Biomedical subjects

G Tavanlis

Publications and source records attributed to G Tavanlis.

4 recordsLinked to original sources

PubMed1988

Papillary necrosis in experimental renal transplantation in the rat.

Renal papillary necrosis is a frequent complication of unsuccessful renal transplantation in rats, occurring in both isografts and allografts. Papillary necrosis does not occur alone, but only and inevitably in association with severe cortical damage. The pattern of the lesion is different from other forms of papillary necrosis in that the least severe lesions occur in the outer medulla and the more severe lesions involve both medulla and papilla. The incidence of papillary necrosis is increased in isografts, but not in allografts, by longer preservation times. It is suggested that the principal underlying cause may be damage to medullary capillaries, occurring either during preservation or as a consequence of rejection and leading to medullary ischemia.

Animals↗

PubMed1987

Glomerular epithelial cell lesions in rat renal isografts.

Visceral glomerular epithelial cell lesions--microvillus formation, loss of foot processes, osmiophilic inclusion droplets, balloon-like malformation of cell processes, degeneration, necrosis, and loss of cell processes from capillary basement membranes--are found in rat renal isografts 1 mth after transplantation. The lesions, which are most readily recognized in perfusion-fixed material, are essentially focal, affecting neither all glomeruli, nor all cells in any glomerulus, bear no relation to the degree of interstitial nephritis in the graft, and are associated with albuminuria and with focal capillary sclerosis in some glomeruli. They are not restricted to renal isografts but are found in aging rats, in different experimental models of glomerular disease and in clinical glomerular disorders, again in association with proteinuria and glomerulosclerosis. It is therefore proposed that glomerular epithelial cell damage increases capillary permeability and impairs maintenance of the integrity of the capillary wall, leading to proteinuria and focal glomerulosclerosis.

Animals↗

PubMed1986

Cyclosporine and the ischemic rat kidney.

The effects of cyclosporine (CsA) on renal function and morphology have been studied in the rat after unilateral nephrectomy and warm renal ischemia. There is evidence of an enhanced CsA nephrotoxic effect after unilateral nephrectomy alone and of an additive or synergistic effect of CsA and renal ischemia upon renal function and morphology. These enhanced effects are most evident after longer periods of ischemia (60 min) and with higher doses of CsA (25 mg/kg/day). The findings may be relevant to clinical practice and suggest that the nephrotoxic effects of CsA upon the donor kidney may be greatest when there is coincident renal damage from other causes.

Animals↗

PubMed1986

Glomerular damage after kidney preservation.

Severe proteinuria occurs during isolated organ perfusion of kidneys removed from SD and DA rats and subjected to 24-hr cold preservation. In both strains increased glomerular permeability was associated with changes in glomerular visceral epithelial cells, particularly cytoplasmic edema and detachment of cells from capillary basement membranes. Foot processes were intact and staining for sialoglycoprotein was retained. The changes were compatible with survival of the isograft kidney after transplantation, but moderate proteinuria was found in some rats after one month. Protein loss in the urine during isolated organ perfusion is very much less in kidneys subjected to 4-hr cold preservation, and the glomerular epithelial cells are normal or show only minimal cytoplasmic edema on electron microscopy. The experiment shows that significant damage to glomeruli may occur during preservation prior to transplantation, and the model itself can be usefully exploited to determine the relation between increased glomerular permeability to albumin and the associated changes in the glomerular capillary wall.

Animals↗