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• W3039354449 abstract "In the report by Neuwirt et al,1Neuwirt H. Burtscher A. Cherney D. Mayer G. Ebenbichler C. Tubuloglomerular feedback in renal glucosuria: mimicking long-term SGLT-2 inhibitor therapy.Kidney Med. 2020; 2: 76-79Abstract Full Text Full Text PDF PubMed Scopus (4) Google Scholar the authors observed that in a patient with renal glucosuria due to a genetic mutation in the sodium-glucose cotransporter 2 (SGLT-2) transporter, the sensitivity of tubuloglomerular feedback is maintained over time. Ultimately, the authors speculate that even in the presence of Na-K-2Cl channel inhibition by loop diuretics, sodium and chloride ions may still activate tubuloglomerular feedback pathways by entering macula densa.1Neuwirt H. Burtscher A. Cherney D. Mayer G. Ebenbichler C. Tubuloglomerular feedback in renal glucosuria: mimicking long-term SGLT-2 inhibitor therapy.Kidney Med. 2020; 2: 76-79Abstract Full Text Full Text PDF PubMed Scopus (4) Google Scholar This conclusion is clinically important; however, in our opinion, some physiologic observations should be made. A strong off-target effect of SGLT-2 inhibitors on the sodium-hydrogen exchangers (NHEs) on the cell surface and intracellular organelles may explain the wide-ranging effects of these agents. In addition, SGLT-2–mediated glucose uptake has been shown to stimulate NHE-3, which is responsible for a considerable amount of sodium reabsorption in the proximal tubule.2Pessoa T.D. Campos L.C. Carraro-Lacroix L. Girardi A.C. Malnic G. Functional role of glucose metabolism, osmotic stress, and sodium-glucose cotransporter isoform-mediated transport on Na+/H+ exchanger isoform 3 activity in the renal proximal tubule.J Am Soc Nephrol. 2014; 25: 2028-2039Crossref PubMed Scopus (119) Google Scholar NHE-1 is not present within the human kidney, so sodium and chloride ions could not activate tubuloglomerular feedback pathways by entering macula densa; however, NHE-3 is located at the proximal tubule and NHE-4, at the thick ascending limb of the loop of Henle.3McCullough P.A. Kluger A.Y. Tecson K.M. et al.Inhibition of the sodium-proton antiporter (exchanger) is a plausible mechanism of potential benefit and harm for drugs designed to block sodium glucose co-transporter.Rev Cardiovasc Med. 2018; 19: 51-63PubMed Google Scholar However, these observations are independent of the coadministration of loop diuretics if we consider that SGLT-2 inhibitors, by inhibiting the Na-K-2Cl channel on the macula densa, act as loop diuretics.4Kimura G. Importance of inhibiting sodium-glucose cotransporter and its compelling indication in type 2 diabetes: pathophysiological hypothesis.J Am Soc Hypertens. 2016; 10: 271-278Abstract Full Text Full Text PDF PubMed Scopus (38) Google Scholar In our opinión, the physiologic effects of SGLT-2 inhibitors on sodium remain largely unknown and an improved understanding is needed to explain their beneficial effects on kidney and cardiovascular outcomes.5Cianciolo G. De Pascalis A. Capelli I. et al.Mineral and electrolyte disorders with SGLT2i therapy.JBMR Plus. 2019; 3e10242Crossref PubMed Scopus (21) Google Scholar The authors declare that they have no relevant financial interests. Received February 14, 2020. Accepted March 8, 2020, after editorial review by the Editor-in-Chief. Tubuloglomerular Feedback in Renal Glucosuria: Mimicking Long-term SGLT-2 Inhibitor TherapyKidney MedicineVol. 2Issue 1PreviewA patient with renal glucosuria due to a congenital knock-out of the sodium-glucose cotransporter 2 (SGLT-2) protein because of a compound heterozygous mutation in the SLC5A2 gene may provide a natural model mimicking the effects of long-term SGLT-2 inhibitor therapy, which has been shown to exert kidney-protective effects beyond its antidiabetic properties. One possible mechanism for the protective effects of SGLT-2 inhibitor therapy might be the activation of tubuloglomerular feedback by increased outflow of sodium, chloride, and glucose to distal parts of the nephron, including the macula densa. Full-Text PDF Open AccessIn Reply to ‘Do SGLT-2 Inhibitors Act Only Through a Functional Tubuloglomerular Feedback Induced by the Increased Outflow of Sodium?’Kidney MedicineVol. 2Issue 4PreviewWe thank De Pascalis and Cianciolo1 for their comment on additional off-target effects of SGLT-2 inhibitors on sodium-hydrogen exchangers (NHEs). However, the purpose of our report was to elucidate whether tubuloglomerular feedback is altered in a natural model mimicking long-term SGLT-2 inhibitor therapy, which was not the case. Full-Text PDF Open Access" @default.
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• W3039354449 title "Do SGLT-2 Inhibitors Act Only Through a Functional Tubuloglomerular Feedback Induced by the Increased Outflow of Sodium?" @default.
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