PP066. Renal artery stenosis revealed by an early-onset preeclampsia: A series of 6 cases.

INTRODUCTION: Renovascular hypertension (HT) due to an renal artery stenosis (RAS) is uncommon. Therefore, it is actually very rare to diagnose RAS during a pregnancy; very few cases have been published. OBJECTIVES: We report here a series of RAS diagnosed after an early-onset preeclampsia (EOPE). METHODS: We reviewed the files of women who had been seen at our Obstetric Medicine Clinic after an EOPE over a 19-year period. EOPE was defined by occurrence of proteinuria ⩾0.30g/d before 32 weeks of gestation (WG) with permanent HT ⩾ 140mmHg for systolic pressure and/or 90 for diastolic pressure. RESULTS: Six cases of RAS complicated with EOPE were included in the study (see table). Mean age at the time of EOPE was 27.8 years (24-35), mean term of appearance of EOPE was 22.8 WG (10-31) and mean parity was 1.5 (1-3). HELLP syndrome was found in one case, no patient had renal failure. Fetal death had occurred in three cases (two medical terminations of the pregnancy and one in utero fetal death). The mean birth weight of surviving neonates was 1235g (1070-1410). Physical examination revealed an abdominal bruit in two cases. RAS was suggested with duplex sonography in two cases, and evidenced with conventional percutaneous contrast angiography in five cases. RAS was secondary to a fibromuscular dysplasia in five cases and to atheromatosis in one case. Angioplasty was performed during conventional angiography procedure in four cases. During the follow-up, two women had a subsequent uneventful pregnancy. Restenosis was diagnosed in one case five years after angioplasty. PE: Pre-eclampsia. WG : Weeks of Gestation. MTP: Medical Termination of Pregnancy. IUFD : Intra-Uterine Fetal Death. RAS : Renal Artery Stenosis. NA : Not Applicable CONCLUSION: This series shows the necessity of exploring every case of HT with clinical features suggestive of secondary HT. Moreover, after an adverse obstetrical event, mainly after an EOPE and namely if it had occurred very early (before 28 WG), renovascular HT must be excluded before a subsequent pregnancy. Doppler ultrasound of the renal arteries is the first imaging modality to use since it is simple and noninvasive. Magnetic resonance angiography or computed axial tomography are also convenient. However, conventional percutaneous contrast angiography remains the gold standard for diagnosis of RAS, since it shows directly renal arteries and allows intervention in the same time with angioplasty and/or stent placement.

Cytomegalovirus prophylaxis with intravenous polyvalent immunoglobulin in high-risk renal transplant recipients.

Cytomegalovirus (CMV) seronegative renal allograft recipients (R-), particularly those with a graft from a CMV-seropositive donor (D+), are at high risk for primary CMV infection. CMV resistance to antiviral oral therapy is an emerging problem in renal transplantation, prompting development of new prophylactic strategies. We retrospectively studied the 1-year posttransplantation incidence of CMV infection in high-risk renal transplant recipients, in whom polyvalent intravenous immunoglobulins (IVIg) were used as prophylaxis. Forty R- patients received immunoprophylaxis by polyvalent IVIg (0.25 g/kg weekly for 8 weeks, starting on the operative day). CMV serological tests remained negative in eight patients (20%). Eight patients (20%) had asymptomatic CMV infection while 24 (60%) developed CMV syndrome and were treated with gancyclovir (10 mg/kg/day intravenously for 3 weeks). None had CMV disease or opportunistic infection. Six patients (15%) had biopsy-proven acute rejection, which followed CMV syndrome in three cases. One-year renal allograft and patient survivals were 95% and 97.5%, respectively. Mean serum creatinine level was 124 +/- 33 micromol/L at 1 year. Clinical tolerance of IVIg was excellent, without any episode of acute renal failure. Polyvalent IVIg provides effective prophylaxis in renal transplant recipients at high risk for CMV infection and is associated with excellent 1-year allograft survival. Because of their immunomodulatory functions, IVIg may have a beneficial effect on the incidence of acute and chronic rejection and allograft survival. A randomized prospective study is required to evaluate long-term effects of CMV prophylaxis with polyvalent IVIg compared to antiviral agents in renal transplant recipients.

