Influence of gestational diabetes mellitus on neonatal weight outcome in twin pregnancies.

AIMS: To evaluate the influence of gestational diabetes mellitus on neonatal birthweight, macrosomia and weight discrepancy in twin neonates. METHODS: An observational retrospective study was performed. One hundred and six women with gestational diabetes and twin pregnancy and 166 twin controls who delivered viable fetuses > 24 weeks were included. Impact of maternal pre-pregnancy BMI, smoking habit, method of conception, chorionicity, gestational age at delivery, mode of delivery and hypertensive complications were also analysed. The effect of maternal hyperglycaemia and metabolic control in gestational diabetes pregnancies was assessed. RESULTS: Gestational hypertension and pre-eclampsia were significantly higher in the group with gestational diabetes (21.5% vs. 6.3%, P = 0.007 and 6.2% vs. 0%, P = 0.025). There were no differences in the incidence of macrosomia (5.7% vs. 7.2%, P = 0.803), large for gestational age (10.3% vs. 13.2%, P = 0.570), small for gestational age (10.3% vs. 12.0%, P = 0.701), severely small for gestational age (6.6% vs. 7.8%, P = 0.814) or weight discrepancy (20.6% vs. 15.2%, P = 0.320) in the group with gestational diabetes compared with twin pregnancies without diabetes. There were no differences when comparing insulin-requiring gestational diabetes pregnancies and twins without diabetes for any of the neonatal weight outcomes. There was no relationship between third trimester HbA1c and neonatal birthweight or infant birthweight ratio. CONCLUSION: Gestational diabetes did not increase the risk of macrosomia or weight discrepancy of twin newborns. Furthermore, glycaemic control did not influence the rate of any of the weight outcomes in our study population. In twin pregnancies, gestational diabetes was associated with a higher risk of gestational hypertension and pre-eclampsia.

The role of new immunosuppressive drugs in nonmelanoma skin cancer in renal transplant recipients.

INTRODUCTION: Nonmelanoma skin cancer (NMSC) is the most common malignancy in patients who have received a solid organ transplant. Multiple factors are involved in the onset of posttransplant NMSC. OBJECTIVES: To analyze the relationship between new immunosuppressive drugs and the onset of NMSC in renal transplant recipients. METHOD: This was a combined retrospective and prospective observational study in which we studied 289 patients who received a kidney transplant between January 1996 and December 2010 at Hospital Universitario Doctor Peset in Valencia, Spain. RESULTS: Seventy-three patients (25.2%) developed 162 NMSCs over a median follow-up of 72 months. There were no statistically significant differences in the onset of NMSC on comparing different induction therapy strategies involving monoclonal and polyclonal antibodies. NMSCs occurred less frequently in patients treated with mammalian target of rapamycin (mTOR) inhibitors than in those treated with other immunosuppressive regimens, although the differences were not statistically significant. Three of 5 patients with recurrent NMSC who were switched from calcineurin inhibitors to mTOR inhibitors developed additional NMSCs despite the change. CONCLUSIONS: Induction therapy with monoclonal and polyclonal antibodies in renal transplant recipients is not associated with an increased risk of NMSC. While mTOR inhibitors are associated with a lower risk of posttransplant NMSC, it remains to be determined whether a switch to these drugs is useful in the management of patients who develop multiple NMSCs.

Diagnosis of acute cortical necrosis in renal transplantation by contrast-enhanced ultrasound: a preliminary experience.

PURPOSE: To evaluate the use of contrast-enhanced ultrasound (CEUS) for diagnosis of cortical necrosis in renal allografts. MATERIALS AND METHODS: We reviewed the medical records and imaging studies of five patients who underwent emergency transplantectomy and a histological diagnosis of cortical necrosis in the period between May 2009 and May 2011. US examinations included initially B-mode and color Doppler and then contrast-enhanced ultrasound with low mechanical index after injection of 2.4 ml of a second generation echo-signal enhancer. Renal transplant vascularization was evaluated during a period of 4 minutes including arterial, corticomedullary and nephrographic phases. Radiologic-pathologic correlation was obtained after transplantectomy in all cases. RESULTS: Five patients with an age range between 30 and 48 years. Post-transplant color Doppler ultrasound showed decreased renal parenchymal vascularization and difficulty to find the spectral waveforms with resistive indexes greater than 0.7 in 4 of 5 patients. CEUS showed enhancement of the main arteries, followed by the enhancement of medullary pyramids, but with an unenhanced peripheral cortical continuous band viewed in all phases, a similar finding to the peripheral rim sign, pathognomonic of cortical necrosis on CT or MRI. The pathologic assessment showed violet kidneys macroscopically with hemorrhagic foci in the outer cortical that drew a well-defined band, findings agreed with CEUS findings. CONCLUSION: CEUS can show the typical peripheral rim sign in cases of cortical necrosis allowing a reliable and fast diagnosis of this condition and it could obviate further imaging studies or biopsy, allowing an earlier decision of nephrectomy.

