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Y Saint-Hillier

Publications and source records attributed to Y Saint-Hillier.

At least 19 recordsLinked to original sources
PubMed2004

T-cell flow-cytometry crossmatch and long-term renal graft survival.

Flow cytometry crossmatch (FCXM) is a more sensitive technique than classical complement-dependent cytotoxicity (CDC) for the detection of donor-directed antibody before renal transplantation. Nevertheless, the role of FCXM in predicting long-term survival of kidney grafts is still unclear. The purpose of our study was to evaluate the impact of a positive T-cell FCXM (T-FCXM) on long-term kidney allografts outcome. Of the 184 consecutive kidney transplantations performed in our center between 1 January1991 and 15 November 1996 a FCXM, performed concurrently to the pre-transplant CDCXM, was available for 170 patients. The CDCXM was negative in all recipients. Among these recipients, 12 (7.1%) had a positive T-FCXM. These patients were not different from patients with a negative T-FCXM for donor and recipient age, sex, frequency of second transplantation, number of human leukocyte antigen matches or mismatches. Frequency of immunized patients was higher in kidney recipients with a positive FCXM (58.3% vs. 24.7%; p=0.02, chi-square test). Survival analysis revealed that kidney graft outcome was better in negative T-FCXM recipients (p=0.03), while patient survival was not statistically different. Our results suggest that a positive pre-transplant T-FCXM despite a negative CDCXM is associated with an impaired long-term graft survival in renal allotransplantation.

Age Factors↗
PubMed1998

Mycophenolate mofetil-induced villous atrophy.

Mycophenolate mofetil (MMF) is a new immunosuppressant developed for the prevention and treatment of acute renal rejection after transplantation. Diarrhea is the most frequent side effect observed during treatment with MMF. Its pathogenic mechanisms remain unknown. We describe a case of severe diarrhea due to villous atrophy in a renal transplant recipient during treatment with MMF. The patient was free of symptoms before MMF. Villous atrophy disappeared a few months after MMF withdrawal.

Adult↗
PubMed1998

Mycophenolate mofetil in renal transplant recipients with cyclosporine-associated nephrotoxicity: a preliminary report.

BACKGROUND: There is a great concern over cyclosporine (CsA) nephrotoxicity in renal transplant recipients, and the effects of conversion from CsA to azathioprine (AZA) remain controversial. Large studies have demonstrated that mycophenolate mofetil (MMF), the morpholinoethyl ester of mycophenolic acid, is superior to AZA as a posttransplant immunosuppressant. METHODS: Six patients with isolated biopsy-proven CsA nephrotoxicity were converted from CsA-AZA to MMF. RESULTS: Mean follow-up was 12+/-2 months. No patient experienced acute rejection. The mean serum creatinine concentration decreased from 225+/-58 to 159+/-66 micromol/L (P<0.0005). Hyperlipidemia and blood pressure improved after CsA withdrawal. CONCLUSION: In a selected transplant population with biopsy-proven CsA nephrotoxicity, CsA withdrawal with a concomitant switch from AZA to MMF seems to be safe and allows a significant improvement of renal function.

Aged↗
PubMed1998

Impaired renal graft survival after a positive B-cell flow-cytometry crossmatch.

BACKGROUND: The clinical and immunological relevance of a positive B-cell flow-cytometry (B-FCXM) crossmatch in renal transplantation is still controversial. METHODS: We retrospectively analysed 145 consecutive cadaveric renal transplantations performed from May 1991 to September 1995 in our institution. All grafts were transplanted following a negative IgG T-cell complement-dependent cytotoxicity crossmatch (T-CDCXM). Concomitantly to CDCXM, B-cell and T-cell FCXM were performed and results were expressed as a mean fluorescence index (FI). Two groups were compared: 116 recipients grafted with a negative B-FCXM vs a group of 19 patients grafted with a positive B-FCXM. RESULTS: The two groups were similar for length of cold ischaemia, donor and recipient's age and degree of HLA mismatching. The proportion of patients with pre-transplant anti-HLA class I antibodies or a retransplantation was significantly increased in the positive B-FCXM group vs the negative B-FCXM group. Recipient survival at 48 months was not significantly different in the two groups. However, graft survival at 12 and 48 months was significantly poorer in the positive B-FCXM than in negative B-FCXM (68% vs 90% at 12 months: P = 0.007, and 57% vs 79% at 48 months: P = 0.02). Within the positive B-FCXM group, no differences were found in pre-transplant anti-HLA class I or II alloimmunization as well as retransplantation frequency between the patients who lost their graft and the patients who did not. CONCLUSION: Our results suggest that a pretransplant positive B-FCXM is associated with an impaired long-term graft survival in renal allotransplantation.

