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Biomedical subjects

P Errasti

Publications and source records attributed to P Errasti.

At least 19 recordsLinked to original sources
PubMed2006

[Kidney transplant].

The kidney transplant is the therapy of choice for the majority of the causes of chronic terminal kidney insufficiency, because it improves the quality of life and survival in comparison with dialysis. A kidney transplant from a live donor is an excellent alternative for the young patient in a state of pre-dialysis because it offers the best results. Immunosuppressive treatment must be individualised, seeking immunosuppressive synergy and the best safety profile, and must be adapted to the different stages of the kidney transplant. In the follow-up to the kidney transplant, cardiovascular risk factors and tumours must be especially taken into account, given that the death of the patient with a working graft is the second cause of loss of the graft following the first year of the transplant. The altered function of the graft is a factor of independent cardiovascular mortality that will require follow-up and the control of all its complications to postpone the entrance in dialysis.

Acute Disease↗
PubMed2005

Preliminary results of the effect of treatment of hyperhomocysteinemia and its relationship with inflammation, coagulation status, and endothelial function after renal transplantation.

The aim of this study was to assess the relationship between total plasma homocysteine (tHC) and several markers of endothelial function, coagulation, and pro-inflammatory status in renal transplant recipients. Our own previous study demonstrated the efficacy of folic acid (FA) and vitamin B(12) (B(12)) treatment to reduce tHC. Using 70 stable recipients, 56 of whom showed hyperhomocisteinemia (HHC) (tHC > or = 14 micromol/L) and a control group (n = 14, tHC < 14 micromol/L), we treated 29 patients in the HHC group (10 mg FA and 500 mg B(12) daily) and determined their endothelial function, inflammatory activity, and coagulation status. We assessed plasma levels of von Willebrand Factor and fibrinogen as the prothrombotic profile and C-reactive protein and plasma albumin as inflammation markers. We performed Doppler sonography of the brachial artery to assess endothelial function. The mean value of plasma tHC of 19.05 +/- 3.70 micromol/L before treatment decreased to 13.45 +/- 3.25 micromol/L after 3 months of treatment (P < .001). The vWF was significantly correlated with tHC (P < .05) and was higher in the HHC patients (P < .05). The fibrinogen mean level was also significantly higher in HHC patients (P < .05). The C-reactive protein level was significantly higher and the albumin level was lower among patients with HHC. The endothelium-dependent dilation (EDD) correlated with baseline tHC (P < .05). In preliminary data we observed that homocysteine-lowering therapy may provide cardiovascular protection by enhancing endothelial function, limiting oxidative stress, and reducing procoagulation status.

Adult↗
PubMed2005

Detection and treatment of post kidney transplant hyperglycemia: a Spanish multicenter cross-sectional study.

INTRODUCTION: The prevalence of diabetes mellitus (DM) is greater among patients with solid organ transplants than in the general population, although the factors associated with posttransplant DM (PTDM) are unknown. OBJECTIVES: The objective of this study was to estimate the prevalence of and assess the risk factors for PTDM. PATIENTS AND METHODS: We included outpatients with functioning isolated solid organ allografts (kidney, liver, heart, and lung). We collected demographic and posttransplant clinical data that included DM diagnostic ADA criteria, DM treatment, DM family history, presence of hepatitis C virus (HCV), immunosuppression treatment, hypertension, and dyslipidemia. RESULTS: A total of 2178 patients included, 1410 kidney recipients, 489 liver transplants, 207 heart transplants, and 72 lung recipients. Seventeen and four-tenths percent of the patients who did not have DM prior to transplantation, developed PTDM (median time: 79 days). A greater prevalence was observed among patients with a family history, HCV, and tacrolimus treatment (with or without steroids P < .05). By logistic regression analyses, OR for these factors were 1.51, 1.65, and 1.38, respectively. Of those patients who did not suffer PTDM, 55.2% showed basal blood glucose values under 100 mg/dL; only 68% presented with a hemoglobin Alc under 6. CONCLUSIONS: The prevalence of PTDM among kidney recipients was higher than that in the general population. DM family history, HCV positive, and tacrolimus were risk factors associated with this entity.

Adult↗
PubMed2003

De novo hemolytic-uremic syndrome/thrombotic microangiopathy in renal transplant patients receiving calcineurin inhibitors: role of sirolimus.

The aim of this study was to evaluate the outcome of ten renal transplant recipients who developed de novo hemolytic uremic syndrome/thrombotic microangiopathy (DnHUS) after treatment with calcineurin inhibitors among 3,862 patients transplanted during the period 2000-2001 in Spain, and the results of switching to sirolimus for resolution of this pathologic condition. No patient had end-stage disease due to primary HUS. The criteria of diagnosis were decreased renal function, biopsy-proven thrombotic microangiopathy, and no signs of acute rejection. Calcineurin inhibitors were completely removed and immediate treatment with sirolimus started after diagnosis. The follow-up period was 19.0+/-4.3 months, at least 12 months after diagnosis. One patient died of sepsis shortly after starting sirolimus therapy. The serum creatinine level in the series decreased from 5.2+/-2.6 mg/dL at the time of biopsy to 2.15+/-1.9 mg/dL 1 month later (P=.011). All but one of the nine recipients, who lost his graft 3 months later (80% success) maintained function, with a serum creatinine of 2.1+/-1.4 mg/dL and Cockroft index of 61.3+/-34 mL/min at the end of follow up. During this time, none of the patients experienced an acute rejection episode and sirolimus was maintained without any remarkable secondary effect. Sirolimus seems to be a promising alternative for the treatment of renal transplant patients who develop calcineurin inhibitor-induced DnHUS.

