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Biomedical subjects

J Jirka

Publications and source records attributed to J Jirka.

At least 37 records · Page 2Linked to original sources
PubMed1990

[Change from treatment with cyclosporin A to conventional treatment in kidney transplantation].

Patients after a first transplantation of the kidney from a dead donor treated with cyclosporin A in combination with one, two or three drugs were switched to conventional treatment with azathioprine and prednisone. Fifty-two patients were switched to the new treatment 11-15 months after transplantation (group I), 9 patients after 6-10 months (groups II), 17 patients after 16-30 months (groups III). Group I was compared with 21 patients where no switched was made after 11-15 months (group IV). The authors did not reveal any change in the survival of grafts nor in the number of rejections during the three-month period following the switch. Survival of grafts in patients with rejection was after two years following the switch significantly lower than in patients without rejection, the loss of grafts, however, did not differ as compared with patients who suffered a rejection during a comparable period but were not switched to conventional therapy. The interval of the switch after transplantation did not influence the incidence of rejections. Rejections after the switch cannot be reliably foreseen from the level of cytotoxic anti-HLA antibodies or previous repections before the switch.

Azathioprine↗
PubMed1990

[Cyclosporin A in preventive therapy after kidney transplantation: a double combination versus a triple combination. I. Therapeutic effectiveness].

Two groups of patient after a first renal transplantation from a dead donor were treated by a double combination of cyclosporin A and prednisone (group A) and triple combination cyclosporin A and azathioprin and prednisone (group B). The groups were similar as regards effectiveness of treatment (evaluated with regard to the survival of recipients and grafts and the number of rejection episodes); they did not differ as to the losses of grafts for other than immunity reasons, which predominated in both groups over losses caused by rejection. Discontinuation of prednisone after four months in group A was complicated by rejection in 54%. Discontinuation of cyclosporin A after one year's treatment and a change to azothioprin and prednisone treatment was in both groups complicated by rejection in cca one fifth of the patients.

Adult↗
PubMed1990

[Cyclosporin A in preventive therapy after kidney transplantation: a double combination versus a triple combination. II. Adverse effects of cyclosporin A and therapeutic complications].

The incidence of irreversibly afunctional grafts, late functional development and period of the initial temporary lack of function did not differ in the two groups. The total number of nephrotoxic episodes was significantly (p less than 0.05) lower in the triple combination, chronic nephrotoxicity developed with equal frequency. Infectious complications were present in 54% of the patients in group A and in 60% in group B, viral complications in 15% patients in group A and in 16% in group B. Serious bacterial infections were the cause of death in one of three patients in group A and in five of six patients in group B.

Adult↗
PubMed1989

[Miliary tuberculosis after kidney transplantation].

The authors describe a case of tuberculosis after kidney transplantation. They discuss diagnostic and therapeutical problems arising from the specific course of this disease which appears in patients with chronic renal insufficiency treated with immunosuppressives after kidney transplantation.

Female↗
PubMed1989

[Tuberculosis after kidney transplantation].

The authors deal with the problem of tuberculosis in patients after transplantation of the kidney. They give an account of eight cases of the disease in 647 patients where during the last 22 years transplantations where performed in the Institute for Clinical and Experimental Medicine. The lungs were affected in six patients, incl. three with miliary dissemination affecting also other organs incl. the graft. In one instance the patient's own kidney was affected and once the talar joint. The authors emphasize this atypical course of the disease and the necessity to search for BK in patients where the febrile condition does not recede after corresponding antibiotic treatment. In case of early antituberculotic treatment the prognosis is on the whole favourable.

Adult↗
PubMed1986

[Rejection nephropathy before and after therapeutic administration of cyclosporin A].

