Iatrogenic pseudoaneurysm of the popliteal artery following corrective tibial osteotomy.

Due to its anatomical location the popliteal artery is exposed to injury during surgical procedures in the region of the knee joint, in particular during high-level corrective osteotomies of the proximal tibial epiphysis. Nevertheless, posttraumatic (iatrogenic) pseudoaneurysm constitutes a very rare complication of the procedure. Only few reports of such complication have been published and they were usually connected with lateral tibial osteotomy - the accidents after medial osteotomy are seldom. The complication we report was observed in a 52-year-old female patient after corrective osteotomy of the medial portion of the proximal tibial epiphysis. The complication was diagnosed 7 days after surgery on US-examination and subsequently confirmed by emergently performed angio-CT. The patient was referred for urgent reconstructive surgery. No significant complications were observed, neither postoperatively nor during follow-up visits.

Activated cells in urine and monocyte chemotactic peptide-1 (MCP-1)--sensitive rejection markers in renal graft recipients.

Chemokines induced during an acute immune alloresponse cause cellular infiltration of the allograft. These chemokines and cells are excreted with urine. The aim of the study was to assess the diagnostic utility of urinary excretion of monocyte chemotactic peptide-1 and certain cells involved in infiltration i.e. CD3+, CD64+ and HLA-DR+ cells. The study entailed 35 patients with acute renal rejection and 65 with a stable graft function. Urinary sediments were prepared by means of cytospin and stained with anti-CD3, anti-CD64, anti-HLA-DR labeled monoclonal antibodies. Urinary expression of MCP-1 was assayed by ELISA. In the patients with acute rejection MCP-1 level was ten-fold higher than in the patients with a stable graft function (6.1+/-3.4 vs 0.6+/-0.4 ng/mg creatinine). The number of CD3+ cells was over 5 times higher than in the non-rejection patients (13.4+/-4.6 vs 2.5+/-2.2). The number of HLA-DR+ cells was 6 times higher in the acute rejection patients (15.7+/-5.9 vs 2.5+/-2.7). The number of CD64+ cells was significantly increased in the patients during an acute rejection episode (p<0.0001). CD3+, HLA-DR+ and CD64+ cell counts strongly correlated with urine excretion of MCP-1. The counts of CD3+ and HLA-DR+ cells correlated with Banff score. The assessment of MCP-1 as well as CD3+, CD64+ and HLA-DR+ cells can provide a useful non-invasive device for the diagnosis of acute rejection. A sole assay of HLA-DR+ cell excretion provides enough specificity and sensitivity for the routine monitoring of patients after kidney transplantation, saving costs and time.

Kidney transplantation and enzyme alpha-galactosidase A therapy in patient with Fabry disease: a case report.

Fabry disease, an X-linked recessive glycolipid storage disease, is caused by a deficiency of the lysosomal enzyme alpha-galactosidase A (alpha-Gal A), which cleaves a fatty substance called globotriaosylceramide (GL3). The abnormal storage of GL3 in blood vessel walls leads to ischemia and necrosis, particularly in blood vessels of the skin, kidneys, heart, brain, and nervous system. The aim of our study was to present the results of cadaveric kidney transplantation with enzyme alpha-Gal A therapy in a patient with Fabry disease. The patient was diagnosed with Fabry disease at the age of 33 years, based on enzymatic tests. Renal manifestations occurred a year later as proteinuria. At the age of 35 years, the glomerular filtration rate (GFR) was within the normal range. The patient received supplemental enzyme treatment with alpha-Gal (1 mg/kg every 2 weeks). At 3 months after starting supplementation, renal function worsened with serum creatinine levels at 1.7 to 1.8 mg/dL. The following months of supplementation (alpha-Gal 1 mg/kg) concurred with progressive renal dysfunction. After 27 months of supplementation at 37 years, with a creatinine value of 5.5 mg/dL, hemodialysis began and months later the patient received a cadaveric kidney graft. The patient no longer required dialysis. On postoperative day 5 the serum creatinine was 3.9 mg/dL; on day 7, 2.2 mg/dL; on day 14, 1.5 mg/dL. Enzyme supplementation began on posttransplant day 13. Renal graft function has been good during 5 months of observation with creatinine levels at 1.2 to 1.3 mg/dL. The treatment does not interfere with tacrolimus metabolism. Simultaneous chronic enzyme supplementation is the optimal treatment in the fifth stage of end-stage renal disease in Fabry disease.