Adult↗
PubMed2003

Autosomal-dominant polycystic kidney disease: high prevalence of graft loss for death-related malignancies and cardiovascular risk factors.

Autosomal-dominant polycystic kidney disease (ADPKD) is a systemic disease with multiple extrarenal manifestations. It accounts for 7% to 11% of patients receiving dialysis or renal transplantation (RT) for end-stage renal disease (ESRD) in Europe. We analyzed retrospectively the causes of death, the prevalence of cardiovascular risk factors (CVRF) and the patient and graft survivals in 62 consecutive ADPKD patients who received 63 cadaveric grafts (29 men and 34 women), of the 600 RTs performed between 1980-2001. The diagnosis of ADPKD was established by family history and ultrasound techniques. At present, 50 patients (79.4%) have functioning grafts, with a mean follow-up of 84.7 months (range, 12-255), and 13 patients have lost their grafts. The main cause of failure was patient death with a functioning graft (9 cases). Malignancies occurred in 5 patients, including 2 lymphomas, 1 renal carcinoma, 1 pancreas sarcoma, and 1 lung cancer associated with infection. Three patients died of cardiocerebrovascular events, and 1 patient of pneumonia. One patient lost the graft after decreasing the immunosuppression for an obstructing colon cancer. Three additional patients now on dialysis lost their grafts due to chronic rejection in 2 cases and primary nonfunction in 1 case. The prevalence of cardiovascular risk factors among the 50 patients with functional grafts were: hypertension, 70%; hypercholesterolemia, 62%; hyperhomocysteinemia, 30%; hyperfibrinogenemia, 68%; increased lipoprotein (a), 18%; microalbuminuria, 22%; hyperuricemia, 48%; hyperparathyroidism, 24%; overweight status, 24%; and nonlethal myocardial infarction, 10%. We conclude that ADPKD patients have good graft and patient survivals, and that the presence of malignancy is the main cause of death and graft failure at our center.

Blood Pressure↗
PubMed2003

Treatment of hyperhomocysteinemia after renal transplantation.

INTRODUCTION: Several epidemiologic prospective studies have provided strong evidence that hyperhomocysteinemia (HHC) is a risk factor for cardiovascular disease (CVD) due to its role in producing endothelial damage due to oxidation stress. Several studies show that combined folic acid (FA) and vitamin B12 (B12) treatment decreases fasting total homocysteine (HC) levels in renal transplant recipients (RTR). The aim of the study was to determine the efficacy and safety during one year of combined FA and B12 treatment in 89 RTR, as well as the relationship between HHC with other known risk factors for CVD and the intrinsic characteristics of the transplantation. METHODS: Among 193 RTR in whom we determined the baseline levels of HC, FA, B12, creatinine, and CV risk factors, 81 had normal (HC < 14 micromol/L) and 112 elevated (HC > or = 14 micromol/L) HC levels, 89 of whom were included in a treatment group (23 nontreated). Analytic measures were performed at baseline and 1, 3, and 12 months. RESULTS: We observed a decrease in HC levels among the treatment group (P<.05) after 12 months without differences in the other groups. There were no differences in age, hypertension, hypercholesterolemia, smoking, presence of diabetes, or type of immunosuppression between the groups. There was a significant correlation between basal creatinine and HC level (P<.05). A higher prevalence of CVD was observed in the HHC group (P<.05). CONCLUSION: HHC is associated with worse renal function and a higher prevalence of CVD. FA and B12 treatment normalize HC levels, representing a safe treatment that could improve the long-term vascular prognosis of RTR.

Adult↗
PubMed2000

Mast cells in chronic rejection of human renal allografts.

An increased number of mast cells (MCs) is found in renal specimens of patients with diseases associated with persistent chronic inflammation. MCs proliferation is partly dependent on the presence of T lymphocytes. Both chronic inflammation and T-lymphocytes are essential in the development of chronic rejection (CR), and probably for the infiltration of MCs. MC-derived products such as heparin, histamine, and serine proteases may be responsible for endothelial proliferation and excess collagen production by fibroblasts. In this study, a quantitative evaluation of the MCs infiltration in kidney allografts with CR is performed. The extent of renal fibrosis was analysed in samples stained with Masson's trichrome. To evaluate the potential relationship between MCs and fibrosis in CR we analysed 30 kidneys with CR (25 from nephrectomies and 5 from autopsies). Ten transplanted kidneys obtained from patients died by causes not related with rejection were used as controls. CR was graded according to the Banff schema, which assesses the degree of vasculopathy, tubular atrophy, interstitial fibrosis and transplantation glomerulopathy. Giemsa-stained sections and immunohistochemistry using anti-MC tryptase and c-kit monoclonal antibodies were used to detect MCs. The mean number of MCs per 20 high-power fields (HPF) in the transplanted kidney with CR was 101.8+/-15.3 in the renal cortex and 46.60+/-6.52 in the medulla. MCs were significantly more numerous in CR with respect to normal kidneys, both in the cortex (P<0.01; Mann-Whitney U test) and in the medulla (P<0.01; Mann-Whitney U test). There was a positive correlation between the number of MCs and extent of fibrosis (P<0.01; Kruskal-Wallis one-way anova test) and tubular atrophy (P<0.01). These results suggest that MCs may play a role in the process of development of interstitial fibrosis in CR.