Coexistence of two different pseudohypoparathyroidism subtypes (Ia and Ib) in the same kindred with independent Gs{alpha} coding mutations and GNAS imprinting defects.

BACKGROUND: Pseudohypoparathyroidism (PHP) defines a rare group of disorders whose common feature is resistance to the parathyroid hormone. Patients with PHP-Ia display additional hormone resistance, Albright hereditary osteodystrophy (AHO) and reduced Gsalpha activity in easily accessible cells. This form of PHP is associated with heterozygous inactivating mutations in Gsalpha-coding exons of GNAS, an imprinted gene locus on chromosome 20q13.3. Patients with PHP-Ib typically have isolated parathyroid hormone resistance, lack AHO features and demonstrate normal erythrocyte Gsalpha activity. Instead of coding Gsalpha mutations, patients with PHP-Ib display imprinting defects of GNAS, caused, at least in some cases, by genetic mutations within or nearby this gene. PATIENTS: Two unrelated PHP families, each of which includes at least one patient with a Gsalpha coding mutation and another with GNAS loss of imprinting, are reported here. RESULTS: One of the patients with GNAS imprinting defects has paternal uniparental isodisomy of chromosome 20q, explaining the observed imprinting abnormalities. The identified Gsalpha coding mutations include a tetranucleotide deletion in exon 7, which is frequently found in PHP-Ia, and a novel single nucleotide change at the acceptor splice junction of intron 11. CONCLUSIONS: These molecular data reveal an interesting mixture, in the same family, of both genetic and epigenetic mutations of the same gene.

[Diagnosing neoplasia in a kidney transplant unit]. / Diagnóstico de neoplasias en una consulta de trasplante renal.

BACKGROUND AND AIM: Cancer is one of the major causes of death with functioning allograft among renal transplant patients. The increasing age of patients in the waiting list has derived in a higher risk of cancer in this population. The aim of this study was to analyze the incidence of cancer in the waiting list and kidney transplant patients. METHODS: Between November/1996 and November/2007 we assisted 825 patients in the outpatient renal transplant clinic, 467 were transplanted, 120 remained in the waiting list and 238 have been removed from the waiting list or died. RESULTS: During this period, 97 malignancies were diagnosed, 33 of 32 kidney transplant candidates and 64 of 62 renal transplant patients. The comparative analysis between this two groups showed that candidates had higher frequency of solid organ tumours compared with a higher incidence of skin cancer in transplanted patients. Mean time between transplant and cancer diagnosis was 42.6 +/- 32.7 months, 48% of malignancies were diagnosed within the first three years postransplant. When comparing kidney transplant patients with and without cancer diagnosis, the formers were older and had worse patient survival at five years. Allograft survival was similar for both groups. CONCLUSIONS: we want to emphasize the extreme importance of a detailed screening in the renal transplant candidates and transplanted patients due to a higher incidence of malignancies in this population.

Treatment of renal transplant failure.

INTRODUCTION: Among graft failures beyond months, we performed progressive reduction and complete withdrawal of immunosuppressive drugs and steroids over a period of 6 months. PATIENTS AND METHODS: We analyzed the treatment and complications associated with all late allograft failures in 34 patients (8.19%) out of 415 patients transplanted from November 1996 to November 2006. RESULTS: In 21 patients (61.8%), the progressive reduction of immunosuppressive treatment was effective and well tolerated; however, in 13 patients (38.2%) there was rejection of the allograft at 10.74 +/- 8.95 months (0.77-34.80) after the failure. With the reintroduction of these drugs, the rejection was controlled in seven patients, but in the other six we had to embolize the allograft, which had to be repeated in one case. Embolization was well tolerated, but in one case there was migration of one coil to the femoral artery. One patient treated with drug withdrawal experienced emphysematous pyelonephritis after repeated urinary infections, requiring a nephrectomy. Thirteen (38.2%) of the patients with late failures have been admitted for a second transplant; five of them showed HLA sensitization. CONCLUSIONS: Conservative treatment with progressive withdrawal of immunosuppression was effective and well tolerated in two-thirds of the patients with late renal allograft failure, but one-third of the patients rejected the graft and needed allograft embolization. Infection of the graft and HLA sensitization can complicate the course of these patients.

