Association of methylenetetrahydrofolate reductase T677 allele with early development of chronic allograft nephropathy.

Objectives: The aim of this study was to evaluate the role of genetic polymorphisms on the development of chronic allograft nephropathy (CAN).

Design And Methods: Using the polymerase chain reaction (PCR), polymorphisms of methylenetetrahydrofolate reductase (MTHFR C677T), interleukin-6 (IL-6 G-174C) and CD14 (C-260T) were evaluated in 92 kidney transplant recipients with stable renal graft function and no signs of acute rejection in a protocol that included graft biopsy at 12 months after kidney transplantation. A normal population sample (n = 365) was also included.

Effect of sirolimus on renal ischaemia/reperfusion injury in normotensive and hypertensive rats.

Renal ischaemia/reperfusion (I/R) injury and hypertension represent major alloantigen-independent factors contributing to the development of chronic allograft nephropathy of renal allografts. In the present study, we investigated the effect of the anti-proliferative immunosuppressant, sirolimus (SIR), in a model of accelerated renal injury in hypertensive transgenic rats (TGRs). Twenty anaesthetized uninephrectomized TGRs with renin overproduction [TGR(mREN2)27] and 20 normotensive Han SD (SD) rats as genetic controls had their renal pedicles clipped for 45 min and were subsequently treated with either SIR (0.

The influence of G-protein beta3-subunit gene and endothelial nitric oxide synthase gene in exon 7 polymorphisms on progression of autosomal dominant polycystic kidney disease.

Background: A significant phenotypical variability is observed in autosomal dominant polycystic kidney disease (ADPKD). The variability cannot be fully explained by the genetic heterogeneity of the disease. We examined the influence of G-protein beta3-subunit C825T polymorphism and endothelial nitric oxide synthase Glu298Asp polymorphism on the progression of ADPKD towards end stage renal failure (ESRF).

[Initial experience with protocol biopsies in transplanted kidneys].

Background: The aim of protocol biopsy after renal transplantation was to assess the prevalence of chronic allograft nephropathy (CTN) and to correlate the degree of CTN with clinical and laboratory data.

Methods And Results: In 105 patients with a stabilized graft function, a protocol biopsy was carried out at 1 year after transplantation. CAN was found in 75% of patients, and in 6% an acute subclinical rejection was revealed.

Predicting the grade of Banff 97 classification of chronic allograft nephropathy based on examination of graft dysfunction (a preliminary report).

Objectives: Progression of chronic allograft nephropathy (CAN) is associated with a progressive decrease in graft function. Prediction of the Banff CAN grade on the basis of correlation between the grade of histological changes and Scr is difficult because of the big spread of individual values. This study sought to predict the Banff CAN grade based on Scr, Ccr and proteinuria using ROC analysis.

Cyclosporine renal dysfunction.

Cyclosporine (CsA), introduced as an immunosuppressive agent in the 1980s, quickly become the first-line treatment in organ transplantation. However, these improvements were associated with an increased incidence of renal dysfunction. CsA causes histopathological changes in renal transplants that are often difficult to distinguish from other processes, especially chronic allograft nephropathy.

Effects of histamine and the h2 receptor antagonist ranitidine on ischemia-induced acute renal failure: involvement of IL-6 and vascular endothelial growth factor.

Background: Vascular endothelial growth factor (VEGF) exerts cytoprotective, antiapoptotic and proangiogenic effects; its synthesis is induced by hypoxia, several cytokines and histamine. The effects of histamine and the H2 receptor antagonist ranitidine on renal VEGF and IL-6 synthesis were investigated in a well-established rat model of renal ischemia/reperfusion injury.

Methods: Following 7 days of pretreatment with histamine (H group; n = 12), ranitidine (R group; n = 10) or vehicle (controls; n = 13), the left vascular pedicle was clamped for 50 min in uninephrectomized male rats and survival assessed in the different treatment groups.

Detection of HLA-G on human extravillous cytotrophoblast and skeletal muscle with a new monoclonal antibody MEM-G/1.

Using immunohistochemistry with the newly available monoclonal antibody MEM-G/1 the reaction patterns on frozen and formaldehyde-fixed paraffin-embedded sections on human placentas, lymph nodes, skeletal muscles, and kidney and liver allografts were compared. HLA-G (a nonclassical major histocompatibility complex class I molecule that is assumed to influence the immune response during pregnancy and some pathological conditions) was found within human extravillous cytotrophoblast but not within villous cytotrophoblast and placental mesenchymal tissue. No HLA-G expression on human lymph nodes, tonsils, and kidney and liver allografts was demonstrated.

TGF-beta1 expression and chronic allograft nephropathy in protocol kidney graft biopsy.

Chronic allograft nephropathy (CAN) represents a frequent and irreversible cause of long-term renal graft loss. TGF-beta1 is a key profibrogenic cytokine associated with CAN pathogenesis. Because of clinical diagnostic inaccuracy, protocol biopsy has been suggested to be a beneficial method for early CAN detection.

Influence of the alpha-adducin and ACE gene polymorphism on the progression of autosomal-dominant polycystic kidney disease.

