Resistance to remnant nephropathy in the Wistar-Furth rat

The Wistar-Furth rat, an inbred strain resistant to actions of mineralocorticoids, was used to study the concept that mineralocorticoids contribute to progressive renal injury. It was postulated that if chronic nephropathy depends on aldosterone and if Wistar-Furth rats are resistant to aldosterone,...

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Published in:	Journal of the American Society of Nephrology Vol. 10; no. 4; pp. 814 - 821
Main Authors:	FITZGIBBON, W. R, GREENE, E. L, GREWAL, J. S, HUTCHISON, F. N, SELF, S. E, LATTEN, S. Y, ULLIAN, M. E
Format:	Journal Article
Language:	English
Published:	Hagerstown, MD Lippincott Williams & Wilkins 01-04-1999
Subjects:	Albuminuria - urine Aldosterone - blood Analysis of Variance Animals Biological and medical sciences Blood Pressure Determination Disease Models, Animal Glomerulonephritis Kidney - pathology Kidney Function Tests Kidney Glomerulus - pathology Kidney Glomerulus - physiopathology Kidneys Male Medical sciences Nephrectomy Nephrology. Urinary tract diseases Nephropathies. Renovascular diseases. Renal failure Nephrotic Syndrome - pathology Nephrotic Syndrome - physiopathology Organ Size Rats Rats, Inbred WF Rats, Wistar Reference Values Statistics, Nonparametric Urinary system involvement in other diseases. Miscellaneous Kidney disease Animal model Urinary system disease Pathophysiology Rat Mineralocorticoid Treatment efficiency Rodentia Case control study Aldosterone Pathology Vertebrata Mammalia Nephropathy Nephrectomy Surgery Animal
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Summary:	The Wistar-Furth rat, an inbred strain resistant to actions of mineralocorticoids, was used to study the concept that mineralocorticoids contribute to progressive renal injury. It was postulated that if chronic nephropathy depends on aldosterone and if Wistar-Furth rats are resistant to aldosterone, remnant nephropathy would be attenuated in Wistar-Furth rats. Wistar-Furth rats and control Wistar rats were subjected to 5/6 nephrectomy or a sham procedure and then followed for 4 wk. Renal ablation resulted in hypertension at 4 wk in both strains (164+/-5 [Wistar-Furth] versus 184+/-7 [Wistar] mm Hg mean arterial pressure), with sham animals remaining normotensive (134+/-6 mm Hg). Renal damage in response to 5/6 nephrectomy was greatly decreased in Wistar-Furth rats compared with Wistar rats. Albuminuria was markedly less in Wistar-Furth rats (12.7+/-4.2 [Wistar-Furth] versus 97.4+/-22.6 [Wistar] mg/d per 100 g body wt, P<0.01). Glomerular damage, consisting of mesangial proliferation, mesangial lysis, and segmental necrosis, was observed in 42% of glomeruli from Wistar rats but in 0% of glomeruli from Wistar-Furth rats (P<0.01). To address the possibility that higher BP in partially nephrectomized Wistar rats mediated the greater renal damage, the study was repeated, with Wistar rats (not Wistar-Furth rats) being treated with a hydralazine-reserpine-hydrochlorothiazide regimen. Although this antihypertensive regimen equalized BP (conscious systolic) (144+/-8 mm Hg [Wistar] versus 157+/-7 mm Hg [Wistar-Furth] at 4 wk), albuminuria remained more than 10-fold greater in Wistar rats. In summary, renal damage upon 5/6 nephrectomy was markedly reduced in Wistar-Furth rats, a finding not attributable to reduced systemic BP. Since Wistar-Furth rats have been shown previously to be resistant to the actions of mineralocorticoids, the data from the present study support the hypothesis that aldosterone mediates, at least in part, the renal injury attendant to renal mass reduction.
Bibliography:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23
ISSN:	1046-6673 1533-3450
DOI:	10.1681/ASN.V104814