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

105: Renal Injury Mechanisms in Motor Vehicle Collisions: Analysis of the Crash Injury Research and Engineering Network (CIREN) Dataset

2007 ◽  
Vol 177 (4S) ◽  
pp. 37-37
Author(s):  
James K. Kuan ◽  
Robert Kaufman ◽  
Jonathan L. Wright ◽  
Charles Mock ◽  
Avery B. Nathens ◽  
...  
Keyword(s):  
Renal Injury ◽  
Motor Vehicle ◽  
Motor Vehicle Collisions ◽  
Vehicle Collisions ◽  
Injury Mechanisms ◽  
Injury Research

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

Effects of losartan, in monotherapy or in association with hydrochlorothiazide, in chronic nephropathy resulting from losartan treatment during lactation

2011 ◽  
Vol 301 (3) ◽  
pp. F580-F587 ◽  
Author(s):  
C. Fanelli ◽  
B. H. V. Fernandes ◽  
F. G. Machado ◽  
C. Okabe ◽  
D. M. A. C. Malheiros ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Renal Injury ◽  
Structural Parameters ◽  
Angiotensin Ii Receptor Blocker ◽  
Angiotensin Ii Receptor ◽  
Injury Mechanisms ◽  
Severe Chronic Kidney Disease ◽  
Insight Into ◽  
Remnant Kidney ◽  
Losartan Treatment

We recently standardized a model (LLact) of severe chronic kidney disease based on impaired nephrogenesis by suppression of angiotensin II activity during lactation (Machado FG, Poppi EP, Fanelli C, Malheiros DM, Zatz R, Fujihara CK. Am J Physiol Renal Physiol 294: F1345–F1353, 2008). In this new study of the LLact model, we sought to gain further insight into renal injury mechanisms associated with this model and to verify whether the renoprotection obtained with the association of the angiotensin II receptor blocker losartan (L) and hydrochlorothiazide (H), which arrested renal injury in the remnant kidney model, would provide similar renoprotection. Twenty Munich-Wistar dams, each nursing six pups, were divided into control, untreated, and LLact groups, given losartan (L; 250 mg·kg−1·day−1) until weaning. The male LLact offspring remained untreated until 7 mo of age, when renal functional and structural parameters were studied in 17 of them, used as pretreatment control (LLactPre), and followed no further. The remaining rats were then divided among groups LLact+V, untreated; LLact+L, given L (50 mg·kg−1·day−1) now as a therapy; LLact+H, given H (6 mg·kg−1·day−1); and LLact+LH, given L and H. All parameters were reassessed 3 mo later in these groups and in age-matched controls. At this time, LLact rats exhibited hypertension, severe albuminuria, glomerular damage, marked interstitial expansion/inflammation, enhanced cell proliferation, myofibroblast infiltration, and creatinine retention. L monotherapy normalized albuminuria and prevented hypertension and the progression of renal injury, inflammation, and myofibroblast infiltration. In contrast to the remnant model, the LH combination promoted only slight additional renoprotection, perhaps because of a limited tendency to retain sodium in LLact rats.

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

Complement-mediated renal injury: Mechanisms and role of membrane regulators of complement

1998 ◽  
Vol 2 (4) ◽  
pp. 276-281 ◽  
Author(s):  
Seiichi Matsuo ◽  
Yoshiki Morita ◽  
Masashi Mizuno ◽  
Kazuhiro Nishikawa ◽  
Yukio Yuzawa
Keyword(s):  
Renal Injury ◽  
Injury Mechanisms

scholarly journals NOD2 promotes renal injury by exacerbating inflammation and podocyte insulin resistance in diabetic nephropathy

2013 ◽  
Vol 84 (2) ◽  
pp. 265-276 ◽  
Author(s):  
Pengchao Du ◽  
Baoxia Fan ◽  
Huirong Han ◽  
Junhui Zhen ◽  
Jin Shang ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Diabetic Nephropathy ◽  
Renal Injury

Renal Injury, Abnormal Vitamin D Metabolism and Bone Homeostasis in Aged Rats With Insulin Resistance or Type 2 Diabetes Mellitus

2008 ◽  
Vol 56 (6) ◽  
pp. 872-877
Author(s):  
Huang Chang-Quan ◽  
Dong Bi-Rong ◽  
Xiao Qian ◽  
He Ping ◽  
Ding Qun-Fang ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Insulin Resistance ◽  
Vitamin D ◽  
Renal Injury ◽  
Urinary Albumin ◽  
Bone Homeostasis ◽  
Aged Rats ◽  
Vitamin D Metabolism ◽  
Hydroxyvitamin D

ObjectiveThe study aimed to explore the relationship among renal injury, abnormal vitamin D metabolism, and bone homeostasis in insulin resistance (IR) or type 2 diabetes mellitus (T2DM).Design and MethodsThe animal models of IR, T2DM, and T2DM treated with 1-alpha hydroxyvitamin D (1-α(OH)D) were established on 18-month-old male Wistar rats. Glucose infusion rates (GIR) and levels of urinary albumin (UA), serum 25-hydroxyvitamin D (25-(OH)D), serum 1,25-dihydroxyvitamin D (1,25-(OH)2D), and bone mineral density (BMD) in lumbar vertebrae and femoral bone were measured.ResultsUrinary albumin level in the rats with T2DM significantly increased, and there existed a significant and negative correlation between GIR and UA level in the rats with T2DM or IR. The levels of serum 25-(OH)D in all models were similar. The levels of serum 1,25-(OH)2D and BMD in the rats with IR were significantly higher than those in the rats with T2DM and were lower than those in normal control rats. In the aged rats with T2DM, administration of 1-α(OH)D had no effect on serum 25-(OH)D level although significantly increased the levels of serum 1,25-(OH)2D and BMD. There existed a negative correlation between the levels of serum 1,25-(OH)2D and UA in the rats with T2DM or IR.ConclusionsIn IR or T2DM, abnormal vitamin D metabolism is characterized by 1,25-(OH)2D deficiency and is related to renal injury, and there also existed bone loss. In T2DM, both 1,25-(OH)2D deficiency and bone loss can be reversed by 1-α(OH)D.

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