Antibodies↗
PubMed1997

No trend toward a spontaneous improvement of hyperparathyroidism and high bone turnover in normocalcemic long-term renal transplant recipients.

Although hyperparathyroidism is a common feature in renal transplant recipients, the long-term course of parathyroid hormone (PTH) secretion in these patients is not well established, and the actual contribution of PTH to posttransplant bone disease remains incompletely understood. Therefore, we studied calcium-regulating hormones and serum osteocalcin, as a marker of bone remodeling, in 82 normocalcemic renal transplant recipients with good renal function who had received a graft 6 to 73 months previously and in 82 healthy subjects matched for age and sex. In all subjects, fasting serum and 24-hour urinary samples were collected. The transplant recipients had excessive PTH secretion (serum PTH, 6.9 +/- 0.5 pmol/L in recipients v 3.0 +/- 0.1 pmol/L in healthy subjects; P < 0.001) and high bone turnover (osteocalcin, 16.6 +/- 0.8 microg/L v 8.0 +/- 0.3 microg/L; P < 0.001). (Values are mean +/- SEM.) In addition, transplant recipients had a slightly higher ionized calcium than the healthy subjects, providing definite evidence of an inappropriate PTH secretion in renal transplant recipients. Furthermore, in subgroups of 25 recipients and 25 healthy controls matched for creatinine clearance, the results superimposed those obtained in the whole groups, suggesting that excessive PTH secretion and high bone turnover in renal transplant recipients did not merely reflect the moderately reduced renal function of some recipients. In the whole group of transplant recipients, PTH correlated positively with osteocalcin (r = 0.40; P < 0.001), suggesting that PTH contributes at least partly to posttransplant bone disease. Conversely, there was no correlation between serum PTH or osteocalcin and the delay from grafting. Therefore, our results provide no evidence for a spontaneous improvement of either persistent hyperparathyroidism or high bone turnover in normocalcemic long-term renal transplant recipients.

Adolescent↗
PubMed1997

Lack of increased urinary calcium-oxalate supersaturation in long-term kidney transplant recipients.

Nephrolithiasis is uncommon after kidney transplantation. However, calcium (Ca) supplementation, which has been proposed as a treatment of post-transplant osteopenia, might increase calciuria and bolster Ca stone formation. Therefore, in 24-hour urine of 82 normocalcemic long-term renal transplant recipients (RT) and in 82 healthy subjects (HS), we assessed some Ca nephrolithiasis risk factors and the Ca-salt saturation estimated by the ion-activity product index (AP) and relative supersaturation (RS). In RT, calciuria was lower (mean +/- SD, 3.20 +/- 2.25 vs. 4.61 +/- 1.71 mmol/day; P < 0.001), urinary volume higher (2.41 +/- 0.83 vs. 1.39 +/- 0.53 liter/day; P < 0.001), oxaluria higher (419 +/- 191 vs. 311 +/- 79 mumol/day; P < 0.001) and citraturia lower (1.40 +/- 1.36 vs. 3.77 +/- 1.36 mmol/day; P < 0.001) than in HS. As a result, Ca-oxalate supersaturation was lower in RT than HS (AP, 1.07 +/- 0.69 vs. 2.07 +/- 1.13, P < 0.001; and RS, 0.62 +/- 0.26 vs. 0.94 +/- 0.21, P < 0.001), and was similar in subgroups of RT (N = 37) and HS (N = 37) matched for urinary volume, demonstrating that even without any larger urinary volume, Ca-oxalate saturation was not higher in RT than HS, and suggesting that opposite changes in Ca and oxalate in RT likely canceled their effects on lithogenic risk. In RT which had similar urinary pH and phosphate (P) than HS, Ca-P supersaturation was lower than in HS for brushite (AP, 3.25 +/- 6.67 vs. 6.01 +/- 4.85, P < 0.001; RS, -0.33 +/- 0.76 vs. 0.48 +/- 0.53, P < 0.001) and octacalcium phosphate (RS, -0.95 +/- 0.72 vs. 0.21 +/- 0.85, P < 0.001), and similar for apatite. Finally, fasting calciuria and calciuric response to a single oral Ca load were similar in RT (N = 19) and HS (N = 8). Together, these results argue strongly against a higher risk of Ca stone formation in RT than HS, even in case of Ca supplementation.