Influence of cytomegalovirus disease on early and late renal graft function.

The role of cytomegalovirus (CMV) disease to induce chronic nephropathy using new immunosuppressive regimens is debated. This study sought to assess the influence of CMV disease on early and late graft function in relation to immunosuppressive therapy. Among 456 renal recipients transplanted from 1997 to 2003, 95 were diagnosed with CMV disease on the basis of clinical symptoms and the presence of pp65 protein. The patients were divided into 2 groups according to their immunosuppressive regimen: group I included 43 patients treated with cyclosporine (CsA), azathioprine (AZA), and prednisone (P); group II, 52 patients treated with calcineurin inhibitor (CI), mycophenolate mofetil (MMF), and P. A control group of 90 CMV disease-free renal recipients were transplanted in 2001. CMV disease occurred in 20.8% of renal recipients: 14.8% from group I and 25.5% from group II. CMV disease was diagnosed in 73 patients (76.8%) before the third month after transplantation. An acute rejection episode (ARE) appeared in 42 patients, of whom 31 had CMV disease diagnosed within 1 month after ARE, while 5 before an ARE. In six patients ARE was not time related to CMV disease. The serum creatinine values at 6 months after transplantation were significantly higher among the CMV versus control groups: 1.69 and 1.76 vs 1.49 (P < .05). In patients with ARE and CMV disease, the serum creatinine value was also higher at 6 and 12 months after transplantation compared with patients without an ARE (P < .03). One- and 3-year graft survival rates were 95.1% and 83.7% in group I versus 93.4% and 86.5% in group II versus 95.4% and 90.2% in the control group. In conclusion, CMV disease showed a negative impact on early graft function independent of the immunosuppressive regimen, an effect that was emphasized by an ARE.

Immunocytological urinalysis and monocyte chemotactic peptide-1 in renal transplant recipients with polyomavirus replication.

In some patients polyomavirus replication induces chronic tubulointerstitial inflammation in the transplanted kidney. The aim of this study was to investigate whether immunocytological urinalysis and monocyte chemoattractant protein-1 (MCP-1) assays could be used for an early diagnosis of nephropathy for patients with polyomavirus replication. We analyzed 1189 urine sediments from 174 renal allograft recipients who were transplanted between 2000 and 2005. Decoy cells were identified by an immunofluorescence method using specific antibodies (JC/BK monoclonal antibody). A similar method was used to detect CD3(+), CD14(+), and HLA-DR(+) cells with appropriate antibodies. The urinary excretion of MCP-1 was assayed by enzyme-linked immunosorbent assay. The results of urine sediment analysis and MCP-1 concentrations were compared with those of patients with stable graft function (control group n = 65). In 17 patients (10%) decoy cells were identified in urine. In 12 patients polyomavirus DNA was detected in plasma or urine by a polymerase chain reaction method. Polyomavirus nephropathy was diagnosed in eight patients by the presence of intranuclear viral inclusions or immunohistochemical staining with SV40 large T-antigen specimens from a renal biopsy, as well as by clinical and histopathological evidence (group I). Polyomavirus replication was diagnosed in four patients by urinary excretion of decoy cells and polyomavirus DNA detection (group III). In five patients only decoy cells were found. The patients of groups I and II showed an increased number of CD3, CD14, HLA-DR surface antigen-positive cells and greater excretion of MCP-1 compared with the control group (P < .02). The number of excreted cells was higher among patients with more severe infiltration. The results of patients from group III were similar to the control group. In conclusion, increased excretion of cells with CD3, CD14, and HLA-DR surface antigens and of MCP-1 were associated with intragraft tubulointerstitial inflammation in patients with polyomavirus nephropathy. Asymptomatic polyomavirus replication was associated with hidden tubulointerstitial inflammation. Monitoring cell excretion and chemokine content may be utilized for early detection of polyomavirus-induced nephropathy.

Incidence and outcome of transplant renal artery stenosis: single center experience.

