Experimental chronic renal failure in the rat by electrocoagulation of the renal cortex

In this paper we describe an experimental model designed for studies of continuous ambulatory peritoneal dialysis (CAPD) in uremic rabbits. We preferred the study of uremic animals because it is not known whether peritoneal membrane differs between normal and uremic animals. Animals made uremic after bilateral nephrectomy could not survive on dialysis. Instead, partial nephrectomy of one kidney and partial (5/6) destruction of the cortex of the remaining kidney by electrocauterization provided a simple and reproducible model. CAPD resulted in adequate control of uremia but the animals showed significant decreases in total plasma proteins and weight. This model is suitable for studies of the metabolic complications of CAPD.

Section: Discussionmentioning

confidence: 99%

Experimental Model for Studies of Continuous Peritoneal’ Dialysis in Uremic Rabbits

Gotloib

Crassweller

Rodella

et al. 1982

“…The various methods for induction of experimental chronic renal failure can be divided into the following groups: (1) the parenteral use of substances which pro duce extensive renal damage, these include nephrotoxins [1] and immune reactive agents [2], (2) interruption of blood supply to a major part of renal parenchyma [3,4]: (3) unilateral destruction of most of the renal cortex by electrocoagulation combined with contralateral ne phrectomy [5]; (4) unilateral papillectomy with contra lateral nephrectomy [6], and (5) unilateral subtotal ne phrectomy with contralateral nephrectomy [7][8][9].…”

Section: Discussionmentioning

confidence: 99%

Induction of Chronic Renal Failure in the Mouse: A New Model

Gabizon¹,

Goren²,

Shaked³

et al. 1985

An animal model with experimental uremia is an important research tool for the study of the sequence of pathophysiological events taking place in the uremic syndrome. An appreciable number of animal models and methods for the induction of chronic uremia have been published. It is surprising that no such method has been reported in the mouse, which is an important laboratory animal. A new method for the induction of chronic uremia in the mouse is described. It consists of unilateral destruction of most of the renal cortex by burns combined with contralateral nephrectomy. This method can be carried out in one or two stages. Follow-up of the experimental animals reveals that significant uremia developed within 4 weeks and remained constant for the rest of the study period, i.e. 10 weeks.

“…Uremic rats were prepared by cortical electrocoagulation of one kidney followed 7 days later by contralateral nephrectomy [12]. The experimental period was of 5 weeks after the day of nephrec tomy, which was considered as day 0.…”

Section: Experimental Designmentioning

confidence: 99%

Chronic Triiodothyronine Supplementation Does Not Improve the Lipoprotein Disorders of Mildly Uremic Rats

Lacour

Roullet²,

Ricordel

et al. 1987

The present study was performed to appreciate the potential role that thyroid deficiency could play in the energy homeostasis and lipid metabolism of experimental chronic renal failure. For this purpose, 12 uremic rats that were supplemented with T₃ (0.4 μg/100 g body weight/day) during 5 weeks by means of osmotically driven minipumps were compared to 12 unsupplemented uremic rats and 12 control rats. The chronic supplementation of uremic rats with T₃ induced no significant change in body weight gain or in the serum concentration of insulin, glucose, glycerol, nonesterified fatty acids, total triglycerides (TG), total cholesterol, and total choline phospholipids. Similarly, the metabolism of TG-rich lipoproteins was not affected by the supplementation with T₃ in these uremic rats as appreciated by TG production or TG degradation (adipose tissue lipoprotein lipase activity). T₃ administration induced a significant decrease in serum β-hydroxybutyrate concentration and an increase in serum lactate concentration. Furthermore, heparin-releasable hepatic TG lipase activity as expressed per total liver mass was decreased in uremic rats treated with T₃. The latter changes were observed in the absence of modifications of serum glucose or TG concentration. We conclude from these observations that rats with a moderate degree of chronic uremia do not seem to have a cellular thyroid deficiency sufficient to disturb their energy or lipid metabolism.