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Editorial
. 2023 Aug;80(8):1611-1613.
doi: 10.1161/HYPERTENSIONAHA.123.21505. Epub 2023 Jul 20.

Paradigm Shift in Hyperglycemic Glomerular Hyperfiltration: Blunted Tubuloglomerular Feedback or Preglomerular Vasodilation?

Jing Wu  1
Affiliations
Editorial

Paradigm Shift in Hyperglycemic Glomerular Hyperfiltration: Blunted Tubuloglomerular Feedback or Preglomerular Vasodilation?

Jing Wu. Hypertension. 2023 Aug.
No abstract available

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Conflict of interest statement

Disclosures None.

Figures

Figure 1
Figure 1. Classical and new mechanisms of glomerular hyperfiltration during hyperglycemia.
The classical concept holds that in hyperglycemia increased sodium (Na+) reabsorption through SGLT1/2 and passive chloride (Cl−) re-uptake in the proximal tubule causes a decreased delivery of Cl− to the macula densa. This blunts tubuloglomerular feedback (TGF) leading to weakened afferent arteriolar constriction and glomerular hyperfiltration. Red arrows denote pathological changes caused by hyperglycemia. The study by Fei et al supports a new paradigm where hyperglycemia and/or hyperosmolality directly stimulate vasodilation in renal microvessels through the Piezo1-CaMKII-eNOS pathway. In response to high glucose, there is greater vasodilation in the afferent arteriole (AA) than in the efferent arteriole (EA), resulting in elevated glomerular capillary pressure (PGC) and augmented GFR. These hemodynamic derangements ultimately lead to proteinuria, glomerulosclerosis, and chronic kidney disease (CKD). EC, endothelial cell. CaMKII, Ca2+/Calmodulin-dependent protein kinase type II. SGLT, sodium-glucose co-transporter.
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Comment on

References

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