Search PubMed⌕ Search

Biomedical subjects

G Thiel

Publications and source records attributed to G Thiel.

At least 199 records · Page 11Linked to original sources
PubMed1988

Risk factors for the development of chronic cyclosporine-nephrotoxicity.

Ninety CSA-treated kidney transplants recipients entered the study. The patients were allocated to three groups based on serum creatinine at 12 months and kidney biopsy findings: control group (serum creatinine less than 177 mumol/l), rejection group (verified by biopsy, serum creatinine greater than 177 mumol/l), nephrotoxicity group (verified by biopsy, serum creatinine greater than 177 mumol/l). Thirty variables were systematically evaluated. The following parameters had a predictive value for the development of chronic CSA-nephrotoxicity: number of CSA-induced episodes of acute deterioration of renal function, CSA trough level (day 0-30, day 31-90), number of unexplained episodes of acute deterioration of renal function, number of nephrotoxic drugs, number of rejection treatments, number of rejection episodes and primary poor renal function. The results indicate that all factors leading to acute renal failure, favor the development of CSA-nephrotoxicity.

Acute Kidney Injury↗
PubMed1987

Factor XII, plasma prekallikrein, alpha 2-macroglobulin and C1-inhibitor levels in renal allograft recipients during immunosuppression with cyclosporin A--sequential measurements over four months in 17 patients.

Factor XII clotting activity (F XII), plasma prekallikrein amidolytic activity (PK), alpha 2-Macroglobulin (alpha 2-M) and C1-Inhibitor (C1-Inh) antigens have been measured in 17 patients immediately before and sequentially for up to four months after kidney transplantation. Before transplantation mean F XII and PK levels were normal (99 +/- 27% and 102 +/- 21%, respectively, mean +/- S.D.) and alpha 2-M and C1-Inh levels were slightly elevated (115 +/- 55% and 129 +/- 32%, respectively, mean +/- S.D.). In the first two weeks after transplantation a significant decrease of F XII to 65 +/- 27%, of PK to 67 +/- 20% and of alpha 2-M to 88 +/- 42%, and a rise of C1-Inh to 201 +/- 44% (mean +/- S.D.) were observed (2 p less than 0.005). F XII levels four month after operation remained significantly (2 p less than 0.05) lower than preoperatively. PK and alpha 2-M values, however, were significantly higher (2 p less than 0.05) at four months as compared to the pretransplant period. Mean F XII levels in the 17 patients at various time points after transplantation correlated positively with PK, alpha 2-M and serum albumin and negatively with CyA level and dose and serum bilirubin. PK and alpha 2-M correlated positively with each other and albumin and negatively with creatinine, bilirubin and CyA (2 p less than 0.01). Whether CyA has a direct influence on production or consumption of F XII, PK, alpha 2-M and C1-Inh, or whether the changes merely reflect altered protein metabolism awaits further study.

Adult↗
PubMed1987

Cyclosporin A and osteonecrosis of the femoral head.

A vascular osteonecrosis has occurred in 5 to 40 per cent of patients who have undergone transplantation of a kidney and generally has been considered to be a complication of the use of corticosteroids. Currently cyclosporin A is in general use for its immunosuppressive property, so that a lower dose of corticosteroids is needed. We analyzed the cases of a series of our patients who underwent transplantation of a kidney in order to find out if our present regimen, using cyclosporin A, influenced the prevalence of osteonecrosis of the femoral head. Of a total of 270 patients, osteonecrosis of the femoral head developed in fifteen of 174 who received conventional immunosuppressive therapy and in only one of ninety-six who received cyclosporin A (p less than 0.05). During the first two months after transplantation, the mean dose of prednisone was approximately 2.5 milligrams per kilogram of body weight per day in the group that received conventional immunosuppressive therapy and approximately 1.1 milligrams per kilogram of body weight per day in the group that received cyclosporin A (p less than 0.001). We concluded that the pathogenesis of the osteonecrosis in patients who underwent transplantation of a kidney was probably related to the higher doses of corticosteroids that were administered.

