[Show abstract][Hide abstract] ABSTRACT: Two single-nucleotide polymorphisms (SNPs) at the calcium-sensing receptor (CASR) gene were previously associated with kidney stones in patients with primary hyperparathyroidism (PHPT): rs1501899, likely associated with a decrease in CASR expression, and Arg990Gly, causing a gain of CASR function. To evaluate the interaction of these two SNPs in the stone risk, we tested the association of stones with the genotype at both SNPs in PHPT patients and the association of rs1501899 with CASR expression as messenger RNA (mRNA) in human kidney samples.
Two hundred and ninety-six PHPT patients were genotyped at the rs1501899 and Arg990Gly SNPs. Minor allele frequency at tested SNPs was higher in PHPT stone formers relative to non-stone forming patients. PHPT patients carrying one or two copies of the minor allele at both rs1501899 and Arg990Gly (n = 16) had the maximal risk of stones (odds ratio, OR 8.3) and higher serum ionized calcium compared with homozygous patients for the wild-type allele at both SNPs. CASR expression as mRNA was measured by real time polymerase chain reaction (PCR) in normal kidney medulla samples from 109 subjects. CASR mRNA was significantly lower in medulla samples from homozygotes for the minor allele at rs1501899 than in subjects with other genotypes.
We conclude that the simultaneous presence of the minor allele at rs1501899 and Arg990Gly may amplify the kidney stone risk in PHPT patients, despite their apparently opposite effects on CASR function in the kidney.
Journal of nephrology 05/2014; · 2.02 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Background:CaSR gene is a candidate for calcium nephrolithiasis. SNPs encompassing its regulatory region were associated with calcium nephrolithiasis.Aims:To test SNPs in the CaSR gene regulatory region associated with calcium nephrolithiasis and their effects in kidney.Subjects and Methods:167 idiopathic calcium stone formers and 214 healthy controls were genotyped for four CaSR gene SNPs identified by bioinformatics analysis as modifying transcription factor binding sites. Strontium excretion after an oral load oral was tested in 55 stone formers. Transcriptional activity induced by variant alleles at CaSR gene promoters was compared by luciferase reporter gene assay in HEK-293 and HKC-8 cells. CaSR and claudin-14 mRNA levels were measured by real-time PCR in 107 normal kidney medulla samples and compared in patients with different CaSR genotype.Results:Only rs6776158 (A>G), located in the promoter 1, was associated with nephrolithiasis. Its minor G allele was more frequent in stone formers than controls (37.8% vs 26.4%, p=0.001). A reduced strontium excretion was observed in GG homozygous stone formers.Luciferase fluorescent activity was lower in cells transfected with the promoter 1 including G allele at rs6776158 than cells transfected with the A allele.CaSR mRNA levels were lower in kidney medulla samples from homozygous carriers for the G allele at rs6776158 than carriers for the A allele. Claudin-14 mRNA levels were also lower in GG homozygous subjects.Conclusion:Minor allele at rs6776158 may predispose to calcium stones by decreasing transcriptional activity of the CaSR gene promoter 1 and CaSR expression in kidney tubules.
The Journal of clinical endocrinology and metabolism 07/2013; · 6.50 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Calcium sensing receptor (CaSR) is a component of the C family of the G protein-coupled receptors. It is ubiquitously expressed in human and mammal cells but is more expressed in parathyroid glands and kidney cells. It is located on the cell plasma membrane and senses the changes of extracellular calcium concentrations. Thus, it may modify cell functions according to serum calcium levels. CaSR has a key role in calcium homeostasis because it allows parathyroid glands and kidney to regulate PTH secretion and calcium reabsorption in order to keep serum calcium concentration within the normal range. CaSR appears as an important player in the regulation of renal calcium handling and body calcium metabolism. Thus, CaSR may protect human tissues against calcium excess. In kidneys, its protective effect includes the stimulation of diuresis and phosphate retention, along with the potential prevention of calcium precipitation and deposition in kidney tubules and interstitium.
[Show abstract][Hide abstract] ABSTRACT: Single nucleotide polymorphisms (SNPs) of the calcium-sensing receptor (CASR) gene at the regulatory region were associated with idiopathic calcium nephrolithiasis. To confirm their association with nephrolithiasis, we tested patients with primary hyperparathyroidism (PHPT).
A genotype-phenotype association study.