Risk factors and prognosis for proteinuria in renal transplant recipients.

INTRODUCTION: Proteinuria in renal transplant recipients has been recognized as a risk factor of progression of chronic allograft nephropathy and for cardiovascular disease, the main causes of transplant failure. PATIENTS AND METHODS: We analyzed the risk factors for persistent proteinuria (>0.5 g/day) among 337 kidney allograft recipients with a minimum follow-up of 6 months, among a series of 375 transplants performed during a decade, as well as their association with allograft and patient survivals. Patients with proteinuria greater than 0.5 g/d were treated with angiotensin-converting enzyme inhibitors (ACEI) and/or angiotensin-receptor blockers. RESULTS: After a mean follow-up of 53.35 +/- 52.63 months, 68 patients (20.17%) had persistent proteinuria greater than 0.5 g/d. Female patients (P = .012), body mass index (BMI) >25 (P = .008), pretransplant HLA sensitization (P = .039), and delayed graft function (DGF; P = .001) were associated with proteinuria. Induction treatment with antithymocyte globulin (P = .030) and treatment with tacrolimus instead of cyclosporine (P = .046) were associated with an increased risk of proteinuria. Multivariate analysis confirmed the independent value of DGF (RR = 2.23; 95% confidence interval [CI] 1.22 to 4.07; P = .009) and BMI >25 (RR = 1.968; 95% CI 1.05 to 3.68; P = .035) to predict postransplant proteinuria. The mean values of serum creatinine (P = .000) and systolic blood pressure (P < .05) were persistently higher from the early stages after transplantation in the proteinuric group. Graft survival at 5 years was 69% among patients who developed proteinuria and 93% in those without proteinuria (P = .000), with no differences in patient survival (P = .062). CONCLUSION: Proteinuria in renal transplant recipients was related to immunological and nonimmunological factors, some of which, such as hypertension and obesity could be modifiable. Proteinuria in renal transplant recipients predicted a worse allograft survival despite of intensive treatment of hypertension including ACEI/angiotensin-receptor blockers.

Benefits derivated from late steroid withdrawal in renal transplant recipients.

Because corticosteroids have adverse metabolic effects, inducing bone-mineral imbalance and contributing to infections among renal transplant recipients, many withdrawal trials have been attempted to reduce adverse events and improve quality of life. We retrospectively analyzed the safety and efficacy of late steroid withdrawal, after the first posttransplant year, among a selected group of kidney allograft recipients. In 42 low immunological risk allograft recipients, among 382 patients transplanted during a decade, corticosteroids were progressively reduced and completely withdrawn. The evolution of clinical and biochemical parameters after the withdrawal were analyzed. Corticosteroid withdrawal was performed as a mean of 52.16 +/- 28.41 months posttransplant, with subsequent follow-up without steroid treatment of 18.13 +/- 16.11 months. Comparing the most recent evaluation with the data previous to steroid withdrawal, patients showed a significant decreases in diastolic pressure (P = .039), total cholesterol (P = .000), and low-density lipoprotein cholesterol levels (P = .039), but not in triglyceride levels (P = .33). Body weight did not change (P = .77), but increased fasting glucose levels were noted (P = .03), in absence of new diagnosed diabetes mellitus. A significant reduction in cyclosporine Neoral (P = .01) or tacrolimus doses were detected (P = .01). At the last visit, serum creatinine in the whole group remained stable (P = .06). Only five patients showed an increase in serum creatinine more than 20% (from 1.44 +/- 0.41 to 1.94 +/- 0.45 mg/dL P = .04) and proteinuria did not increase (P = .94). No patient was diagnosed with a rejection episodes or required corticosteroid resumption. Graft and patient survivals were 100% at the end of follow-up. In conclusion, our data showed that late corticosteroid withdrawal in renal transplant recipients of low immunological risk is safe and is followed by an improvement in their metabolic profile and in blood pressure.