Azathioprine↗
PubMed1986

[Cyclosporin A and hyperlipidemia after kidney transplantation. Prospective study].

Hyperlipidemia is common after renal transplantation and has been attributed, at least in part, to corticosteroid therapy. We therefore studied serum lipids in a group of nondiabetic transplant recipients on conventional immunosuppression with azathioprin and prednisone (Aza/P), in comparison with a transplanted group on cyclosporin A monotherapy (CyA) without steroids. Frequency and degree of hyperlipidemia in the two groups showed no significant difference. Atherogenic hypercholesteremia was found as frequently in patients on CyA as in those on Aza/P. Possible factors preventing normalization are discussed.

Adult↗
PubMed1986

[Glomerular erythrocytes in urine. Identification and significance].

The glomerular origin of microhematuria can often be identified by typical changes in erythrocyte morphology when the urinary sediment is examined with a phase contrast microscope. The so-called "glomerular erythrocytes" appear in uneven annular shape (ring forms) or as fragmented, crushed and ruptured cells (destroyed forms). Non-glomerular erythrocytes originating from the urinary tract have different morphological characteristics. The occurrence of only a few glomerular erythrocytes (0-2 per high power field) is a normal finding. The morphological characteristics of the erythrocytes should be analyzed as the first step in the work up of microhematuria. In the case of clearcut glomerular microhematuria, unnecessary urological or radiographical investigation can thus be avoided.

Erythrocytes↗
PubMed1986

Cotton-wool exudates not observed in recipients of renal transplants treated with cyclosporine.

Retinal cotton-wool patches, not previously observed in bone marrow recipients, have been reported in three patients who received Sandimmun (cyclosporine) as prophylaxis for graft-versus-host-disease after bone marrow transplantation. These patients all had acute lymphoblastic leukemia and had received, in addition to the standard conditioning regimen, central nervous system irradiation before transplantation. We were thus prompted to examine 55 renal transplant recipients (15 of them prospectively) who were receiving cyclosporine for evidence of similar fundal changes. No cotton-wool patches were found in any of the renal transplant recipients.

Adolescent↗
PubMed1986

Value of urinary sediment in the diagnosis of interstitial rejection in renal transplants.

The occurrence of lymphocyturia, or a sharp increase in preexisting lymphocyturia, has been found to correlate with immunological rejection. In most studies time-consuming staining techniques or counting chambers have been used. A new staining technique, with prestained slides, is investigated as a predictor of cellular rejection and to distinguish between cellular rejection and cyclosporine (CsA) toxicity, or other causes of renal function impairment. In 18 consecutive renal transplant recipients, treated with CsA, urinary sediments were analyzed almost daily for two months, and prediction of cellular rejection was related to renal biopsies and retrospective clinical evaluation. In addition 24 transplant biopsies were compared with urinary sediment prediction; in both parts of the study a lymphocyturia of more than 20% and polymorphs less than 55% (of 100 nucleated cells, excluding squamous epithelial cells) were considered to suggest interstitial rejection. Episodes of lymphocyturia (greater than 20%), with simultaneous increase of the number of epithelial cells, resulting in a relative decrease of polymorphs (less than 55%), were found 10 times. Of these, 9 corresponded well with biopsy or clinical evaluation and 1 was false-positive. Correlating urinary sediment analysis with biopsy histology (n = 24), 19 were accurate, 3 equivocal, and 2 false; this corresponds to a sensitivity of 77% and a specificity of 91%. In conclusion, the analysis of urinary sediments with prestained slides is a quick and simple method to diagnose cellular rejection and to distinguish it from toxic of ischemic renal damage. Results are comparable to those of the fine-needle aspiration technique without invasive insult to the patient.

Adult↗
PubMed1986

Mannitol potentiates cyclosporine nephrotoxicity.

