Insulin Resistance, Elevated Glomerular Filtration Fraction, and Renal Injury

Hypertension ◽  
1996 ◽  
Vol 28 (1) ◽  
pp. 127-132 ◽  
Author(s):  
Donald R. Dengel ◽  
Andrew P. Goldberg ◽  
Ronaldo S. Mayuga ◽  
Gretchen M. Kairis ◽  
Matthew R. Weir
Keyword(s):  
Insulin Resistance ◽  
Glomerular Filtration ◽  
Renal Injury ◽  
Filtration Fraction

scholarly journals Celastrol, an NF-κB Inhibitor, Improves Insulin Resistance and Attenuates Renal Injury in db/db Mice

PLoS ONE ◽  
2013 ◽  
Vol 8 (4) ◽  
pp. e62068 ◽  
Author(s):  
Jung Eun Kim ◽  
Mi Hwa Lee ◽  
Deok Hwa Nam ◽  
Hye Kyoung Song ◽  
Young Sun Kang ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Renal Injury

scholarly journals Chronic administration of furosemide augments renal weight and glomerular capillary pressure in normal rats

1998 ◽  
Vol 275 (2) ◽  
pp. F230-F234 ◽  
Author(s):  
Pascale H. Lane ◽  
Larry D. Tyler ◽  
Paul G. Schmitz
Keyword(s):  
Renal Injury ◽  
Wistar Rats ◽  
Chronic Administration ◽  
Relative Increase ◽  
Hydraulic Pressure ◽  
Ang Ii ◽  
Filtration Fraction ◽  
Renal Growth ◽  
Glomerular Capillary ◽  
Arteriolar Resistance

Angiotensin II (ANG II) is believed to promote progressive renal injury via augmented glomerular capillary hydraulic pressure (PGC). Acute volume reduction secondary to diuretic administration increases circulating ANG II and augments PGC, yet the hemodynamic effects of sustained diuretic administration are unknown. Therefore, glomerular micropuncture studies were performed in male Munich-Wistar rats after 6–8 wk of treatment with daily furosemide (F, 40 mg/day), furosemide plus the AT1 receptor antagonist, losartan (F + L, 5 mg/day), or no therapy (C, control). Renal weight was increased in F rats (1.23 ± 0.7 g) vs. C (1.00 ± 0.06 g) or F + L (0.97 ± 0.01 g). In addition, PGC was elevated in F animals (52.1 ± 1.5 mmHg) vs. C (43.7 ± 1.5) or F + L-treated rats (41.3 ± 1.7). F-treated rats were also characterized by a relative increase in efferent arteriolar resistance and filtration fraction. The latter was markedly attenuated in F + L-treated animals. Collectively, these findings are consistent with an ANG II-mediated alteration in intrarenal hemodynamics. In contrast to acute volume manipulations, however, chronic furosemide augmented renal growth, whereas losartan administration completely arrested this phenomenon. Further studies are warranted to determine whether the hemodynamic and growth adaptations elicited by chronic F administration induce or accelerate renal injury.

scholarly journals Matching Human Unilateral AKI, a Reverse Translational Approach to Investigate Kidney Recovery after Ischemia

2019 ◽  
Vol 30 (6) ◽  
pp. 990-1005 ◽  
Author(s):  
Danielle E. Soranno ◽  
Hyo-Wook Gil ◽  
Lara Kirkbride-Romeo ◽  
Christopher Altmann ◽  
John R. Montford ◽  
...  
Keyword(s):  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Renal Injury ◽  
Filtration Rate ◽  
Human Study ◽  
Renal Ischemia ◽  
Research Approach ◽  
Urine Biomarkers ◽  
Injured Kidney