In all, 332 PHPT patients and 453 healthy controls were genotyped for the rs7652589 (G>A) and rs1501899 (G>A) SNPs sited in the noncoding regulatory region of the CASR gene. Allele, haplotype, and diplotype distribution were compared between PHPT patients and controls, and in stone forming and stone-free PHPT patients.
The allele frequency at rs7652589 and rs1501899 SNPs was similar in PHPT patients and controls. The A minor alleles at these two SNPs were more frequent in stone forming (n=157) than in stone-free (n=175) PHPT patients (rs7652589: 36.9 vs 27.1%, P=0.007; rs1501899: 37.1 vs 26.4%, P=0.003). Accordingly, homozygous or heterozygous PHPT patients for the AA haplotype (n=174, AA/AA or AA/GG diplotype) had an increased stone risk (odds ratio 1.83, 95% confidence interval 1.2-2.9, P=0.008). Furthermore, these PHPT patients had higher serum concentrations of ionized calcium and parathyroid hormone (1.50 ± 0.015 mmol/l and 183 ± 12.2 pg/ml) than patients with the GG/GG diplotype (n=145, 1.47 ± 0.011 mmol/l (P=0.04) and 150 ± 11.4 pg/ml (P=0.049)). Using a logistic regression model, the increase in stone risk in PHPT patients was predicted by AA/AA or AA/GG diplotype, the highest tertile of serum ionized calcium values and the lowest tertile of age.
Polymorphisms located in the regulatory region of the CASR gene may increase susceptibility of the PHPT patients to kidney stone production.
European Journal of Endocrinology 03/2011; 164(3):421-7. · 3.14 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Endogenous ouabain (EO) is markedly raised in patients with chronic renal failure. As high EO induces myocardial cell hypertrophy in vitro and it is associated with left ventricular hypertrophy (LVH) in essential hypertensives and in patients with heart failure we investigated the relationship between plasma EO and LV mass and geometry in 156 end-stage renal disease (ESRD) patients. EO was measured by a specific radioimmunoassay and by mass spectrometry.
On univariate analysis, plasma EO was directly related to LV mass (r = 0.26, P = 0.001) and LV end diastolic volume (r = 0.25, P = 0.002) and these relationships held true in multiple linear regression models including a series of potential confounders. Patients with eccentric LVH (n = 41, i.e. 26%) had the highest plasma levels of EO when compared to patients with other patterns of LV geometry (P = 0.001). Furthermore, plasma EO had diagnostic value for eccentric LVH because the area under the corresponding ROC curve (68%) was significantly greater (P = 0.002) than the threshold of diagnostic indifference. In this analysis, the sensitivity was 91% and the specificity was 36%. The positive predictive value was 33% but EO had a remarkably high negative predictive value (92%) for the exclusion of eccentric hypertrophy.
In ESRD patients, plasma EO is independently associated with LV mass, LV volume and eccentric LVH. The results of this study are compatible with the hypothesis that EO is involved in alterations of LV mass in ESRD.
Journal of Internal Medicine 04/2008; 263(3):274-80. · 6.46 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Myocardial disorders are a remarkable cause of morbidity and mortality in chronic haemodialysed patients (HD). They could be favoured by alteration of cell Ca(2+) handling. In previous studies we characterized an erythrocyte Ca(2+) influx, sensitive to membrane potential and inhibited by Ca(2+) antagonists. Since its maximal influx rate was decreased in HD patients, this study investigates if Ca(2+) influx alterations are related to myocardial disorders in HD patients.
Voltage-sensitive erythrocyte Ca(2+) influx was measured in 30 healthy controls and in 53 patients (47 HD patients and six patients with left ventricular hypertrophy and normal kidney function), using fura 2. In 29 HD patients and in six healthy subjects Ca(2+) influx was also determined in the presence of parathyroid hormone (PTH) in vitro. Patients were classified according to Lown's ventricular arrhythmias classification after 24-h Holter electrocardiograph (ECG) monitoring. Forty-six patients underwent echocardiography.
Voltage-sensitive erythrocyte Ca(2+) influx was significantly reduced in HD patients. Maximal influx rate was significantly higher in HD patients of Lown's classes 3 and 4 (0.789 +/- 0.156 nmol/s, n = 8; P < 0.01) than in patients of classes 1 and 2 (0.499 +/- 0.055 nmol/s, n=15), or without ventricular arrhythmias (0.400 +/- 0.041 nmol/s, n = 24). Maximal influx rate was directly correlated to left ventricular mass index (LVM) (r = 0.353, P < 0.05). Subjects with left ventricular hypertrophy and normal kidney function displayed erythrocyte Ca(2+) influx similar to that of normal subjects. Multiple regression indicates that LVM and Ca(2+) influx were independently related to severity of arrhythmias. When added to the influx assay, PTH increased the maximal influx rate only in patients with ventricular arrhythmias.