A possible drug interaction between cyclosporine (CyA) and mannitol was tested for in female Wistar rats infused continuously with CyA 10 mg (40-50 mg/kg BW) in 24 ml mannitol 20% daily for 3 to 4 days (group CIM). For comparison, two other groups of rats were infused either with the same amount of CyA in 24 ml NaCl 0.9% (group CINa) or with the same amount of mannitol without CyA (group M). No animal of groups CINa or M, but 6 out of 10 group CIM rats developed severe oligo-anuric acute renal failure (ARF). Histologically massive vacuolisation of proximal tubular epithelia was found in the kidneys of CIM rats with ARF, while CIM rats without ARF showed minor to moderate degrees of vacuolisation. No vacuolisation was seen in groups CINa and M. Moderate amounts of tubular inclusion bodies and microcalcifications were detected in the kidneys of CIM rats without ARF and in those of CINa rats. To elucidate the mechanism of ARF, renal blood flow, creatinine clearance and proximal tubular pressures were measured in the kidneys of another series of CIM rats infused for 48-96 hours with CyA and mannitol. Renal blood flow and proximal tubular pressures in the kidneys of animals that had not or not yet developed ARF did not differ from those in rats infused with mannitol alone despite histological alterations with minor to moderate degrees of vacuolisation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Cyclosporine A nephrotoxicity in Goldblatt renovascular hypertension in rats.

Experiments were conducted on a renovascular model of hypertension to investigate the effect of high blood pressure and CyA nephrotoxicity combined on arteriolar and tubular morphology and renal function. A two kidney, one clip model of Goldblatt hypertension was selected in which were given 20 or 40 mg/kg/d CyA by gastric gavage for 3-4 weeks while receiving isotonic saline as drinking fluid. CyA was found to suppress feeding and drinking and, as a result, lead to volume depletion and weight loss, with a corresponding lowering of blood pressure and renal function and an increase in plasma renin. When CyA and control animals were pair-fed these effects disappeared, except for a modest depression of renal function, unaccompanied by a reduction in urinary concentrating power. Histological damage to the tubules was equally prevalent in both kidneys despite different levels of renal perfusion, suggesting that plasma concentration, rather than toxin delivery, determines tubular damage. The occurrence of arteriolopathy and glomerulosclerosis was infrequent, and if present, it was only found in the unclipped kidney and was not potentiated by CyA. Glomerular prostaglandin synthesis after substrate incubation was suppressed by CyA to an equal extent in both kidneys, clipped and unclipped.

Animals↗
PubMed1986

Effect of cyclosporine in rats with reduced renal mass.

The longterm effect of cyclosporine (CyA) on chronic renal failure was studied in female Wistar rats subjected to 4/5 to 5/6 nephrectomy by partial infarction of the left kidney followed by contralateral nephrectomy. CyA was added to a standard rat diet containing 25% protein. Each rat received 14 g of food daily containing 0 (control), 1.2 (group A), 2.4 (group B), or 4.8 (group C) mg CyA. The number of rats that did not survive the whole experimental period of 20 weeks on the CyA containing diets was similar to the control. In the surviving rats no difference between groups could be detected regarding body weight, serum creatinine and creatinine clearance. Proteinuria rose progressively up to 15 weeks in the control group and similarly in groups A and B. Mean proteinuria in group C was about half the control mean at 5-20 weeks. Systolic blood pressure differed little between groups A, B and control, but was significantly lower than control in group C at 10-20 weeks. Histologically groups B and C showed significantly less glomeruli with segmental sclerosis and less hypertensive vasculopathy than groups A and control. Histological signs of tubular CyA toxicity correlated with the doses applied: inclusion bodies were more frequent in all groups while the score of vacuolisation was increased significantly in group C only. In conclusion, CyA appears not to adversely affect or - at moderately toxic dosage - even to slow down progressive glomerular sclerosis in rats with reduced renal mass.

Animals↗