Calcineurin inhibitor reduction based on maintenance immunosuppression with mycophenolate mofetil in renal transplant patients: POP study.

Since calcineurin inhibitors (CNI) have been introduced, they have become the cornerstone of immunosuppression for renal transplant patients, but their cardiovascular and neurological toxicities, and primarily their renal toxicity, have brought about an increased effort to find combinations of immunosuppressants that are either CNI-free or that use minimum doses of these drugs. The weight of immunosuppression therefore lies with drugs that have a better toxicity profile. The POP observational transverse study including 213 renal transplant patients was designed to study CNI minimization strategies. The mean time of transplant evolution to the time of reduction was 9.9 +/- 11.8 months. The acute rejection rate to the start of reduction was 9.4%. Almost all the patients were undergoing treatment with CNI + mycophenolate mofetil (MMF) + steroids in the immediate posttransplantation period. When reduction was chosen, all patients were undergoing treatment with MMF (mean dose at the start of reduction = 1490.7 +/- 478.0 mg/d). Among the cohort, 66.7% of patients were being treated with tacrolimus (mean C0 levels 13.3 +/- 6.6 ng/mL) and 33.3% with cyclosporine (mean C0 levels 192.2 +/- 94.0 ng/mL; mean C2 levels 1097.5 +/- 457.6). The main reasons for withdrawal were nephrotoxicity (55.9% of the cases), as well as prevention of adverse effects (21.6%). The mean target CNI dose reduction was 41.4% +/- 21.45% in the tacrolimus group and 28.6 +/- 10.0% in the cyclosporine group. In conclusion, CNI toxicity, primarily renal toxicity, makes reduction of these drugs based on the use of full MMF doses an alternative to manage renal transplant patients.

Effect of overweight on kidney transplantation outcome.

INTRODUCTION: Obesity is a prevalent problem in renal transplant recipients that is followed by reduced graft and patient survivals. Because the prevalence of overweight (OW) is increasing in the renal transplant population, we studied the influence of OW on graft and recipient evolution. PATIENTS AND METHODS: We analyzed a series of 337 patients with renal allografts having a mean follow-up of 53.4 +/- 30.6 months. We excluded 39 patients obese at transplantation. We compared the evolution of 134 OW patients (45.5%), and 160 patients (54.4%) with a body mass index <25 (NW group). RESULTS: OW patients were older (P = .000) with a higher prevalence of hypertension (P = .028), left ventricular hypertrophy (P = .014), and dyslipidemia (P = .001). They had received kidneys from older donors (P = .019). OW patients showed a higher incidence of acute tubular necrosis (ATN) (P = .006), without a higher incidence of acute rejection episodes (P = .756). Postransplant diabetes mellitus was more frequent (P = .000), and systolic blood pressure (P < .05), total cholesterol (P < .05), and tryglicerides were higher (P < .05) in the OW group. Serum creatinine at 6 months (P = .007) and proteinuria >0.5 g/24 hours, (P = .023) were higher among the OW group. Graft survival was not different between groups, but patient survival was lower in the OW group (P = .002). A logistic regression analysis showed that the recipient age (RR: 5.243) and the presence of OW (RR: 1.100) were independent prognostic factors for patient death. CONCLUSIONS: OW was a common situation among renal transplant candidates. It was associated with worse cardiovascular and metabolic profiles. OW patients showed worse allograft function and lower patient survival. A major effort must be exerted to avoid excessive weight gain, particularly among those OW at transplantation.

Renal function in patients with cadaveric kidney transplants treated with tacrolimus or cyclosporine.