Myocardial dysfunction and altered ventricular excitability could be related in uraemic HD patients to alterations of calcium transport, as found in the erythrocyte model. Reduced resistance to PTH could contribute to this phenomenon.
[Show abstract][Hide abstract] ABSTRACT: Platelet hyperfunction is a typical feature of the prothrombotic state that frequently complicates the natural history of diabetes. In uremia, a bleeding diathesis is present, which principally involves the primary phase of hemostasis. Thus, in patients with uremia of diabetic origin, the infrequent coexistence of two opposite alterations of hemostasis takes place. In patients with uremia, an increased incidence of cardiovascular events and related mortality is observed. This phenomenon is greatly amplified in uremia of diabetic origin. Calcium homeostasis is a critical aspect of platelet function, which has recently become available in human diseases. The aim of this study was to evaluate calcium homeostasis in platelets from patients with uremia of diabetic and nondiabetic origin.
We evaluated, by means of Fura 2, the intracellular concentration of ionized calcium ([Ca2+]i) in platelets from 18 patients with uremia of diabetic origin, 12 patients with uremia of nondiabetic origin and 16 healthy control subjects [Ca2+]i was evaluated in resting conditions and after stimulation with 0.05, 0.1, 0.5 U/ml thrombin.
Platelets from uremic patients with diabetes had higher resting [Ca2+]i than both control subjects (P = 0.01) and uremic patients without diabetes (P = 0.001). Similarly, after stimulation with thrombin, the absolute increase of [Ca2+]i was higher (P < 0.05) in platelets from uremic patients with diabetes compared with both control subjects and uremic patients without diabetes. The relative increase of [Ca2+]i was higher (P < 0.05) than normal in platelets from uremic patients after weak or intermediate strength thrombin. No correlation were present between [Ca2+]i values and other clinical and laboratory variables potentially associated with platelet hyperfunction.
Diabetes and uremia in combination further deteriorate the abnormal platelet calcium homeostasis observed in uremia.
Diabetes Care 11/1996; 19(10):1062-6. · 7.74 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: The pharmacokinetics of pidotimod ((R)-3-[(S)-(5-oxo-2-pyrrolidinyl) carbonyl]-thiazolidine-4-carboxylic acid, PGT/1A, CAS 121808-62-6) in elderly volunteers and in patients with renal failures were investigated. No differences in absorption, excretion and pharmacokinetic parameters was evident between old volunteers and the youngs of a previous work. Patients with impaired renal function showed different pharmacokinetic parameters of pidotimod in relation to different grade of kidney function. There were linear relationships between elimination half-lives and plasma levels of creatinine and urea; longer half-lives correspond to higher levels of creatinine and urea. As the half-life of the compound did never exceed 8-9 h, the data do not support any change of pidotimod administration schedule (every 24-12 h).
[Show abstract][Hide abstract] ABSTRACT: As many antihypertensive drugs have negative effects on glucose metabolism, we conducted a multicenter study to evaluate the efficacy of isradipine slow release oral (SRO) 5 mg/d in patients with hypertension and diabetes. A total of 111 patients (mean age, 56 years) with mild-to-moderate hypertension and non-insulin-dependent diabetes mellitus were enrolled. After a 15-day run-in period with placebo, they were treated with isradipine SRO 5 mg/d for 26 weeks. Enalapril 10 to 20 mg/d was added to the treatment at the end of the first 6 weeks if blood pressure (BP) was not adequately controlled (ie, diastolic blood pressure [DBP] ⩾90 mm Hg). During each study visit (every 15 days the first 6 weeks and every 30 days thereafter) casual BP and heart rate measurements were performed. At baseline and 6 and 26 weeks, noninvasive 24-hour BP monitoring was done. Mean casual BP values, which were 163/100 mm Hg at baseline, were 10 mm Hg lower at 2 weeks; at the end of the study, systolic BP had fallen by 23 mm Hg and DBP by 16 mm Hg. Analysis of the 24-hour BP profile, at 6 and 26 weeks indicated that the physiologic circadian rhythm was maintained throughout the study, although these BP values decreased over the course of the study. BP reduction was more pronounced in the daytime (7 am to 11 pm) than the nighttime (11 pm to 7 am). Heart rate remained almost unchanged at all the observation times. Side effects, related mainly to systemic vasodilation, occurred in 12 patients, only one of whom suspended the study treatment. Overall, ten patients dropped out of the study. The main blood chemistry findings remained unchanged; microalbuminuria and glycosylated hemoglobin showed a tendency to decrease, whereas blood glucose remained virtually unchanged. These results, obtained in a large series, indicate that isradipine SRO provides gradual, uniform control of BP in hypertensive diabetic patients without negative effects on the blood glucose profile.