Since the incidence of transplant renal artery stenosis (TRAS) in renal allografts varies from 1% to 23%, we sought to examine its incidence, to analyze treatment options, and to ascertain its outcomes. Retrospective analysis of 793 kidney allograft recipients transplanted between 1996 and 2004 revealed an incidence of 0.9% (n = 7). Time from kidney transplantation to the first symptoms varied from 1 week to 3 years (median, 4 months). Three patients experiences refractory hypertension and six patients developed allograft dysfunction. Screening color Doppler ultrasonography showed hemodynamic changes in six patients with the definitive diagnosis confirmed by angiography in all patients. One patient with an anastomotic stenosis was treated with a surgical operation and six patients, percutaneous transluminal angioplasty (PTA), with stenting in three cases. Both surgical as well as PTA treatment were successful in all but one patient, who underwent PTA alone, developed chronic renal insufficiency necessitating hemodialysis and finally lost his allograft. In the other patients all symptoms resolved after treatment and the patients are doing well with functioning allografts. Although TRAS was an uncommon complication, if recognized promptly it could be treated by surgery or PTA with a high success rate.

Conversion to sirolimus from cyclosporine may induce nephrotic proteinuria and progressive deterioration of renal function in chronic allograft nephropathy patients.

Antiproliferative and non-nephrotoxic properties of sirolimus have been exploited for treatment of patients with chronic graft dysfunction. In this paper we point to the possible association of nephrotic syndrome and renal impairment with rapid conversion from cyclosporine (CsA) to sirolimus in patients with chronic nephropathy. Five male patients, ages 34 to 56 years, with chronic renal failure in the course of glomerulonephritis, were transplanted between 1997 and 1999. For the first 49 to 65 months, the immunosuppressive regimen consisted of CsA, azathioprine (AZA), and prednisone. Thereafter, due to chronic nephropathy evidenced by biopsy, conversion to sirolimus was performed with sharp withdrawal of CsA. The serum creatinine level prior to conversion was 1.9 +/- 0.3 mg/dL. Trace to 86 mg/dL proteinuria was found in 3 patients, while 2 patients had about 200 mg/dL. After 2 to 4 months of sirolimus treatment the proteinuria progressed (558 +/- 183 mg/dL); edema, hypoproteinemia, hypoalbuminemia, and hyperlipidemia developed; and the serum creatinine increased to 3.5 +/- 0.8 mg/dL. Biopsies performed in three patients revealed new pathologic changes. After 4 to 5 months, we performed reconversion to calcineurin inhibitor. Proteinuria decreased to 0 to 150 mg/dL; nevertheless the serum creatinine was continuously rising. Six to 15 months after the conversion, 3 patients returned to dialysis. The fourth patient, who was earlier reconverted, has a serum creatinine level of 2.0 mg/dL after 15 months. In conclusion, conversion from CsA to sirolimus may induce nephrotic syndrome with progressive deterioration of renal function. Converted patients require careful monitoring of proteinuria and renal function. Early reconversion to calcineurin inhibitor may prevent progressive deterioration of graft function.

Favorable resolution of hepatic infarctions in transplanted liver after portal vein thrombosis treated by surgical thrombectomy: a case report.

Portal vein thrombosis (PVT) after orthotopic liver transplantation (OLT) is a life-threatening complication associated with a high rate of graft loss and patient death, with reported incidence of 1% to 2% in adults. We report a case of an early PVT after OLT complicated by hepatic infarctions in the liver graft. After surgical thrombectomy and restoration of the portal inflow, hepatic infarctions resolved spontaneously within 6 months, which was confirmed by computed tomography.

Renal function and tubular phosphate handling in long-term cyclosporine- and tacrolimus-based immunosuppression in kidney transplantation.