INTRODUCTION: Renal function predicts graft survival in kidney transplant patients. This study compared the 2-year evolution of renal function in patients treated with cyclosporine or tacrolimus in combination with mycophenolate mofetil (MMF) and prednisone. METHODS: We studied 1558 cadaveric renal transplant recipients from 14 Spanish hospitals between January 2000 and December 2002. Of these, 1168 were treated with tacrolimus and 390 with cyclosporine. The primary efficacy endpoint was long-term renal function. Renal function was measured by serum creatinine and glomerular filtration rate (GFR) by creatinine clearance calculated from the Cockcroft-Gault formula. This report summarizes the 2-year results. RESULTS: At 24 months the tacrolimus group showed significantly better serum creatinine (1.5 +/- 0.7 vs 1.8 +/- 0.8 mg/dL, P < .001) and GFR (60.5 +/- 20.9 mL/min vs 47.9 +/- 10.0, P < .001) than the cyclosporine group. Additionally, recipients with ideal graft donors (23.5 +/- 2.8 vs 24.0 +/- 2.9 years) had a better serum creatinine at 2 years (1.23 +/- 0.2 vs 1.5 +/- 0.4 mg/dL, P < .05). Multivariate analysis showed that tacrolimus was an independent factor associated with better renal function: odds ratio 1.6, 95% confidence interval (1.2 to 2.2), P < .001. CONCLUSIONS: Patients with a renal transplant treated with tacrolimus in combination with MMF and prednisone displayed better renal function at 2 years than those who received cyclosporine.

[Seasonal perodicity in vascular access thrombosis for haemodialysis]. / Ritmo estacional en la trombosis del acceso vascular para hemodiálisis.

Different studies have shown that some clinical events, particularly cardiovascular and thrombotic events, show a regularity in its appearance. The aim of our study was to analyse the possible existence of seasonal periodicity in the incidence of the vascular access thrombosis in patients on chronic haemodialysis. Prospectively, we collected information of 164 patients with 250 episodes of vascular access thrombosis referred to our hospital from january 1995 to december 1999. An ANOVA test for comparison of the means, and a time series analysis were performed. During the five year study the consecutive number of thrombosis were 43, 57, 55, 59 and 36. When the different seasons were analysed, the cumulative number of events in summer during the study period were 91, a significant increase compared to spring, autumn, and winter (54, 54, and 51, respectively; p<0.001). Time series analysis confirmed that thrombolic events during summer showed an increased incidence over the mean (p<0.001), and it occurred every year. The same results were obtained when the PTFE grafts were analyzed separetely (july RR 2.62, p=0.002; august, RR 2.37, p=0.04), but not with the arteriovenous fistulae. In conclusion, this study showed a seasonal periodicity of vascular access thrombosis, with a PTFE graft. Although the causes were unknown, these data alert us on the convenience of an increased attention to the vascular access during the summer months in order to prevent its thrombosis.

Transplant renal artery stenosis: association with acute vascular rejection.

BACKGROUND: Transplant renal artery stenosis, the prevalence of which varies from 2% to 12%, is an important cause of hypertension and allograft dysfunction. We sought to determine the clinical characteristics of this disorder, assessing, predisposing factors, establishing treatment options, and examining patient outcomes. PATIENTS AND METHODS: Among 321 renal allograft recipients between November 1996 and December 2004, six patients were identified with this finding. We analyzed their clinical data before and after treatment compared with the 315 recipients face of the disorder. RESULTS: The six patients with the disorder were diagnosed within the first year (2 to 8 months; median 5.5 months). All patients displayed renal dysfunction, peripheral edema, and new-onset or uncontrolled hypertension at presentation. Abnormal Doppler findings were observed in 5 (83.3%) patients. The hemodynamically significant stenosis was successfully treated with percutaneous transluminal angioplasty (PTA) in all six. However, 3 (50%) patients displayed recurrent stenosis requiring a second PTA. The mean serum creatinine level decreased from a pre-PTA value of 4.4 +/- 1.8 mg/dL to a 1-month post-PTA value of 2.2 +/- 0.5 mg/dL (P = .027). Patients had no significant improvement in mean systolic and diastolic pressure. Vascular acute rejection episodes were more frequent among the affected than the control group (3/6; 50% vs 18/315; 5.7%; P < .001). No differences were found in age, sex, donor type, etiology of renal disease, immunosuppression, acute tubular necrosis, acute cellular rejection, cold ischemia time, or HLA matching. CONCLUSION: Transplant renal artery stenosis is a common cause of hypertension and renal allograft dysfunction. Acute vascular rejection is associated with this disorder.

Erythropoietin treatment in the sixth posttransplant month as a prognostic factor for renal allograft survival.

