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dc.contributor.author
Tang, Jeannette
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Wysocki, Jan
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Ye, Minghao
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Garramuño, Patricia
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Rein, Johannes
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Shirazi, Mina
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Bader, Michael
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Gomez, Roberto Ariel
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Sequeira Lopez, Maria Luisa S.
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Afkarian, Maryam
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Batlle, Daniel
dc.date.available
2020-07-13T19:34:59Z
dc.date.issued
2019-07
dc.identifier.citation
Tang, Jeannette; Wysocki, Jan; Ye, Minghao; Garramuño, Patricia; Rein, Johannes; et al.; Urinary renin in patients and mice with diabetic kidney disease; Lippincott Williams; Hypertension; 74; 1; 7-2019; 83-94
dc.identifier.issn
0194-911X
dc.identifier.uri
http://hdl.handle.net/11336/109182
dc.description.abstract
In patients with diabetic kidney disease (DKD), plasma renin activity is usually decreased, but there is limited information on urinary renin and its origin. Urinary renin was evaluated in samples from patients with longstanding type I diabetes mellitus and mice with streptozotocin-induced diabetes mellitus. Renin-reporter mouse model (Ren1d-Cre;mT/ mG) was made diabetic with streptozotocin to examine whether the distribution of cells of the renin lineage was altered in a chronic diabetic environment. Active renin was increased in urine samples from patients with DKD (n=36), compared with those without DKD (n=38; 3.2 versus 1.3 pg/mg creatinine; P<0.001). In mice with streptozotocin-induced diabetes mellitus, urine renin was also increased compared with nondiabetic controls. By immunohistochemistry, in mice with streptozotocin-induced diabetes mellitus, juxtaglomerular apparatus and proximal tubular renin staining were reduced, whereas collecting tubule staining, by contrast, was increased. To examine the role of filtration and tubular reabsorption on urinary renin, mice were either infused with either mouse or human recombinant renin and lysine (a blocker of proximal tubular protein reabsorption). Infusion of either form of renin together with lysine markedly increased urinary renin such that it was no longer different between nondiabetic and diabetic mice. Megalin mRNA was reduced in the kidney cortex of streptozotocin-treated mice (0.70±0.09 versus 1.01±0.04 in controls, P=0.01) consistent with impaired tubular reabsorption. In Ren1d-Cre;mT/mG with streptozotocin-induced diabetes mellitus, the distribution of renin lineage cells within the kidney was similar to nondiabetic renin-reporter mice. No evidence for migration of cells of renin linage to the collecting duct in diabetic mice could be found. Renin mRNA in microdissected collecting ducts from streptozotocin-treated mice, moreover, was not significantly different than in controls, whereas in kidney cortex, largely reflecting juxtaglomerular apparatus renin, it was significantly reduced. In conclusion, in urine from patients with type 1 diabetes mellitus and DKD and from mice with streptozotocin-induced diabetes mellitus, renin is elevated. This cannot be attributed to production from cells of the renin lineage migrating to the collecting duct in a chronic hyperglycemic environment. Rather, the elevated levels of urinary renin found in DKD are best attributed to altered glomerular filteration and impaired proximal tubular reabsorption.
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application/pdf
dc.language.iso
eng
dc.publisher
Lippincott Williams
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dc.rights
info:eu-repo/semantics/openAccess
dc.rights.uri
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.subject
diabetes mellitus
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kidney
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mice
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renin
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renin-angiotensin system
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Otras Ciencias Biológicas
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dc.subject.classification
Ciencias Biológicas
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CIENCIAS NATURALES Y EXACTAS
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dc.title
Urinary renin in patients and mice with diabetic kidney disease
dc.type
info:eu-repo/semantics/article
dc.type
info:ar-repo/semantics/artículo
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info:eu-repo/semantics/publishedVersion
dc.date.updated
2020-06-30T14:24:34Z
dc.journal.volume
74
dc.journal.number
1
dc.journal.pagination
83-94
dc.journal.pais
Estados Unidos
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dc.journal.ciudad
Philadelphia
dc.description.fil
Fil: Tang, Jeannette. Northwestern University; Estados Unidos
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Fil: Wysocki, Jan. Northwestern University; Estados Unidos
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Fil: Ye, Minghao. Northwestern University; Estados Unidos
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Fil: Garramuño, Patricia. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; Argentina
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Fil: Rein, Johannes. Northwestern University; Estados Unidos
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Fil: Shirazi, Mina. Northwestern University; Estados Unidos
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Fil: Bader, Michael. Charité Universitätsmedizin; Alemania
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Fil: Gomez, Roberto Ariel. University of Virginia; Estados Unidos
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Fil: Sequeira Lopez, Maria Luisa S.. University of Virginia; Estados Unidos
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Fil: Afkarian, Maryam. University of California at Davis; Estados Unidos
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Fil: Batlle, Daniel. Northwestern University; Estados Unidos
dc.journal.title
Hypertension
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dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/doi/http://dx.doi.org/10.1161/HYPERTENSIONAHA.119.12873
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/https://www.ahajournals.org/doi/10.1161/HYPERTENSIONAHA.119.12873
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