During 1983 to 1986 41 patients were treated with Cyclosporin A (CyA) following kidney allotransplantation (TPL). 31 received the first (29 extra- and 2 intrafamilial) graft; in 10 there was second TPL, in 9 cases under high-risk conditions, where the first graft had been destroyed by (hyper)acute rejection or by rapidly progressive rejection with early vascular lesion. 21 needle biopsies and 5 excised grafts which had been collected 5 days to 18 months after TPL were examined by light microscopy and in addition 6 of the former also underwent electron and immunofluorescence microscopic study. The glomeruli showed discrete, inconstant segmental lesions but the ultrastructure also revealed severe general endothelial swelling. The tubular system had nonspecific degenerative changes of varying extent. In 11 patients focal cytoplasmic microvacuoles appeared in proximal tubular epithelia; there were also inconstant hyaline droplets, microcalcifications, and intratubular crystals. Electron microscopy revealed multiple round dense intramitochondrial inclusions in proximal tubules. The ultrastructure of the microvacuoles resembled that of "osmotic nephropathy". The rejection infiltrate and interstitial fibrosis of various degree did not essentially differ from those of conventionally treated grafts. In 7 patients cortical arterioles and small arteries exhibited a stenosing lesion (toxic?). In 3 cases metachromatic "mucoid" thickening of intima was prominent. Ultrastructure studies showed swollen endothelial cells with numerous globular dense bodies and a severe defect in the leiomyofibrils of muscle cells of the media. Hyperplasia of juxtaglomerular apparatus was apparent in 7 patients. Immunofluorescent microscopy of two biopsies from subsequently excised grafts visualized IgM, C3, and fibrinogen in small arteries and some glomerular capillary loops. Three early nephrectomies were caused by infarct-like necrosis. The discussion deals with differences between CyA- and conventionally treated grafts, diagnostic features, interpretation of findings, and measures following biopsy. In our patients with continual CyA-treatment no case of clinically and morphologically typical obliterative arterio-arteriolopathy (OA) and rapidly progressive irreversible rejection has as yet been noted.

Biopsy↗
PubMed1985

The effect of perioperative hydration in allogenic renal graft recipients.

The authors evaluated the effect of perioperative hydration by 20% human albumin, packed red blood cells (RBC) and saline in allogenic renal graft recipients. In the group of recipients selectively hydrated, the incidence of postoperative oligoanuria decreased from the initial 62 to 25.7% compared with 50% in the group of nonhydrated patients. However, in the former group graft ruptures occurred in 10% as against 1.6% only in the latter. Potential causal relation between the higher incidence of ruptures and perioperative hydration has not been demonstrated and will be subject to further study. With respect to the lower risk imposed on the patients with rupture than on those with postoperative oligoanuria (higher survival rate of grafts and lower mortality of patients) the authors recommend routine introduction of body fluid expansion during operation in allogenic renal graft recipients from cadaver donors.

Fluid Therapy↗
PubMed1985

Rejection nephropathy: course and prognosis.

A clinical-morphological study in 134 recipients of first renal allografts (15 related and 119 non-related) was performed with the aim to establish prognosis of different types of rejection nephropathy. Following order of prognosis (from the worst to the best) was found: necrotic lesion, early vascular lesion, late vascular lesion, late interstitial lesion. Several factors of importance were discussed.

Graft Rejection↗
PubMed1984

Ultrastructural immunohistochemistry of glomerulonephritis in needle biopsy.

In two patients with glomerulonephritis (GN) IgG and C 3 were visualized in ultrastructure by means of HRP-conjugated antisera. The first patient had an acute postinfectious extra-intracapillary GN lasting for about two months with granular fluorescence of anti-IgG, -C 3, and -C 1q. Electron microscopy revealed widespread endothelial defects, a well-pronounced polymorphonuclear stasis, and typical perimembranous "humps". These deposits reacted with HRP-anti-C 3 but the ultrastructural proof of IgG was negative. A weak and sporadic reaction of both these conjugates was seen in the swollen mesangial matrix while intraluminal plugs of coagulated plasma and extracapillary exudates yielded a dense coarse reaction product. In the second patient (allograft, three years after transplantation) the membranous and proliferative probably recurrent GN with nephrotic syndrome showed massive perimembranous deposits in the late involution stage. Granular fluorescence of the main Ig classes and of C 3 was sporadic or absent. In the ultrastructural immunoenzyme assay, too, the residues of deposits failed to react with HRP-anti-IgG or -C 3 and the mesangial matrix harboured only sporadic foci of faint positivity; however, dense product was again seen in capillary plasmatic "microthrombi". The discrepancy between immunofluorescence microscopy and immunoenzyme histochemistry, noted also by others in experimental glomerulopathies, may reflect the instability and dynamic properties of immune deposits with an early loss of antibody reactivity and a more protracted though not persistent local activation of complement. In light microscopy, fluorescent granules may correspond not only to the sites of immune deposition but also to accidental intracapillary plasma precipitates.

Adult↗