The purpose of this work was to assess the prognostic value of the need for erythropoietin (EPO) treatment at 6 months after transplantation. We retrospectively reviewed the outcomes of 143 consecutive cadaveric kidney transplants performed between January 2000 and April 2004, functioning at 6 months postransplantation. Patients were divided into two groups: group EPO6m (n = 24) received EPO treatment in the sixth month, and a control group (n = 119) did not receive EPO. Renal function deterioration (RFD) was considered to be a sustained decrease in creatinine clearance (CrCl) greater than 20% between the sixth month postransplant and the last visit. Mean follow-up was 38 +/- 16 months. The mean ages of the donor (57 +/- 9 vs 49 +/- 12 years; P = .001) and the recipient (59 +/- 12 vs 47 +/- 17 years; P = .000) were greater in the EPO6m group. Delayed graft function (83% vs 48%; P = .001) was more frequent in the EPO6m group. At 6 months after transplantation the EPO6m group showed lower hemoglobin (11.52 +/- 1.71 vs 13.32 +/- 1.69 g/dL; P = .000), higher serum creatinine (2.31 +/- 0.72 vs 1.65 +/- 0.53 mg/dL; P = .000), lower CrCl (33.53 +/- 10.83 vs 53.6 +/- 17.58 mL/min; P = .000), and similar proteinuria. RFD was more common in the EPO6m group (38% vs 10%; P = .026), with a different pattern of evolution of CrCl (-0.098 +/- 0.176 vs +0.093 +/- 0.396 mL/min/mo, P = .000). Multivariate analysis demonstrated that treatment with EPO at 6 months was the only predictor of RFD (RR 4.46; 1.58 to 12.58; P = .005). The need for EPO at 6 months postransplant was a good predictor of later renal allograft deterioration, more sensitive than serum creatinine or proteinuria.

Posttransplant diabetes mellitus in renal allograft recipients: A prospective multicenter study at 2 years.

The purpose of this study was to investigate the incidence and risk factors for the development of diabetes mellitus after kidney transplantation (PTDM). A total of 1783 nondiabetic renal allograft recipients transplanted from January 2000 to December 2002 were included. Diabetes was diagnosed following American Diabetes Association criteria. While 1276 patients were treated with tacrolimus (Tac), mycophenolate mofetil (MMF), and steroids, 507 patients received cyclosporine-ME (CsA), MMF, and steroids. PTDM incidence at 6, 12, and 24 months was 14.2%, 12.8%, and 13.3%, respectively. Cumulative incidence during the follow-up was 21.6%. Only 121 of the diabetic patients (47.6%) at 6 months remained diabetic at 24 months. Furthermore, 60 patients of 116 patients on insulin at 6 months (51.7%) remained on treatment at 24 months. The cumulative incidence of PTDM was similar in the two immunosuppressive treatments (19.7% on CsA-MMF vs 22.3% on Tac-MMF; P = NS). However, at 24 months, 14 of 50 diabetic patients on CsA-MMF (28%) and 74 of 161 patients on Tac-MMF (45.9%) were on insulin treatment (P < .05). By Cox regression analysis, age older than 60 years (RR 1.61; 95%CI 1.28-2.04; P < .001), body mass index (BMI) > 30 kg/m2 at transplantation (RR 1.66; 95%CI 1.27-2.16; P < .001), and immunosuppression with Tac (RR 1.30; 95%CI 1.02-1-66; P = .033) were associated with PTDM. In conclusions, the incidence of PTDM at 24 months in immunosuppressive protocols including MMF is about 22%, and it is associated with older age, increased BMI, and immnunosuppression with Tac.

[Chronological aggregation of subcutaneous mycosis in renal transplant recipients]. / Agregación cronológica de cuatro casos de micosis subcutánea invasiva en receptores de trasplante renal.

We present four cases of subcutaneous invasive mycosis in renal transplant recipients that happened in our Unit during a period of eight months. The Microbiology Department did not find any fungi when they studied possible reservoirs and vectors for transmission. We speculate about the reasons of this chronological aggregation. We discuss the treatment that we used for these infections.

[Renal transplantation with positive crossmatch]. / Trasplante renal en presencia de una prueba cruzada positiva.