BackgroundThe duration of renal ischemia that is associated with (or leads to) renal injury in patients is uncertain, and a reverse translational research approach has been proposed to improve animal models of AKI to facilitate clinical translatability. We developed a two murine models of unilateral renal ischemia to match a recently published human study that investigated renal injury after unilateral renal ischemia during partial nephrectomy.MethodsEight 10-week-old C57BL/6 male mice underwent left UiAKI or sham procedure, with or without intra-operative ice packs. Functional, histological, and biomarker outcomes were followed at 2, 6 and 24 hours, or 14 or 28 days later. The 14 and 28 day cohorts were duplicated such that contralateral nephrectomy could be performed 3 days prior to sacrifice with functional measurements obtained to isolate the glomerular filtration rate of the injured kidney.ResultsThe short-term outcomes correlated with the human study findings with urine and serum biomarkers of injury peaking around 24 hours and then normalizing, and reassuring immediate histological outcomes. Functional and histological outcomes at the later time-points (14 and 28 days) demonstrate an increase in fibrosis markers, and a reduction in glomerular filtration rate in the injured kidney, corresponding to the duration of ischemia, while serum and urine biomarkers remained reassuring.ConclusionsOur findings suggest that clinically available biomarkers of renal function are falsely reassuring against long-term injury following UiAKI, and that the duration of ischemia correlates with impaired function and increased fibrosis.

Insulin Resistance, Hyperinsulinemia, and Renal Injury: Mechanisms and Implications

2006 ◽  
Vol 26 (3) ◽  
pp. 232-244 ◽  
Author(s):  
Pantelis A. Sarafidis ◽  
Luis M. Ruilope
Keyword(s):  
Insulin Resistance ◽  
Renal Injury ◽  
Injury Mechanisms

The Prevalence of Renal Dysfunction in Young Adults with Sickle Cell Disease.

Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 3804-3804
Author(s):  
Raymond U. Osarogiagbon ◽  
Laura M. McHugh ◽  
Lori E. Kronish ◽  
Elisabeth A. Chismark
Keyword(s):  
Sickle Cell Disease ◽  
Renal Dysfunction ◽  
Glomerular Filtration ◽  
Sickle Cell ◽  
Renal Injury ◽  
Healthcare Providers ◽  
Early Death ◽  
Cell Disease ◽  
Early Screening ◽  
Stage Renal Disease

Abstract Sickle cell disease is typified by dramatic acute painful episodes, which consume the majority of patients’ and healthcare providers’ attention. However, the cumulative damage to vital organs that occurs in this disease is often the determinant of early death. The kidneys are a major target organ in sickle cell disease and renal failure is a highly morbid event. It is also strongly associated with early death. Glomerular hyperfiltration is often the earliest sign of renal injury. This is followed by return to apparently normal filtration rates, then successively lower rates, culminating in end-stage renal disease. Microalbuminuria follows hyperfiltration and progresses to frank proteinuria. We evaluated the prevalence of renal dysfunction in a cohort of patients with sickle cell disease managed at the University of Tennessee Cancer Institute’s adult sickle cell program. At entry into the program, patients underwent a routine battery of tests, including 24 hour urine collection for measurement of creatinine clearance and urine protein. Our findings are summarized in the table below. By the age of 25 years, almost 80% of patients with sickle cell disease showed significant abnormality of glomerular filtration and 40% had significant proteinuria. This worsens with age. By a median of 37 years, 2 in 3 patients have developed significant proteinuria and hypofiltration has become the predominant pattern of glomerular filtration abnormality. Since renal injury is reversible in the early stages, more emphasis needs to be placed on aggressive early screening, surveillance and intervention. Intervention at the stage of hyperfiltration and microalbuminuria is easier and much more likely to be successful. Patients and their healthcare providers need to be educated on the high prevalence of renal damage. Efforts at education, screening, surveillance and, where necessary, treatment should begin well before adolescence.

Insulin Resistance, Renal Injury, Renal 1-α Hydroxylase, and Bone Homeostasis in Aged Obese Rats

2008 ◽  
Vol 39 (4) ◽  
pp. 380-387 ◽  
Author(s):  
Huang Chang-Quan ◽  
Dong Bi-Rong ◽  
He Ping ◽  
Lu Zhen-Chan ◽  
Peng Xiao-Dong
Keyword(s):  
Insulin Resistance ◽  
Renal Injury ◽  
Bone Homeostasis ◽  
Obese Rats

scholarly journals Resistin, Glomerular Filtration Rate, and Insulin Resistance

Hypertension ◽  
2008 ◽  
Vol 51 (2) ◽  
Author(s):  
Yasuharu Tabara ◽  
Michiya Igase ◽  
Haruhiko Osawa ◽  
Hideichi Makino ◽  
Tetsuro Miki ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Filtration Rate
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