The aim of the study was to assess impaired tubular phosphate reabsorption and renal function among patients on cyclosporine- or tacrolimus-based immunosuppression for 2 years after kidney transplantation. Among 60 cadaveric kidney allograft recipients observed for 48 months, 40 received cyclosporine, azathioprine, and prednisone (group A and B). Group C consisted of 20 patients receiving tacrolimus with steroid withdrawal at 3 months after transplantation. Renal function and calcium-phosphate metabolism-iPTH, 25-OHD, 1,25(OH)(2)D concentration, phosphate reabsorption (TRP; mmol/L), and tubular maximum phosphate reabsorption per glomerular filtration rate (TmPO(4)/GFR; mmol/L)-were assessed at 1, 6, 12, 18, and 24 months (groups A and C) or 24, 30, 36, 42, and 48 months (group B). Renal function after 24 months of observation was significantly better among tacrolimus-treated patients (serum creatinine concentration mumol/L; C: 94.6 +/- 16.8 vs A: 110.5 +/- 22.1 vs B: 121.1 +/- 30.9; P < .05). Among tacrolimus-treated recipients, TRP and TmPO(4)/GFR remained within normal values during the whole observation period. In groups A and B, TRP improved during the first year of observation; after 2 years it reached values observed in group C (TRP: A: 0.67 +/- 0.1; B: 0.72 +/- 0.13; C: 0.76 +/- 0.07; P = NS), whereas TmPO(4)/GFR remained low in group A after 2 years (A: 0.78 +/- 0.19; B: 0.91 +/- 0.25; C: 0.94 +/- 0.15; P < .05). Tacrolimus-treated patients exhibit significantly faster recovery from tubular phosphate reabsorption impairment compared with cyclosporine-treated recipients. Tacrolimus-based immunosuppression led to better kidney allograft function during 2-year observation.

Sirolimus delays recovery from posttransplant renal failure in kidney graft recipients.

The aim of this study was to evaluate the impact of sirolimus and cyclosporine (CsA) combined therapy on the incidence and duration of delayed graft function (DGF), and the impact of the latter on 1-year graft function. The study entailed 23 cadaveric renal recipients treated with sirolimus-CsA-prednisone regimen (sirolimus group). The reference group entailed 23 patients treated with CsA-azathioprine-prednisone. In the sirolimus group the frequency of DGF was 39% and was essentially the same as in reference group (34.8%). The duration of DGF was significantly longer in SRL group and lasted 21.2 +/- 12.2 days versus 6.8 +/- 2.5 in reference group (P = .004). Serum creatinine level decreased below 3.0 mg/dL after 36 +/- 22 days in sirolimus group versus 16.8 +/- 6 days in reference group (P < .04). Cold ischemia was slightly longer and donors were older in DGF patients in both groups. Sirolimus dose during first month was higher in DGF patients (3.5 versus 2.6 mg), whereas level of CsA was lower (230 versus 310 ng/mL). Biopsy-proven acute rejection (AR) occurred in most of DGF patients and during the DGF period. Serum creatinine level at the 12th month posttransplant was higher in DGF versus non-DGF patients (2.0 +/- 0.5 versus 1.5 +/- 0.4 mg/dL). One-year patient and graft survival was 100% in sirolimus group and 100% and 95% in reference group. In conclusion, sirolimus significantly retards the recovery from posttransplant renal failure; however, it does not increase the incidence of DGF. Patients who suffered from posttransplant acute renal failure had worse renal function at 1 year after transplantation, independent of the treatment protocol.

Intragraft mRNA expression of cytokines and growth factors in human kidney allograft biopsies by in situ RT-PCR analysis.

The aim of our study was to correlate intragraft mRNA expression of cytokines and growth factors with histopathologic features in renal allograft biopsies. Fifty-six core biopsies performed in 51 kidney transplant recipients were assessed by the Banff '97 classification. Tubular and glomerular expressions of IFN-gamma, TGF-beta1, and PDGF-B as well as IL-2, IL-6, and IL-10 mRNA were assessed using semiquantitative RT-PCR in situ. No significant differences were noted between acute cellular and vascular rejection with regard to the glomerular and tubular mRNA expression of cytokines examined. We observed a positive correlation between tubular and glomerular IL-10 and IFN-gamma mRNAs during acute rejection. In chronic rejection the mRNA expression levels of IFN-gamma and IL-2, IL-6, and IL-10 did not differ from those of acute rejection; moreover, the glomerular expression of mRNA for TGF-beta1 (P < .05) and PDGF-B (P < .1) was even lower than during acute rejection episodes. Both tubular and glomerular IL-2, TGF-beta1, and PDGF-B mRNA expression levels in biopsies with acute rejection were significantly higher than in acute tubular necrosis (ATN). Biopsy samples with borderline changes exhibited the lowest levels of cytokine gene expression and were close to the intensity of control specimens obtained from living donor kidney biopsies taken during organ harvest. Our data failed to show a dichotomy between Th1 and Th2 cytokine activation in biopsy specimens from kidney allograft recipients; both Th1- and Th2-derived cytokines were involved to similar extents in rejection processes.