Adolescent↗
PubMed1999

Benefits of a dietary intervention on weight loss, body composition, and lipid profile after renal transplantation.

The nutritional status of a group of 23 renal transplanted patients with a body mass index > 27, hyperlipidemia, and stable renal function were studied before and after 6 mo of dietary intervention with the American Heart Association (AHA) Step One pattern. The dietary records showed that the intake of total fat decreased from 42.2 +/- 5.5 to 33.0 +/- 4.2% (P < 0.001) and the intake of saturated fat decreased from 12.8 +/- 1.8 to 9.2 +/- 3.1% (P < 0.01) of total calories. The cholesterol intake fell from 352 +/- 10 to 221 +/- 12 mg/d. The mean weight loss was 3.2 +/- 2.9 kg (P < 0.001), followed by a significant decrease in mean body fat mass (%) measured by triceps skinfold (34.2 +/- 3.3 versus 32.9 +/- 3.7; P < 0.05), bioelectrical impedance (30.8 +/- 5.7 versus 26.5 +/- 5.9; P < 0.001), and infrared interactance (37.5 +/- 6.3 versus 34.7 +/- 5.5; P < 0.01). After the dietary intervention, lipid profile improved in all patients, with a decrease in the mean total cholesterol (237 +/- 32 versus 224 +/- 36 mg/dL; P < 0.05), which was higher in males. Also, low-density lipoprotein cholesterol was reduced in male patients (156 +/- 19 versus 136 +/- 11 mg/dL, P < 0.05), whereas in females low-density lipoprotein cholesterol levels remained unaltered. The high-density lipoprotein cholesterol and triacylglycerol values were not affected in both males and females by the dietary treatment. The reduction in serum cholesterol was inversely correlated with the initial values of triceps skinfold (r = 0.52, P < 0.01) and was lower in patients with a body mass index > 30 (5.7 versus 2.8%, NS). It is concluded that the obesity and hyperlipidemia following renal transplantation may be improved by dietary intervention and subsequent weight loss.

Adult↗
PubMed1999

Decrease of apoptosis rate in patients with renal transplantation treated with mycophenolate mofetil.

BACKGROUND/AIMS: Mycophenolate mofetil (MMF) is a powerful immunosuppressant that inhibits the proliferation of lymphocytes by blocking the enzyme inosine monophosphate dehydrogenase. MMF prevents acute graft rejection in organ transplants. The aim of this investigation is to study whether MMF has any influence on apoptosis and proliferation rates of cells other than lymphocytes. METHODS: We conducted a retrospective study of renal allograft biopsies taken during the 1st week after transplantation in 25 patients receiving triple therapy with prednisone, ciclosporin and azathioprine 75 mg/day and in 25 patients treated with MMF at a dose of 2 g/day instead of azathioprine, in order to investigate the differences in the proliferation and apoptosis rates of the glomerular, tubular, interstitial and endothelial cells of the kidney. Twelve normal kidneys were used as controls. Conventional histopathological techniques were applied as usual for pathological diagnosis. Proliferative activity was assessed by use of MIB-1 antibody. Sections of formalin-fixed, paraffin-embedded tissue blocks were stained for the presence of apoptotic cells by TUNEL assay. Evaluation of proliferative or apoptotic rates was made by counting the number of positive cells in 10 glomeruli and in 10 transversely cut tubuli in each biopsy. The positive cells in the interstitium were counted in ten high-power fields. Positive cells in the endothelium were scored semiquantitatively from 0 to 3: 0 = none, 1 = isolated cells, 2 = small groups of cells, 3 = most endothelial cells. Mann-Whitney U and chi-square tests were used for intergroup comparisons. RESULTS: All biopsies were normal or had borderline (Banff classification) acute rejection. MIB-1 rates were similar in both groups, without statistical differences (p > 0.05) between them. Significantly lower apoptotic rates were found in the group treated with MMF in tubular epithelium (23.41 +/- 8.86 vs. 57.4 +/- 13.42; p = 0.021), in glomerular (1.25 +/- 0.78 vs. 5.3 +/- 1.66; p = 0.027), and interstitial cells (1.58 +/- 0.6 vs. 5.8 +/- 1.54; p = 0.043). Apoptosis in endothelial cells (p > 0.05) was similar in both groups. CONCLUSION: We conclude that treatment with MMF of kidney transplant patients does not affect the proliferative rate of cells of the allograft, but decreases the number of apoptotic cells in tubular epithelium.

Adult↗