Current Therapeutic Research 01/1995; 56(2):190-199. · 0.45 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Conventional insulin therapy does not correct the counter-regulatory abnormalities of insulin-dependent diabetes mellitus. Pancreas transplantation is an alternative therapy that restores the endogenous insulin secretion in diabetes. In this study, the effects of segmental pancreas transplantation on counter-regulation to mild hypoglycaemia were evaluated. Glucose kinetics and the counter-regulatory hormonal responses were assessed in eight insulin-dependent diabetics with end-stage renal failure who had received pancreas and kidney transplantation 1 year previously, seven diabetic uraemic subjects (candidates for combined transplantation), five patients with chronic uveitis on immunosuppressive therapy comparable to pancreas recipients and 10 normal subjects. Insulin (0.3 mU kg-1 min-1) was infused for 2 h to induce mild hypoglycaemia (plasma glucose 3.2-3.5 mmol l-1) and exogenous glucose was infused as required to prevent any glucose decrease below 3.1 mmol l-1. After transplantation, two of eight recipients had hypoglycaemic episodes reported in their medical records. During the study, hepatic glucose production was rapidly suppressed in the controls and in the patients on immunosuppression (-80 +/- 7 and -54 +/- 7%, P < 0.001 vs. basal), and rebounded to the baseline values within 1 h (-3 +/- 1 and -6 +/- 2%, P = NS vs. basal). The transplant recipients had similar suppression in the first hour (-88 +/- 8%, P < 0.001 vs. basal), but the suppression persisted in the second hour (-69 +/- 11%, P < 0.001 vs. basal) indicating a lack of glucose counter-regulatory response.(ABSTRACT TRUNCATED AT 250 WORDS)
European Journal of Clinical Investigation 11/1994; 24(11):751-8. · 3.37 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: In order to assess the combined and separate effects of pancreas and kidney transplant on whole-body protein metabolism, 9 insulin-dependent diabetic-uremic patients (IDDUP), 14 patients after combined kidney-pancreas transplantation (KP-Tx), and 6 insulin-dependent diabetic patients with isolated kidney transplant (K-Tx), were studied in the basal postabsorptive state and during euglycemic hyperinsulinemia (study 1). [1-14C]Leucine infusion and indirect calorimetry were utilized to assess leucine metabolism. The subjects were studied again with a combined infusion of insulin and amino acids, given to mimic postprandial amino acid levels (study 2). In the basal state, IDDUP demonstrated with respect to normal subjects (CON): (a) higher free-insulin concentration (17.8 +/- 2.8 vs. 6.8 +/- 1.1 microU/ml, P < 0.01) (107 +/- 17 vs. 41 +/- 7 pM); (b) reduced plasma leucine (92 +/- 9 vs. 124 +/- 2 microM, P < 0.05), branched chain amino acids (BCAA) (297 +/- 34 vs. 416 +/- 10 microM, P < 0.05), endogenous leucine flux (ELF) (28.7 +/- 0.8 vs. 39.5 +/- 0.7 mumol.m-2.min-1, P < 0.01) and nonoxidative leucine disposal (NOLD) (20.7 +/- 0.2 vs. 32.0 +/- 0.7 mumol.m-2. min-1, P < 0.01); (c) similar leucine oxidation (LO) (8.0 +/- 0.1 vs. 7.5 +/- 0.1 mumol.m-2.min-1; P = NS). Both KP-Tx and K-Tx patients showed a complete normalization of plasma leucine (116 +/- 5 and 107 +/- 9 microM), ELF (38.1 +/- 0.1 and 38.5 +/- 0.9 mumol.m-2.min-1), and NOLD (28.3 +/- 0.6 and 31.0 +/- 1.3 mumol.m-2.min-1) (P = NS vs, CON). During hyperinsulinemia (study 1), IDDUP showed a defective decrease of leucine (42% vs. 53%; P < 0.05), BCAA (38% vs. 47%, P < 0.05), ELF (28% vs. 33%, P < 0.05), and LO (0% vs. 32%, P < 0.05) with respect to CON. Isolated kidney transplant reverted the defective inhibition of ELF (34%, P = NS vs. CON) of IDDUP, but not the inhibition of LO (18%, P < 0.05 vs. CON) by insulin. Combined kidney and pancreas transplanation normalized all kinetic parameters of insulin-mediated protein turnover. During combined hyperinsulinemia and hyperaminoacidemia (study 2), IDDUP showed a defective stimulation of NOLD (27.9 +/- 0.7 vs. 36.1 +/- 0.8 mumol.m-2.min-1, P < 0.01 compared to CON), which was normalized by transplantation (44.3 +/- 0.8 mumol.m-2.min-1).