Mycophenolate mofetil but not the type of calcineurin inhibitor (cyclosporine vs tacrolimus) influences the intragraft mRNA expression of cytokines in human kidney allograft biopsies by in situ RT-PCR analysis.

The aim of the study was to assess the molecular background of the alloimmune response by the detection of low-abundance mRNA of cytokines in 34 core needle biopsies from kidney allografts with histopathological findings of acute rejection (AR). Recipients were immunosuppressed with a calcineurin inhibitor (CNI), cyclosporine or tacrolimus, and prednisone and azathioprine or mycophenolate mofetil (MMF). Tubular and glomerular expression of IL-2, IL-6, IL-10, IFN-gamma, TGF-beta1, and PDGF-B mRNA were assessed using semiquantitative evaluations of RT-PCR in situ on paraffin tissue sections. This procedure resulted in light microscopy visualization of granular precipitates at the sites of the corresponding mRNA chains. The tubular expression of mRNA for IL-6 and TGF-beta1 was significantly lower in biopsies with AR (n = 34) obtained from patients treated with MMF (n = 12) than in biopsies obtained from patients treated with azathioprine (n = 22) (P < .02). Responsiveness to corticosteroids tended to be more frequent among the MMF group (11 of 12 recipients vs 15 of 22 recipients, P = ns). Moreover, 8 of 12 recipients in the MMF-treated group displayed serum creatinine levels equal or less than 167 mmol/L 1 year after biopsy compared to 7 of 22 recipients in the azathioprine-treated group. There was no significant difference between the groups that had or had not received corticosteroids or between those treated with each type of CNI. These results suggest stronger inhibition of humoral responses and down-regulation of fibrosis by MMF among recipients with AR.

Gingival overgrowth in kidney transplant recipients treated with cyclosporine and its relationship with chronic graft nephropathy.

Our previous study of a group of renal transplant recipients treated with CsA showed a significantly faster development of chronic graft failure among patients with gingival hyperplasia (GH) compared to unaffected patients. The aim of the present research was to establish the impact of CsA dose and blood levels on the incidence of chronic graft nephropathy and gingival overgrowth as well as to assess risk factors for chronic graft nephropathy. The study included 64 renal graft recipients (32 patients with GH and 32 without GH) transplanted between 1989 and 1994. There were no significant differences between the pretransplant demographic and clinical data of the patients with and without GH. Patients with GH received a significantly higher total yearly dosages of CsA compared those without GH (P <.03). Serum creatinine in the first year posttransplant in patients with GH was 1.9 mg/dL versus 1.6 mg/dL in those without GH. During 9 to 14 years follow-up, end-stage renal failure due to chronic nephropathy occurred in 18 patients (56%) with GH and eight patients (25%) without GH. Ten-year renal graft survival was 35% in GH patients and 69% in patients without GH. Ten-year patient survival was 69% in the GH group and 91% in the group without GH. CsA dosage was a risk factor for GH and for graft loss, which implies a role of CsA toxic effects on the pathological mechanisms of GH and of chronic allograft nephropathy.

Mycophenolate mofetil severely depresses antibody response to CMV infection in early posttransplant period.