Background: A significant phenotypical variability is observed in autosomal dominant polycystic kidney disease (ADPKD). The variability can not be fully explained by the genetic heterogeneity of the disease. We examined the influence of the ACE I/D polymorphism, adducin Trp460Gly polymorphism and the association of both polymorphisms on the progression of ADPKD towards end-stage renal failure (ESRF).

[Increased sP-selectin and other cardiovascular risk factors: fibrinogen, tissue plasminogen activator (t-PA Ag) and acute phase proteins after kidney transplantation].

Background: Our study was designed to monitor the presence of the "coronary artery disease (CAD) risk factors" after kidney transplantation.

Methods: 26 kidneys transplant recipients with well-functioning (creatinine clearance > 0.8 mL/s) renal allografts receiving cyclosporine A (CsA) as the basic component of immunosuppressive therapy and 60 healthy age-matched controls were included into the study.

[An unusual manifestation of tuberculosis in a female patient after kidney transplantation. Case report].

Organ transplant recipients are at the increased risk of infection complications. Herein, we present a case of unusual localisation of tuberculosis in renal allograft recipient treated by combination of cyclosporine A, mycophenolate mofetil and steroids. After the non specific prodromes, surgery due to ileus discovered ileocaecal tumour.

[The kidneys, ageing and transplantation].

The discrepancy between the increasing number of patients listed for kidney transplantation and limited cadaver donor sources has led the transplant community towards indication of elderly people as potential kidney donors. Based on clinical data, the kidney grafts explanted from aged donors have limited survival rates compared with younger ones. The donor age has been also implicated as the important alloantigen-independent risk factor for later onset of chronic allograft neprohopathy called chronic rejection.

[Transforming growth factor (TGF-beta) and kidney transplantation].

Transformation growth factor (TGF-beta) is a cytokine, which takes part in many clinical conditions linked to different chronic disease states. Its production is regulated by genes and polymorphism of TGF-beta gene individually predetermines levels of its production. TGF-beta is produced by a number of normal, predominately haemopoietic and tissue cells.

G-protein beta-3-subunit and eNOS gene polymorphism in transplant recipients with long-term renal graft function.

Background: Despite new immunosuppressive drugs, only a minority of graft survive over 15 years. The aim of our study was to determine the influence of gene polymorphisms in the G-protein-beta(3) subunit (Gbeta3) and endothelial nitric oxide synthase (eNOS) on the long-term outcome of kidney grafts.

Methods: Using PCR, corresponding genotypes in Gbeta3 (C825T) and eNOS (G894T) gene polymorphism were evaluated in patients with preserved graft function over 15 years and in a control group of transplant recipients.

Influence of the endothelial nitric oxide synthase polymorphism on the progression of autosomal dominant polycystic kidney disease and IgA nephropathy.

Background: The reason of variability of clinical course and progression to end-stage renal failure (ESRF) of two widespread chronic nephropathies--autosomal dominant polycystic kidney disease (ADPKD) and IgA nephropathy (IGAN) is not clear. The endothelial dysfunction is considered in the number of factors possibly influencing the prognosis of these nephropathies. Our study tried to verify the hypothesis that endothelial nitric oxide synthase (ecNOS) gene polymorphisms in intron 4 could have some relevance to the progression of ADPKD and/or IgA nephropathy.

Influence of the endothelial nitric oxide synthase polymorphism on the progression of autosomal dominant polycystic kidney disease and IgA nephropathy.

Background: The reason of variability of clinical course and progression to end-stage renal failure (ESRF) of two widespread chronic nephropathies-autosomal dominant polycystic kidney disease (ADPKD) and IgA nephropathy (IGAN) is not clear. The endothelial dysfunction is considered in the number of factors possibly influencing the prognosis of these nephropathies. Our study tried to verify the hypothesis that endothelial nitric oxide synthase (ecNOS) gene polymorphisms in intron 4 could have some relevance to the progression of ADPKD and/or IgA nephropathy.

Renal ischemia--reperfusion injury: an inescapable event affecting kidney transplantation outcome.

Ischemia--reperfusion (I-R) injury has been shown to be a common cause of late and irreversible complications during a variety of standard medical and surgical procedures. The pathogenesis of events which follow the I-R involves both injured endothelium and activated leukocytes and their interaction. In kidney transplantation, an I-R injury occurs in situations such as graft harvesting, cold storage and surgery.

Atherogenesis markers in patients with chronic rejection of renal allografts.

Patients with renal insufficiency are thought to be at the higher risk of atherosclerosis complications. In the present study we evaluated some atherogenesis risk factors in patients with biopsy proven chronic vascular rejection of transplanted kidney and compared them with matched groups of transplant recipients. Patients with chronic rejection had higher plasma levels of alfa-I-acid glycoprotein and fibrinogen as well as soluble P-selectin level.

TGF-beta I gene polymorphism in heart transplant recipients--effect on renal function.

Renal dysfunction is a severe late complication of heart transplantation (HTx). Transforming growth factor beta I (TGF beta I) is a potent multifunctional cytokine with profibrogeneic effect. TGF beta I gene polymorphism correlates with cytokine production.