Journal of Clinical Investigation 05/1994; 93(5):1948-58. · 12.81 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Bioelectrical impedance is a technique allowing a quick, repeatable and reliable assessment of body composition. This method was applied to detect total body water (TBW), fat (FAT) and fat-free mass (FFM) in 80 normal subjects, 65 diabetic (45 insulin-dependent [IDD], 20 non insulin-dependent [NIDD]) and 34 uremic diabetic patients (20 IDD, 14 NIDD) submitted to hemodialysis three times a week. Uremic patients were tested at the end of the dialytic session. Multivariated analysis adjusted for age, sex and disease showed the following results: body mass index (BMI) increased with age (p < 0.005) and in the presence of NIDD (p < .001); TBW was lower in nephropathic patients (p < 0.05) and in the female sex (p < 0.0001); FFM decreased with age (p < 0.005), female sex (p < 0.0001) and in nonuremic NIDD (p < 0.001). Correspondingly FAT increased with age (p < 0.005), female sex (p < 0.0001) and in nonuremic NIDD (p < 0.001). Sixteen uremic subjects, randomly selected from both IDD and NIDD groups, tested at the beginning and at the end of the same hemodialytic session, showed a significant decrease of TBW which corresponded to the correction of their overhydratation. In our patients uremia does not seem to influence the nutritional status and the bioelectrical analysis could be applied to determine the real dry weight in hemodialyzed diabetic patients.
[Show abstract][Hide abstract] ABSTRACT: In this study, pancreas transplantation is used as a clinical model of pancreas denervation in humans. To assess the role of innervation on the feedback autoinhibition of insulin secretion, we studied four groups of subjects--group 1: 16 patients with combined pancreas and kidney transplantation (plasma glucose = 5.1 mM, HbA1c = 6.4%, creatinine = 86 mM); group 2: 8 patients with chronic uveitis on the same immunosuppressive therapy as transplanted patients (12 mg/day prednisone, 5 mg.kg-1.day-1 CsA); group 3: 4 uremic, nondiabetic patients in chronic hemodialysis; group 4: 7 normal, nondiabetic control subjects. The following means were used to study the groups: 1) a two-step hyperinsulinemic euglycemic clamp (insulin infusion rate = 1 mU and 5 mU.kg-1.min-1); and 2) a 0.3 mU.kg-1.min-1 hypoglycemic clamp (steady-state plasma glucose = 3.1 mM). Basal plasma-free IRI (84 +/- 6, 42 +/- 12, 72 +/- 12, and 30 +/- 6 pM in groups 1, 2, 3, and 4, respectively), basal C-peptide (0.79 +/- 0.05, 0.66 +/- 0.05, 3.04 +/- 0.20, and 0.59 +/- 0.06 nM in groups 1, 2, 3, and 4, respectively), and glucagon (105 +/- 13, 69 +/- 4, 171 +/- 10, and 71 +/- 5 pg/ml in groups 1, 2, 3, and 4, respectively) were increased in groups 1 and 3 with respect to groups 2 and 4 (P < 0.01). During euglycemic hyperinsulinemia, plasma C-peptide decreased by 45, 20, and 44% in groups 2, 3, and 4, respectively, but showed no significant change from the basal in patients with transplanted pancreases.(ABSTRACT TRUNCATED AT 250 WORDS)
[Show abstract][Hide abstract] ABSTRACT: Total acquired lipoatrophic diabetes (LD) is characterized by muscle mass hypertrophy, non-ketotic hyperglycaemia and insulin resistance with respect to glucose and lipid metabolism. To assess whether the defect in insulin action extends to leucine/protein metabolism, a female subject (age=33 years; body weight=44 kg; HbAlc=9.5%) with LD was studied twice: in study I we used a three-step euglycaemic hyperinsulinaemic clamp (40, 80 and 200 mU m–2 min–1) combined with [3-3H]glucose and [1-14C]leucine infusions along with indirect calorimetry. In study II we used a 40 mU m–2 min–1 euglycaemic hyperaminoacidaemic (plasma leucine 160 mol/l) hyperinsulinaemic clamp. Five controls were also studieD. In the basal state the patient with LD had plasma leucine (130 mol/l), isoleucine (63), valine (169) and phenylalanine levels (48) comparable