ReviewWorld journal of diabetes2015
How the kidney hyperfiltrates in diabetes: From molecules to hemodynamics.
Review in World journal of diabetes, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Metabolic Reprogramming and Immunometabolic Dysregulation in Diabetic Kidney Disease: From Pathogenesis to Precision Multi-target Therapies.Research (Washington, D.C.) · 2026Review
- Intrarenal Mechanisms of Sodium-Glucose Cotransporter-2 Inhibitors on Tubuloglomerular Feedback and Natriuresis.Endocrinology and metabolism (Seoul, Korea) · 2023Review
- Update on Pathogenesis of Glomerular Hyperfiltration in Early Diabetic Kidney Disease.Frontiers in endocrinology · 2022Review
- Is There a Diabetes-Kidney-Heart Continuum? Perspectives From the Results of the Cardiovascular and Renal Outcome Clinical Trials With SGLT2 Inhibitors.Frontiers in cardiovascular medicine · 2021Article
- Angiotensin-(1-7): A Novel Peptide to Treat Hypertension and Nephropathy in Diabetes?Journal of diabetes & metabolism · 2015Article
Corrections and comments
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Authors and funding
3 authors.
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Abstract
In this review, we focused on two molecules, connexin and sodium-glucose cotransporter, which can link to diabetic hyperfiltration. In diabetic kidney, the activation of renin-angiotensin system occurs simultaneously with glomerular hyperfiltration. The latter largely depends on pathophysiological afferent arteriolar dilation in the presence of high angiotensin II. As a mechanistic basis for the above, tubular hypothesis has been proposed for type 1 diabetic patients as well as experimental models. Although tubular hypothesis has not been well evaluated in type 2 diabetes, clinical observations support that tubular hypothesis is true also in type 2 diabetes. Recent results on tubular hypothesis along with connexin abnormality in type 2 diabetes were revisited. In addition, the importance of sodium-glucose cotransporter in diabetic hyperfiltration is discussed. The link between salt paradox and the activation of renin-angiotensin system will be also reviewed.
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