Literature DB >> 7919155

Method of renal mass reduction is a critical modulator of subsequent hypertension and glomerular injury.

K A Griffin1, M Picken, A K Bidani.   

Abstract

The hypertension, proteinuria, and glomerulosclerosis that develop in the remnant kidney model (uninephrectomy plus infarction of approximately 2/3 of the other kidney) have been generally considered to represent the adverse consequences of a severe reduction in nephron number. To differentiate the blood pressure (BP) responses to infarction from those of reduced renal mass per se, BP was continuously monitored radiotelemetrically in rats whose total renal mass was reduced by 2/3 (infarction) and by 5/6 (infarction or surgical excision of both poles) and in sham-operated controls. Hypertension only developed in the two infarcted groups. Overall averages of systolic BP monitored every 10 min over 6 wk were 144 +/- 8 and 156 +/- 5 mm Hg in the 2/3 and 5/6 infarction groups (N = 10 each), respectively, as compared with 120 +/- 2 mm Hg (N = 12) in the approximately 5/6 surgical excision group (P < 0.01) and 117 +/- 5 mm Hg (N = 8) in controls. Changes in kidney weights, glomerular volumes, RBF, GFR, and renal autoregulatory ability after renal mass reduction by the two methods were qualitatively similar in additional animals from each group monitored for 2, 4, or 6 wk without radiotelemetry. Significant proteinuria and glomerulosclerosis only developed in the two infarction (hypertensive) groups. At 6 wk, 18 +/- 4 and 19 +/- 3% of the glomeruli exhibited injury in the 2/3 (N = 22) and the 5/6 infarction groups (N = 21), respectively, in contrast to 3 +/- 1% glomerular injury in the 5/6 surgical excision group (N = 24) (P < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

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Year:  1994        PMID: 7919155     DOI: 10.1681/ASN.V4122023

Source DB:  PubMed          Journal:  J Am Soc Nephrol        ISSN: 1046-6673            Impact factor:   10.121


  58 in total

1.  Large BP-dependent and -independent differences in susceptibility to nephropathy after nitric oxide inhibition in Sprague-Dawley rats from two major suppliers.

Authors:  Karen Griffin; Aaron Polichnowski; Hector Licea-Vargas; Maria Picken; Jianrui Long; Geoffrey Williamson; Anil Bidani
Journal:  Am J Physiol Renal Physiol       Date:  2011-09-21

2.  Nebivolol does not protect against 5/6 ablation/infarction induced chronic kidney disease in rats - comparison with angiotensin II receptor blockade.

Authors:  Jennifer M Sasser; Natasha C Moningka; Tatsiana Tsarova; Chris Baylis
Journal:  Life Sci       Date:  2012-06-19       Impact factor: 5.037

3.  Uremic Toxic Blood-Brain Barrier Disruption Mediated by AhR Activation Leads to Cognitive Impairment during Experimental Renal Dysfunction.

Authors:  Mickaël Bobot; Laurent Thomas; Anaïs Moyon; Samantha Fernandez; Nathalie McKay; Laure Balasse; Philippe Garrigue; Pauline Brige; Sophie Chopinet; Stéphane Poitevin; Claire Cérini; Philippe Brunet; Françoise Dignat-George; Stéphane Burtey; Benjamin Guillet; Guillaume Hache
Journal:  J Am Soc Nephrol       Date:  2020-06-11       Impact factor: 10.121

4.  Tissue, urine and blood metabolite signatures of chronic kidney disease in the 5/6 nephrectomy rat model.

Authors:  Munsoor A Hanifa; Martin Skott; Raluca G Maltesen; Bodil S Rasmussen; Søren Nielsen; Jørgen Frøkiær; Troels Ring; Reinhard Wimmer
Journal:  Metabolomics       Date:  2019-08-17       Impact factor: 4.290

5.  Warfarin-related nephropathy modeled by nephron reduction and excessive anticoagulation.

Authors:  Kyle Ware; Polina Brodsky; Anjali A Satoskar; Tibor Nadasdy; Gyongyi Nadasdy; Haifeng Wu; Brad H Rovin; Udayan Bhatt; Jon Von Visger; Lee A Hebert; Sergey V Brodsky
Journal:  J Am Soc Nephrol       Date:  2011-09-01       Impact factor: 10.121

6.  Sympathetic nerves and the progression of chronic kidney disease during 5/6 nephrectomy: studies in sympathectomized rats.

Authors:  Robert A Augustyniak; Maria M Picken; David Leonard; Xin J Zhou; Weiguo Zhang; Ronald G Victor
Journal:  Clin Exp Pharmacol Physiol       Date:  2009-06-29       Impact factor: 2.557

Review 7.  Does significant renal ablation truly and invariably lead to hyperfiltration and progressive chronic kidney disease?

Authors:  Andrew Wang; Ramin Sam
Journal:  Clin Exp Nephrol       Date:  2016-10-13       Impact factor: 2.801

Review 8.  Failed Tubule Recovery, AKI-CKD Transition, and Kidney Disease Progression.

Authors:  Manjeri A Venkatachalam; Joel M Weinberg; Wilhelm Kriz; Anil K Bidani
Journal:  J Am Soc Nephrol       Date:  2015-03-25       Impact factor: 10.121

Review 9.  Potential risks of calcium channel blockers in chronic kidney disease.

Authors:  Karen A Griffin; Anil K Bidani
Journal:  Curr Cardiol Rep       Date:  2008-11       Impact factor: 2.931

10.  Inhibition of the soluble epoxide hydrolase promotes albuminuria in mice with progressive renal disease.

Authors:  Oliver Jung; Felix Jansen; Anja Mieth; Eduardo Barbosa-Sicard; Rainer U Pliquett; Andrea Babelova; Christophe Morisseau; Sung H Hwang; Cindy Tsai; Bruce D Hammock; Liliana Schaefer; Gerd Geisslinger; Kerstin Amann; Ralf P Brandes
Journal:  PLoS One       Date:  2010-08-04       Impact factor: 3.240

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