Estimation of anti-CMV-IgG and anti-CMV-IgM is considered a relatively inexpensive screening tool of CMV status. The aim of study was to estimate how the immunosuppressive protocol influence serum anti-CMV IgG and IgM concentration in renal graft recipients and to estimate the adequacy of anti-CMV-IgG concentration and anti-CMV-IgM index as screening parameters of active CMV disease in patients receiving different immunosuppression. The study group consisted of 33 patients with clinical signs of CMV disease who received one of three types of immunosuppression: (1) azathioprine (Aza) + cyclosporine (CyA) + prednisone (Pr), 20 patients; (2) mycophenolate mofetil (MMF) + CyA + Pr, eight patients; tacrolimus (Tac) + MMF, five patients. Patients were enrolled when the pp65-antigen (pp65) of PBL was positive within 1 to 5 months after transplant (75 patients tested). The IgM-i in the Aza + CyA + Pr group was higher than in MMF + CyA + Pr group (2.73 + 1.8 vs 1.08 +/- 1.07, P =.021). The IgM-i in the Aza + CyA + Pr group was higher than in Tac + MMF (2.73 +/- 1.8 vs 0.78 +/- 0.69; P =.014). There was no difference in IgM-i between MMF + CyA + Pr and Tac + MMF. There was no difference in relative increase of IgG-c among all groups but there was a difference in relative increase of IgM-i between Aza + CyA + Pr and MMF + CyA + Pr groups (6.7 +/- 9.4 vs 2.3 +/- 5.9; P =.007) and between Aza + CyA + Pr and MMF + Tac groups (6.7 +/- 9.4 vs 0.6 +/- 0.54; P =.003). Immunosuppressive protocols including MMF exert an inhibitory influence on B-cell response and synthesis of anti-CMV-IgM. It makes the anti-CMV-IgM index an inadequate rough screening diagnostic parameter of active CMV disease.

Influence of hypercholesterolemia and acute graft rejection on chronic nephropathy development in renal transplant recipients.

Graft endothelial lesions resulting from acute rejection may be sustained by concomitant hypercholesterolemia, thus increasing the risk of chronic graft failure. The present study was undertaken to examine the influence of hypercholesterolemia and acute graft rejection (AGR) episodes on graft function and graft loss due to chronic nephropathy. A cohort of 336 patients transplanted between 1993 and 2000 having graft function at 12 months after transplantation were examined. Immunosuppressive therapy consisted of CsA, azathioprine, and corticosteroids in 90% with 10% of patients receiving mycophenolate mofetil in place of azathioprine. During the first year after transplantation, AGR occurred in 134 (39.8%) and hypercholesterolemia (6.2 mmol/L) in 132 (39.2%) of patients. The population was divided into four groups according to AGR occurrence and cholesterol concentrations during the first year after transplantation for analysis of serum creatinine concentrations and graft loss at 5 years of follow-up. Patients with AGR irrespective of cholesterol levels displayed significantly higher creatinine concentrations. Graft loss in these patients increased over twofold compared to the remaining groups. Patients without hypercholesterolemia and AGR showed normal creatinine concentrations and low graft loss rates during 5 years of follow-up.

Cytokine gene expression in kidney allograft donor biopsies after cold ischemia and reperfusion using in situ RT-PCR analysis.

It was previously reported that ischemia-reperfusion injury initiates an inflammatory response and may significantly affect the transplanted organ function. The aim of this study was to assess changes of intragraft cytokine mRNA expression in kidneys after cold ischemia (CI) and following reperfusion. We examined mRNA of a product of activated T lymphocytes (IFN-gamma) and a monocyte product (IL-6). Eleven kidneys were transplanted after CI time ranging from 16 to 39 hours. Renal needle core biopsies were obtained from donors after cold ischemia and approximately after 20 minutes of reperfusion. Tubular and glomerular expression of IFN-gamma and IL-6 mRNA were assessed using semiquantitative evaluation of the RT-PCR in situ. After reperfusion an intense increase of IL-6 mRNA expression was observed in four specimens, a slight increase was noticed in five specimens, and a very slight decrease in two specimens. Changes in IL-6 mRNA expression were limited only to tubules. In contrast, the glomerular and tubular mRNA expression of IFN-gamma and glomerular of IL-6 remained stable. Mean CI time for patients with an intense increase was higher than for patients with a slight increase and with the decrease of IL-6 mRNA expression (32.0 +/- 6.8 vs 25.2 +/- 7.3 and 26.0 +/- 5.7 hours). Our results suggest that early inflammatory changes at the time of implantation of renal allografts depends mainly on monocyte/macrophage-associated products. The observed intensity of their expression in tubules was connected to longer CI time.