Adult↗
PubMed1997

Effect of losartan on haemoglobin concentration in renal transplant recipients--a retrospective analysis.

PURPOSE OF STUDY: To evaluate the effect of the angiotensin II type 1 receptor antagonist, losartan, on post-transplant erythrocytosis. METHODS: We retrospectively analyzed the influence of losartan therapy on haemoglobin levels of renal transplant recipients. Twenty-eight patients who received losartan therapy to control hypertension were divided into two groups. In 10 patients, losartan therapy was initiated after treatment with ACE inhibitors which was discontinued due to adverse reactions (Group A). Group B consisted of 18 patients treated with losartan who had never received ACE inhibitors. RESULTS: There was no difference in mean haemoglobin concentration and haematocrit between the two groups before the onset of losartan therapy. In Group B, mean haemoglobin concentration and haematocrit decreased from 137 +/- 20 g/l and 0.4 at the start of losartan therapy to 120 +/- 16 g/l (P < 0.0005) and 0.35 (P < 0.0005), respectively 3 months later. In Group A, neither haemoglobin nor haematocrit differed between the onset of losartan therapy and the end of the study. Serum creatinine increased from 158 mumol/l +/- 78 to 172 mumol/l +/- 80 in Group B (P < 0.005), but remained stable in Group A. Plasma protein concentrations remained stable in each group and there was no change in diuretic therapy during the study. CONCLUSION: Our study suggests that losartan therapy decreases haemoglobin in renal transplant recipients.

Adult↗
PubMed1995

Lack of evidence that cyclosporine treatment impairs calcium-phosphorus homeostasis and bone remodeling in normocalcemic long-term renal transplant recipients.

Since the effects of cyclosporine on mineral and bone metabolism are controversial, we studied calcium regulating hormones, calcium-phosphorus (Ca-P) metabolism, and bone remodeling, assessed by serum osteocalcin, in long-term renal transplant recipients (RT). Forty-seven normocalcemic patients with good renal function receiving cyclosporine (CT, n = 27) or not (NC, n = 20) were studied at baseline and after an oral Ca load. CT and NC had similar age, daily dose of steroids, GFR level, and duration of transplantation. Baseline evaluation included 24-hr urinary Ca, P, TRP, TmP/GFR, fasting serum intact PTH, 1,25-(OH)2D, 25OHD, osteocalcin, Ca, and P. Subjects of the two groups had excessive secretion of PTH, tubular P wasting, and high serum osteocalcin level, as is usual in RT. However, there was no difference between CT and NC regarding any baseline variable. Ten CT and ten NC, matched for duration of transplantation and serum PTH level, ingested 1g Ca to achieve an acute dynamic study of PTH secretion and Ca-P metabolism. In both CT and NC, this Ca load caused the same decreases in serum PTH (P < 0.001), NcAMP (P < 0.05), and urinary P (P < 0.001) and the same increases in serum and urinary Ca (P < 0.001), and in both TmP/GFR and TRP (P < 0.001). These results strongly suggest that cyclosporine treatment had no significant effect on calcium-regulating hormone secretion, P-Ca metabolism, and bone remodeling level. We therefore consider that cyclosporine is unlikely to have any prominent role in the abnormalities of bone endocrine and mineral metabolism that are common in long-term kidney recipients.

Administration, Oral↗
PubMed1995

Acute oral calcium load decreases parathyroid secretion and suppresses tubular phosphate loss in long-term renal transplant recipients.

