The renin-angiotensin system in cats with chronic renal failure

• Published in: Journal of comparative pathology Vol. 115; no. 3; pp. 239 - 252
• Main Authors: TAUGNER, F, BAATZ, G, NOBILING, R
• Format: Journal Article
• Language: English
• Published: London Elsevier 01.10.1996
• Subjects: Animals; Biological and medical sciences; Cat Diseases - physiopathology; Cats; Female; Immunohistochemistry; Juxtaglomerular Apparatus - chemistry; Juxtaglomerular Apparatus - cytology; Juxtaglomerular Apparatus - physiopathology; Kidney - chemistry; Kidney - cytology; Kidney - physiopathology; Kidney Failure, Chronic - physiopathology; Kidney Failure, Chronic - veterinary; Kidneys; Male; Medical sciences; Microscopy, Electron; Nephrology. Urinary tract diseases; Renin - analysis; Renin-Angiotensin System - physiology; Urinary system involvement in other diseases. Miscellaneous; Fissipedia; Carnivora; Urinary system disease; Pathophysiology; Renal disease; Kidney; Vertebrata; Chronic; Renin angiotensin system; Mammalia; Histopathology; Urinary system; Animal; Cat; Renal failure; Juxtaglomerular apparatus
• ISSN: 0021-9975; 1532-3129
• DOI: 10.1016/S0021-9975(96)80082-X

The kidneys of eight male and two female cats with subacute (clinical illness 1-3 months) to chronic (clinical illness > 3 months) renal failure were examined histopathologically, electron microscopically and immunohistochemically. Semiquantitative morphometric data, obtained by measurement of the reninpositive portion of the afferent arteriole (RPP) and evaluation of the juxtaglomerular index (JGI), were compared with data from three healthy control cats. On the basis of the morphometric data, the animals with renal failure could be classified in three groups showing either a stimulated (group A), an unaltered (group B) or an inhibited (group C) renin-angiotensin system. In the three group A cats the JGI and RPP were increased (45.5 +/- 3.5%; 130 microns); in the four group B cats these values were comparable with those of the controls; in the three group C animals the JGI was decreased but the RPP was unaltered (11.7% +/- 3.2%; 56 microns). The increase in kidney renin in animals affected by chronic renal failure (CRF) may have been due to a volume depletion. Prolonged CRF seemed to result in increasing hypertrophy of renal blood vessels, leading to renal hypoxia and increasing preglomerular resistance. Reduced kidney renin status may have been caused by inhibition of renin synthesis in prolonged CRF as a result of renal ischaemia.