to those of the controls. Basal hepatic glucose production (3.2 vs 2.00.2 mg kg–1 min–1), endogenous leucine flux (ELF=45.4 vs 401 mol m–2 min–1) and non-oxidative leucine disposal (NOLD=37.2 vs 341 mol m–2 min–1) were increased in the patient with LD, while basal leucine oxidation (LO=8.2 vs 6.02 mol m–2 min–1) was similar in LD and controls. Following the three-step insulin infusion, insulin-stimulated glucose metabolism was defective in the subject with LD (glucose oxidation=60%, 50%, and 52% of controls; non-oxidative glucose disposal =39%, 34% and 30% of controls at 40, 80 and 200 mU m–2 min–1 respectively). The decrease of leucine, isoleucine, valine and phenylalanine, as well as the suppression of ELF, LO and NOLD was defective in the subject with LD at each insulin step. In vitro studies demonstrated a defect in receptor insulin binding on erythrocytes, the absence of anti-insulin receptor antibodies and the presence of insulin antibodies in the serum of the patient with LD. Following combined hyperaminoacidaemia/hyperinsulinaemia a similar stimulation of protein synthetic rate (20 vs 30%) was demonstrated in the patient with LD and controls respectively. In conclusion the patient with LD shows a reduced insulin sensitivity and a reduced maximal response to insulin in both glucose and protein metabolism. The present data support the hypothesis that in LD the defect in insulin action is both at the receptor and post-receptorial sites. The patient with LD showed a normal stimulation of protein synthesis under combined hyperinsulinaemic/hyperaminoacidaemic conditions. Our results may explain the muscle mass hypertrophy in LD.
[Show abstract][Hide abstract] ABSTRACT: The aim of our study was to evaluate the effects of haemodialysis, kidney transplantation and simultaneous kidney and pancreas transplantation on survival of diabetic subjects and on kidney function. 40 Type 1 (insulin-dependent) diabetic patients received a kidney transplantation: in 31 cases the kidney was transplanted simultaneously to a pancreas graft from the same donor (KP group), while in 9 cases the pancreas was not available (K group). 44 uraemic Type 1 (insulin-dependent) diabetic patients on dialysis and in waiting list for kidney transplantation, constituted the control group (HD group). Patient survival rate 1, 3 and 5 years following transplantation was better in KP group (93%, 89%, 89%, respectively) and in K group (88%, 88%, 73%, respectively) and in HD group (88%, 62%, 51%, respectively). Kidney graft survival at 1, 3 and 5 years post-transplant was better in KP group (93%, 72%, 72%, respectively) than in K group (76%, 61%, 31%, respectively). 1 year after transplantation, patients of the KP group who had lost the pancreas for technical reasons (thrombosis) were included in the K group so as to evaluate the effect of the transplanted pancreas on long-term patient and kidney survival. Patient survival rate in the KP group (17 patients) at 2 and 4 years was 100%, while at the same intervals it was 78% in the K group (13 patients). Kidney graft function rate at 2 and 4 years was 93% in the KP group (17 grafts) and 54% and 27% respectively in the K group (14 grafts).(ABSTRACT TRUNCATED AT 250 WORDS)
[Show abstract][Hide abstract] ABSTRACT: The aim of this study carried out on 33 uremic diabetic patients submitted to chronic hemodialytic treatment was to assess the kind of complications related to the vascular approach used as well as their short- and long-term incidences. Out of the 46 anastomoses prepared, 39 were arteriovenous fistulae according to Brescia-Cimino and 7 were PTFE grafts. The actuarial survival rate was 88%, 79%, and 63% after one, two and four years, respectively. The most frequent compliance was thrombosis. Our experience demonstrates that the distal arteriovenous fistula may be considered a valid vascular access for hemodialysis also in diabetic patients.