INTRODUCTION: Lymphocytotoxic antibodies reduce the expectancy of renal transplantation due to the increased risk of a positive crossmatch. MATERIAL AND METHODS: We analyzed the evolution of eight kidney transplants performed in our unit in presence of a positive crossmatch with historical T and/or B lymphocyte positive crossmatches. RESULTS: Mean panel reactivity was 76,6 +/- 25,7% (r: 22-100%), been higher than 75% in six patients. Six patients were recipients of a second or third transplant. Immunosuppression consisted of quadruple therapy including induction with thymoglobuline. Five patients had delayed graft function, and one had primary non-function of the graft. One patient lost her graft due to chronic allograft nephropathy in the second year postransplantation. Six patients maintained a good renal function (serum creatinine 1,2 +/- 0,5 mg/dl, proteinuria 0,20 +/- 0,34 g/day). CONCLUSION: Renal transplantation in presence of a positive cross-match with historical serum and T lymphocytes and/or B lymphocytes, was followed by a satisfactory graft survival.

Longitudinal study of plasma lipoproteins and hormones during pregnancy in normal and diabetic women.

Plasma lipoproteins were studied longitudinally at the 1st, 2nd, and 3rd trimester of gestation and at postpartum and postlactation in 12 age-matched PGDM women, 9 GDM women, and 12 healthy control subjects. FPG and HbA1c were higher in every case in PGDM women than in control subjects, whereas in GDM patients, glucose was augmented only after parturition. FFA and beta-hydroxybutyrate levels were higher in both PGDM and GDM patients than in control subjects during gestation but not after parturition. Total TGs and VLDL, LDL, and HDL TGs increased with gestational time in the three groups and declined at postpartum, and although total cholesterol and VLDL, LDL, and HDL cholesterol followed a similar trend, their rise was less pronounced, and the decline after parturition was slower than that of the TGs in the three groups, with no difference among them. The VLDL TG/cholesterol ratio declined in the three groups at the 3rd gestational trimester, whereas in both LDL and HDL, the TG/cholesterol ratio, but not the cholesterol/phospholipid ratio, increased during gestation in the three groups, indicating a specific enrichment of TGs in these particles. The increase in apoA-I and apoB with gestation was parallel to the respective changes in HDL and LDL cholesterol and, again, no difference was observed between the three groups. Plasma levels of beta-estradiol, progesterone, and prolactin increased sharply with gestation and declined at postpartum in the three groups, but absolute values of beta-estradiol and prolactin, at the three trimesters of gestation, were lower in PGDM patients, but progesterone levels were lower than controls in GDM women only at the 3rd trimester. (ABSTRACT TRUNCATED AT 250 WORDS)

Plasma molecular forms of gastrin, neurotensin and somatostatin in pregnancy and gestational diabetes after an oral glucose load or a mixed meal.

At present the physiological role of gastrin, neurotensin and somatostatin in pregnancy and gestational diabetes is scarcely known. We have measured their different molecular forms in plasma of six female controls, six normal pregnant (NP) women and six gestational diabetic (GD) women under basal conditions and 30 min after an oral glucose load (100 g) and a liquid mixed meal in order to study if their alteration could contribute to the impaired glucose tolerance in GD. Total basal concentrations of neurotensin and somatostatin were higher in GD than in controls and NP, and no change was found after the glucose load or mixed meal in GD. Neurotensin-1-13 was the main molecular form of all neurotensins at basal time in the three groups studied, being higher in GD in comparison with controls and NP. Somatostatin-1-14 was the predominant molecular form in controls and GD under basal conditions and did not show any change any change after stimuli. In NP, somatostatin-1-14 showed a significant increase following both kinds of stimuli. Total gastrin concentrations in NP and GD showed a significant increase after the glucose load, which was not observed in controls. Gastrin-17 was the main molecular form at basal time and 30 min post-stimuli in GD but not in NP and controls. We suggest that the basal elevation of neurotensin and somatostatin levels could contribute to the impaired glucose tolerance observed in gestational diabetes, as well as to the lack of post-stimuli responses for neurotensin and somatostatin in GD.(ABSTRACT TRUNCATED AT 250 WORDS)

[Post-transplant diabetes mellitus associated with acute hepatitis C virus infection in a renal transplant recipient]. / Diabetes mellitus postrasplante asociada a hepatitis aguda por virus de la hepatitis C en un receptor de injerto renal.

There are some controversial reports about the pathogenic role of hepatitis C virus infection on diabetes mellitus in renal graft recipients. We report a case of a renal transplanted who developed diabetes mellitus post-transplantation during an acute hepatitis C virus infection. We discuss the multifactorial etiology of post-transplant diabetes mellitus, and the possible interaction between tacrolimus and an acute virus C infection on its pathogenesis.