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. 2022 Oct 21;9:1029224. doi: 10.3389/fmed.2022.1029224

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Copyright © 2022 Afangbedji and Jerebtsova.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Mechanism of SCD-induced glomerular hyperfiltration. The hypoxic, acidic, and hyperosmolar environment of the renal medulla promotes the polymerization of HbS and the sickling of RBCs. Slow blood rheology in the vasa recta aggravates the vaso-occlusion and leads to ischemia that can advance to infarction. As a compensatory mechanism, medullary prostaglandins and nitric oxide (NO) are secreted leading to an increased renal cortical flow. It was suggested that prostaglandins are released by renal interstitial cells. Genetic modifiers such as APOL1, HMOX1, MYH9, HbA1, and HbA2 and increased renal perfusion coupled with increased glomerular permeability and glomerular filtration surface area may enhance glomerular hyperfiltration in SCD. Figure created with BioRender.com.