking each receptor. Deletion of both B1R and B2R reduces nitric oxide (NO) production and aggravates renal diabetic phenotypes, relevant to either lack of B1R or B2R, demonstrating that both B1R and B2R exert protective effects on diabetic nephropathy presumably via NO. Here, we review previous epidemiological and experimental studies, and discuss novel insights regarding the therapeutic implications of the importance of the KKS in averting diabetic nephropathy.
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What OpenQuestion holds
Registered trials
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.