Biopsy eosinophilia as a predictor of renal graft dysfunction.

AIM: The aim of this research was to assess the impact of eosinophilia in renal biopsy specimens obtained during an acute rejection (AR) episode on the severity and reversibility of rejection and on long-term graft function. MATERIAL: Among 165 renal graft recipients who underwent transplantation (Tx) in 2001 and 2002 whose biopsy specimens revealed AR, 49 with tissue eosinophilia were compared with control group of 48 without this feature. The average biopsy time was 60.6 and 95.8 days, respectively. Biopsies during delayed graft function were performed in 46.9% of patients with eosinophilia and 29% in the control group. The immunosuppressive regimen was based on tacrolimus or cyclosporine. RESULTS: Tissue eosinophilia was observed in 49 of 165 patients (29.6%): 5 patients had eosinophilia <10/mm(2), 31 patients 10-100/mm(2), 13 patients >100mm(2) (3 patients >300/mm(2)). Severity of AR according to Banff score was statistically lower in the control group (P <.002). Patients with tissue eosinophilia who initially received steroid-free treatment presented with significantly higher (P =.02) biopsy/patients index (2.3 vs 1.81) than the total eosinophilic group. Serum creatinine values at 6 and 12 months after transplantation (Tx) were higher among eosinophilic when compared with the control group (2.41 vs 1.82 mg/dL, P <.002; 2.10 vs 1.98 mg/dL, P =.006, respectively). Chronic rejection within the first year occurred in 25% of patients with tissue eosinophilia, and 8.3% of patients in the control group. One-year graft survival rate among patients with tissue eosinophilia was lower compared with the control group (89.8% and 93.7%, respectively). CONCLUSIONS: Biopsy eosinophilia is a negative predictor that indicates a more severe course of AR and a worse response to treatment with the threat of chronic graft dysfunction.

The influence of calcineurin inhibitors on mycophenolic acid pharmacokinetics.

Despite the fact that concentrations of mycophenolic acid (MPA) are not routinely measured, accumulating data suggest the usefulness of this monitoring to optimize therapy. The aim of this study was to assess the influence of CsA and tacrolimus on MPA pharmacokinetics. Concentrations of MPA were measured using HPLC. An assay was performed before dose (the C(0)), as well as at 40 minutes and 1, 2, 4, 6, 8, 10, 12 hours after administration of mycophenolate mofetil (MMF). MPA profiles were assessed in 51 patients receiving tacrolimus at a dose of 1.0 g/d and prednisone as well as in 97 patients receiving CsA (2.0 g/d) and prednisone. Significant correlations of MPA levels with serum albumin and GFR were observed in both groups. Women presented with higher levels of MPA than men. C(0) MPA level among the tacrolimus group were significantly higher than those in CsA group: 3.18 +/- 2.21 microg/mL versus 1.68 +/- 1.03 microg/mL (P

Vascular complications after the treatment with Ilizarov external fixators.

Iatrogenic vascular injuries from external fixation in orthopaedics and traumatology are frequent. Three cases of vascular injuries after the treatment with Ilizarov external fixators were treated at our institution. These include two cases of pseudoaneurysms and one case of acute ischaemia of the lower limb. Two patients became symptomatic only after removal of the fixator. In all cases, the diagnosis was made by color flow duplex sonography. All vascular injuries needed surgical repair.

The detection of Chlamydia pneumoniae in aneurysm of abdominal aorta and in normal aortic wall of organ donors.

Sixty patients underwent surgery due to abdominal aortic aneurysms; the group included 30 patients with asymptomatic aneurysm and 30 with ruptured aneurysm. A control group comprised 30 organ donors. Surgical specimens derived from aneurysm or aorta fragments were investigated for Chlamydia pneumoniae DNA using PCR. In asymptomatic aneurysms, DNA was found in 9 cases (29%), and in ruptured aneurysms in 14 cases (49%). In the control group, C. pneumoniae DNA was not detected in an aortic wall. These results suggest that healthy aortic wall is not susceptible to chlamydial infection. A large number of aneurysm infections implies C. pneumoniae role in proteolysis and degradation of the aneurysm wall. The biological effect of this process may cause an enlargement of the aneurysm.