ArticleClinical and experimental nephrology2011
Growth factor Midkine is involved in the pathogenesis of renal injury induced by protein overload containing endotoxin.
Article in Clinical and experimental nephrology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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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.
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Who cites it
6 citing papers in PubMed, 16 citations in OpenAlex.
- Elevated Midkine Serum Levels Are Associated with Long-Term Survival in Critically Ill Patients.International journal of molecular sciences · 2023Article
- Midkine: a novel and early biomarker of contrast-induced acute kidney injury in patients undergoing percutaneous coronary interventions.BioMed research international · 2015Article
- CD147/basigin reflects renal dysfunction in patients with acute kidney injury.Clinical and experimental nephrology · 2014Article
- Measuring midkine: the utility of midkine as a biomarker in cancer and other diseases.British journal of pharmacology · 2014Review
- Midkine in nephrogenesis, hypertension and kidney diseases.British journal of pharmacology · 2014Review
- Loss of heparin-binding protein prevents necrotizing glomerulonephritis: first clues hint at plasminogen activator inhibitor-1.International urology and nephrology · 2013Review
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundGrowth factor Midkine (MK), which expresses on endothelial cells and renal proximal tubules, has been implicated in inflammation-related kidney diseases such as ischemic reperfusion-induced tubulointerstitial injury and diabetic nephropathy. The biological actions of MK are elicited through its chemotactic activity and chemokine-driven inflammatory pathway. Post-infectious glomerulonephritis is caused by the deposition of immune complexes into glomeruli by infiltrating a number of inflammatory cells. Therefore, we investigated whether MK might be involved in the pathogenesis of acute glomerulonephritis.
methodsWe induced endocapillary proliferative glomerulonephritis in 129/SV mice using intraperitoneal injections of a large amount of protein.
resultsIn contrast to mice deficient in MK (Mdk (-/-)), Mdk (+/+) mice induced by protein overload demonstrated more diffuse cellular proliferation in the mesangial areas and capillary lumens, eventually leading to glomerular damage and tubulointerstitial injury. This pathological observation could be attributable to neutrophil infiltration through the chemotaxis and stimulation of the MK-macrophage inflammatory protein (MIP)-2 pathway, but appeared to be due to the MK-related immunoglobulin (Ig)G deposition and C3 activation. These findings are often seen in infectious-related glomerular injury. Furthermore, the profile of MK expression was strongly consistent with that of glomerular damage and tubulointersititial injury.
conclusionThis study might provide a new insight into understanding the deleterious role of MK in endocapillary proliferative glomerulonephritis induced by protein overload.
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