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Comment
. 2017 Jan;66(1):14-16.
doi: 10.2337/dbi16-0056.

Back to the Future: Glomerular Hyperfiltration and the Diabetic Kidney

Katherine R Tuttle  1
Affiliations
Comment

Back to the Future: Glomerular Hyperfiltration and the Diabetic Kidney

Katherine R Tuttle. Diabetes. 2017 Jan.
No abstract available

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Figures

Figure 1
Figure 1
Glomerular structural and functional relationships as determinants of GFR. In the study by Ruggenenti et al. (17) of participants with type 2 diabetes and obesity, weight loss by calorie restriction lowered systemic blood pressure, blood glucose, and GFR. This may be interpreted as a decrease in glomerular hyperfiltration and, inferentially, intraglomerular hypertension by both decreasing transmitted blood pressure and modulating tubuloglomerular feedback. A: Normal glomerulus. The balance between vasodilation and vasoconstriction in the afferent (upstream) and efferent (downstream) arterioles determines intraglomerular pressure, a major regulator of GFR. Distal tubular delivery of solute, particularly sodium chloride, at the macula densa regulates afferent arteriolar tone via tubuloglomerular feedback. B: Glomerulus in diabetes. The afferent arteriole opens in response to vasodilatory factors such as hyperglycemia and high blood levels of amino acids. Because of a high filtered load of glucose, reabsorption of glucose and sodium chloride is increased in the proximal tubule. The afferent arteriole also dilates in response to decreased delivery of sodium chloride to the distal tubular macula densa via tubuloglomerular feedback. The efferent arteriole vasoconstricts in response to high local production of angiotensin II. Overall, the balance shifts to glomerular hyperfiltration as a result of high intraglomerular pressure from afferent arteriolar vasodilation and efferent vasoconstriction.
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