Persistent hyperparathyroidism and impaired tubular reabsorption of phosphate (P) are common after kidney transplantation. In order to assess the suppressibility of these abnormalities, we studied the effects of a single oral calcium (Ca) load (1 g) in 7 healthy subjects (HS) and in 14 normocalcemic long-term renal transplant recipients with good renal function (RT). In HS and RT, serum and urinary Ca were similar at baseline, and increased (p < 0.001) to the same extent after Ca ingestion. Serum parathyroid hormone (PTH) and nephrogenic cAMP (NcAMP) levels were higher at baseline in RT than HS (mean +/- SEM; respectively, PTH 7.8 +/- 0.8 vs. 3.5 +/- 0.6 pmol/l, p < 0.001, and NcAMP 24.8 +/- 2.3 vs. 13.9 +/- 2.3 nmol/l GFR, p < 0.01). After Ca, PTH (p < 0.001) and NcAMP (p < 0.01) decreased markedly in both RT and HS. Maximal changes in PTH and NcAMP were larger in RT than HS (PTH - 3.3 +/- 0.4 vs. -2.1 +/- 0.03 pmol/l, p < 0.01, and NcAMP -18.2 +/- 3.3 vs. -8.1 +/- 2.6 nmol/l GFR, p < 0.05). Although PTH levels remained significantly higher in RT than HS from baseline to the end of the study (p < 0.001), PTH decreased to the normal range in RT after Ca load. Moreover, NcAMP reached similar values in RT and HS after Ca (16.0 +/- 3.3 vs. 13.2 +/- 2.8 nmol/l GFR at the end of the survey, NS).(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1992

[Discovery of an undetected thrombosis of the artery of the graft during kidney transplantation. Value of resolution of the obstruction and high pressure kidney washing].

During the transplantation of a kidney, we have discovered an undetected recent thrombosis of the renal artery of the graft, which was revealed after clamp removal by infarction of the kidney. We performed an immediate arterial desobstruction and a secondary high flow rate washing of the kidney, which allowed properly restoring the vascularity of the graft and successfully grafting it.

Female↗
PubMed1992

[Syndrome of the pyelo-ureteral junction of the graft after kidney transplantation. Apropos of 2 cases].

We report 2 cases of decompensation of a pelviureteric obstruction in a transplanted kidney. In one case, the pyeloureteral obstruction was discovered intraoperatively during grafting (cadaver kidney) and was corrected at that time. In the other case, the obstruction was decompensated one month after grafting (kidney taken from a living donor with a very discrete bilateral junction syndrome) and required surgical treatment. The procedure used in both cases was a pyelopyelic anastomosis after nephrectomy of the recipient's kidney.

Adolescent↗
PubMed1991

Soluble interleukin-2 receptors in chronic renal failure.

A depression of the general immune response in uremia is well documented, and hemodialyzed (HD) patients present deficient interleukin-2 (IL2) secretion. Since soluble IL2 receptors (SIL2R) could affect the immune response through interaction with circulating immune cells, we studied the potential relationship between SIL2R concentration and lymphocyte subsets in 44 HD patients. HD patients present lymphopenia, higher CD4/CD8 ratio. CD16 counts and SIL2R concentrations than controls. A significant negative correlation was found between SIL2R concentration and lymphocyte count (p less than 0.01), and between SIL2R concentration and T4/T8 ratio (p less than 0.01). An increase of SIL2R concentration due to abnormal T cell preactivation in HD patients with nonreused cuprophan membranes could perhaps contribute to cell immunity impairment through IL2 binding and inhibition of T cell activation.

CD4-CD8 Ratio↗
PubMed1989

[Hypercalcemia: diagnostic and therapeutic procedures].

The management of hypercalcaemia is easy for a trained medical group, but it is difficult and confusing for others. The most tricky treatment is that severe acute hypercalcaemia, although biphosphonates, which are very effective agents, are now available. In 60 p. 100 of the cases, hypercalcaemia is due to a malignant disease, but the so-called benign causes, such as parathyroid adenoma, must not be missed since acute hyperparathyroidism may be life-threatening.

Humans↗