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R Kain

Publications and source records attributed to R Kain.

26 records · Page 2Linked to original sources
PubMed1994

Immunological risk factors are solely responsible for primary non-function of renal allografts.

Primary non-function (PNF) of renal allografts has been attributed to various risk factors, among them immunological ones, as well as unfavourable preservation conditions. To investigate the impact of these risk factory on the occurrence of PNF, 1335 consecutive kidney transplants performed at a single centre over a 10-year period were analysed. All patients received immunosuppression based on cyclosporine. As the method of analysis a conditional stepwise logistic regression model was chosen, comparing each graft suffering PNF with its partner kidney retrieved from the same donor. Thus, all donor-related variables could be omitted from the analysis, as they are the same in every pair of grafts. Risk factors analysed included panel-reactive antibodies, number of pretransplant transfusions, pregnancies, number of prior transplants, cold and second warm ischaemia time, mismatches on HLA loci A, B and DR and recipient age. The overall incidence of PNF was 87 grafts (6.5%). One patient suffered immediate rejection due to transplantation of an ABO incompatible graft. This case was excluded from further analysis. PNF occurred three times in recipients of living related grafts, twice in recipients of en-bloc grafts and four times in grafts, in which the paired kidney was either not transplanted or shipped outside the Eurotransplant region, so that no paired graft was available for matched case-control analysis. Of the remaining 77 pairs, twice both organs of one donor failed immediately. The remaining 73 complete pairs were analysed. Two of the investigated risk factors have independently a significant impact on the occurrence of PNF. Increasing the number of pretransplant transfusions raises the relative risk of graft failure up to six fold (P=0.02), while a history of prior transplants bears a relative risk of 0.21E05 (P=0.005). Ischaemia has no significant impact on the occurrence of PNF. Our data strongly suggest that immunological rather than donor risk factors are responsible for the non-function of kidney grafts.

ABO Blood-Group System↗
PubMed1993

Renal biopsy: in vitro and in vivo comparison of a new automatic biopsy device and conventional biopsy systems. Work in progress.

A nondisposable full-cut biopsy gun with a disposable needle (system 1, prototype of system 2) and a disposable gun-needle combination (system 2) were compared with conventional needles and Tru-Cut-type biopsy systems in renal parenchymal biopsy procedures. In cadaveric kidneys, more glomeruli were harvested with system 1 than with four other biopsy systems. In native kidneys, more glomeruli were harvested and core quality was better with system 2 than with a Tru-Cut-type biopsy gun.

Adult↗
PubMed1992

Polyetiology of renal allograft dysfunction. Does calculation of the resistive index still make sense?

In 101 consecutive patients with renal allograft dysfunction a correlation of Duplex Doppler sonography (DDS) with histopathologic reports of simultaneously performed biopsies was made. Renal vascular impedance was estimated by calculating the resistive index (RI). A total of 290 different specific histologic diagnoses (mean 2.1 +/- 0.84 diagnoses/biopsy) was noted. With increasing time interval to transplantation, single diagnoses as cause of allograft dysfunction decreased. DDS could not reliably differentiate, exclude, or grade any of the common causes of renal allograft dysfunction like vascular and/or cellular rejection, chronic rejection, acute tubular necrosis, cyclosporin nephrotoxicity, relapse of glomerulonephritis and infection. Follow-up studies after established histologic diagnosis in 19 patients with persisting allograft dysfunction demonstrated a lack of sensitivity of DDS to significant superimposed causes of transplant malfunction. We conclude that biopsy is still necessary to direct proper therapy of renal allograft dysfunction.

Adolescent↗
PubMed1991

Duplex Doppler sonography in renal parenchymal disease. Histopathologic correlation.

To evaluate the histopathologic changes influencing Doppler measurements of the resistive index (RI) in renal arteries in renal parenchymal diseases, 68 kidneys in 34 consecutive patients with various forms of renal parenchymal diseases were studied by duplex Doppler ultrasound (duplex US) immediately before percutaneous renal biopsy. The RI, renal length, and renal cortical echogenicity were correlated with the amount of glomerular, interstitial, and vascular changes graded on a scale from 0 to 100. The renal vascular resistance and therefore the RI are significantly correlated with the prevalence of arteriolosclerosis, glomerular sclerosis, arteriosclerosis, edema, and focal interstitial fibrosis. There was no significant difference of the RI in five groups of different renal parenchymal diseases. Of 34 patients, 24 presented with an RI less than 0.7, which was thought to be within the normal range so far. Additionally, the RI increases as the patient's age increases, due to higher incidence of arteriosclerosis. Of our patients, 44% presented with normal cortical echogenicity. Quantitative duplex US using the RI does not reliably distinguish different types of renal medical disorders.

Adult↗
PubMed1990

[Vascular kidney transplant rejection--is a duplex sonographic diagnosis possible?].

The diagnostic value of quantitative Duplex Doppler sonography (DS) in renal allograft evaluation is being viewed increasingly critically. We undertook a retrospective analysis of DS in 51 consecutive patients to assess the capability of DS in the diagnosis of vascular rejection. At the time of renal allograft biopsy, a mean resistive index (RI) was calculated from Doppler measurements within main, segmental, interlobar and arcuate arteries and correlated with histological diagnosis. Our results indicate a low specificity (36% for RI greater than 0.7), low sensitivity (35% for RI greater than 0.9) as well as a low positive predictive value (54% for RI greater than 0.7) for the diagnosis of vascular rejection. Therefore, elevation of the RI is an unspecific finding in different causes of allograft dysfunction. Thus, renal biopsy to establish specific histologic diagnosis of allograft dysfunction remains mandatory.

Adolescent↗
PubMed1989

Transcellular transport and membrane insertion of the C5b-9 membrane attack complex of complement by glomerular epithelial cells in experimental membranous nephropathy.

Deposition of the C5b-9 complex of C in glomeruli of rats with experimental membranous nephropathy (MN) is essential for the development of proteinuria. In this investigation C5b-9 was localized in the passive Heymann nephritis (PHN) by immunoelectron microscopy with a mAb specific for C5b-9(m) neoantigen. Its distribution was compared with that in another model of MN induced by successive injections of cationic human IgG and rabbit anti-human IgG into rats. In PHN C5b-9 was found: 1) in the immune deposits (ID), and on the cell membranes of foot processes close to the ID; 2) in clathrin-coated pits of the glomerular epithelial cells (GEC) close to the ID and in membrane vesicles in the cytoplasm, separated from sheep IgG and the gp330 Ag; 3) in high concentration in multivesicular bodies of GEC; and 4) in association with membrane vesicles in the urinary space which presumably are the exocytosed content of membrane vesicular bodies. By contrast, in the cationic IgG-MN model C5b-9 was found mostly in ID, but rarely within the GEC. By freeze-fracture electron microscopy we have further identified 200- to 250-A intramembrane particles in PHN in the cell membranes of the "soles" of the foot processes which resemble membrane inserted human C5b-9(m). Degradation products of C5b-9 were further detected by immunoblotting of a 100,000 x g pellet of PHN rat urine. These results indicate that, in PHN, C5b-9 is inserted into the cell membranes of GEC, and that it is selectively endocytosed and transported across GEC by a cellular mechanism which apparently protects the cell from accumulation of membrane-inserted C5b-9.

Animals↗