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      A forgotten method to induce experimental chronic renal failure in the rat by ligation of the renal parenchyma.

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          Abstract

          Animal models of chronic renal failure have been widely used in the experimental nephrology laboratories. The most common technique used is the 5/6 reduction of renal mass, either by surgical resection or by infarction.

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          Evaluation of two protocols of uremic rat model: partial nephrectomy and infarction.

          Zun Chang Liu, Kai Chow, Thomas Chang (2003)
          Animal models of chronic renal failure have been mostly achieved by partial ablation of renal parenchyma, the two most common techniques employed being surgical resection or infarction. Evaluation of the uremic model using these two techniques was carried out in Wistar rats. Two weeks after operative procedure, measured serum urea levels in the resection and infarction models were 59.1 and 64.3 mg/dL (normal range 15.6-24.4 mg/dL) respectively. However, the standard deviation in the former was significantly lower, 6.3 vs. 97.1 mg/dL from infarction model, p = 0.007. A consistent degree of glomerular filtration rate reduction was obtained in the resection model, resulting in 20-30% of normal creatinine clearance. This compared favorably with the creatinine clearance range (0.3-74% of normal) from the infarction model, in which two animals died of uremia and seven had higher than 50% of normal creatinine clearance. It is reasonable to attribute reproducibility and homogeneity demonstrated in the resection model to (i) more precise control of renal ablation extent with surgical techniques and (ii) less interplay of confounding injury mechanism to remnant kidney. These data support superiority of the resection model as an experimental tool for pathophysiological and/or interventional investigations of chronic renal failure.
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            A new method of inducing experimental chronic renal failure by cryosurgery.

            Kazuo Kumano, Kyuya Kogure, Toshio Tanaka … (1986)
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              Pathogenesis of the glomerulopathy associated with renal infarction in rats.

              Mabel Purkerson, Phillip E. Hoffsten, Saulo Klahr (1976)
              The present studies were designed to characterize the extent and pathogenesis of the glomerular lesions which occur in the viable portion of the kidney following partial renal infarction in rats. Control rats with two normal kidneys had a mean blood pressure of 112 mm Hg, minimal proteinuria and no glomerular pathology on light (LM), electron (EM) or immunofluorescence microscopy (IFM). Rats with two-thirds infarction of one kidney (stage II) became hypertensive, although less than 4% of the glomeruli from either kidney were abnormal. Rats with two-thirds infarction of one kidney and contralateral nephrectomy (stage III) developed proteinuria and hypertension whether fed a normal, low or high Na+ diet. By light microscopy 37% of glomeruli were abnormal 28 days after partial infarction and contralateral nephrectomy and thereafter the percent of abnormal glomeruli increased. Detectable amounts of immunoglobulin and complement (C3) were present in kidneys of stage II or III rats but were always accompanied by more extensive albumin and fibrin deposits. Basement membrane deposits characteristic of immune complexes were not seen on EM. Administration of antihypertensive medication to stage III rats significantly lowered blood pressure and reduced the number of abnormal glomeruli on LM; however, IFM abnormalities remained prominent. Platelet thrombi seen by EM and abundant glomerular fibrin deposits seen on IFM suggested that coagulation mechanisms may be prominent in the pathogenesis of the renal lesion. Heparin-treated stage III rats had significantly lower blood urea nitrogen concentrations, blood pressures and proportion of abnormal glomeruli although glomerular deposition of serum proteins was still present on IFM. These observations suggest that this glomerulopathy is initiated by an unknown agent(s) which increased capillary permeability. This lesion progresses via thrombotic mechanisms which are prevented by heparin administration.
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                Author and article information

                Journal
                Journal ID (iso-abbrev): Nephron Exp. Nephrol.
                Title: Nephron. Experimental nephrology
                Publisher: S. Karger AG
                ISSN (Electronic): 1660-2129
                ISSN (Print): 1660-2129
                Publication date (Electronic): 2006
                Volume: 103
                Issue: 3
                Affiliations
                [1 ] Surgery Deparment, Hospital Universitario Arnau de Vilanova, Laboratorio de Investigación UDL-HUAV, Lleida, Spain.
                Article
                Publisher Item ID: 92198
                DOI: 10.1159/000092198
                PubMed ID: 16554663
                SO-VID: 7f8ab86c-169a-45be-b0c4-e353d34dc17c
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