[Role of the time of administration of calcium carbonate (before or during mealtime) in the control of hyperphosphatemia in patients on maintenance hemodialysis]. / Rôle du moment d'administration du carbonate de calcium (avant ou pendant les repas) sur le contrôle de l'hyperphosphorémie des patients hémodialysés chroniques.

UNLABELLED: A study has claimed that at equal elemental calcium dose, CaCO3 was not less but equally efficient in controlling predialysis hyperphosphatemia as calcium acetate provided both calcium salts were given five minutes before the meals instead of during the meals because the higher acidity of a fasting gastric juice would allow a better dissociation of CaCO3. To examine the point that CaCO3 is more efficient if it is taken five minutes before compared to during the meal, we performed a two month randomised cross-over trial in twelve reliable and stable patients maintained on chronic hemodialysis while their treatment and diet remained constant. Comparison of the plasma concentrations measured during the two modes of administration showed no significant difference in creatinine, urea, bicarbonate, intact-PTH. Mean (+/- SD) plasma PO4 was significantly higher (1.93 +/- 0.50 versus 1.72 +/- 0.40 mmol/l; p = 0.02) whereas corrected plasma Ca was significantly lower (2.30 +/- 0.15 versus 2.38 +/- 0.17 mmol/l; p = 0.01) when CaCO3 was given before the meals than during the meals. CONCLUSIONS: a) administration of CaCO3 before the meal decreases its efficiency in controlling hyperphosphatemia since plasma PO4 was actually slightly higher with this timing of administration; b) administration of CaCO3 before the meal is associated with significantly lower plasma corrected calcium suggesting a smaller absorption of calcium which may be an advantage but only in hypercalcemic patients; c) there is no reason other than the prevention of its hypercalcemic effect to recommend the administration of CaCO3 just before the meals than during the meals.

[Inhibition of gastric secretion by omeprazole and efficacy of calcium carbonate in the control of hyperphosphatemia in patients on maintenance hemodialysis]. / Inhibition de la sécrétion gastrique par l'oméprazole et efficacité du carbonate de calcium sur le contrôle de l'hyperphosphorémie des patients hémodialysés chroniques.

UNLABELLED: Apparent contradictions exist in the literature regarding the effect of gastric secretion inhibition on phosphatemia. In healthy adults, omeprazole has been reported to prevent the increase of plasma phosphate or of phosphaturia observed after an acute phosphate load suggesting an inhibition of phosphate absorption. In patients on chronic hemodialysis their hyperphosphatemia is associated to gastric hypersecretion but the inhibition of this latter by ranitidine in patients taking CaCO3 has been reported to increase their plasma phosphate. Because of this contradiction, we have made an open cross-over study in 16 stable and compliant patients in chronic hemodialysis taking a mean daily dose of 9.4 +/- 4 g of CaCO3 and compared their predialysis plasma concentration of phosphate, calcium, protides, bicarbonates, intact PTH, urea and creatine for two successive periods of two months without or with 20 mg of omeprazole. Plasma phosphate did not increased significantly with omeprazole (from 1.80 +/- 0.38 to 1.89 +/- 0.42 mmol/l) whereas plasma corrected calcium significantly decreased from 2.41 +/- 0.18 to 2.36 +/- 0.16 mmol/l (p = 0.04) and plasma bicarbonate decreased significantly from 26.7 +/- 3.5 to 25.7 +/- 3.1 mmol/l (p < 0.05). No significant change was observed in plasma creatine and urea suggesting stability of dialysis efficiency and of protein and therefore phosphate intake. CONCLUSION: These data do not support that CaCO3 efficiency as phosphate binder is decreased with inhibition of the gastric secretion by omeprazole.

[Cutaneous vasculitis after hepatitis B vaccination with recombinant vaccine in a renal transplant patient]. / Vascularite cutanée après vaccination contre l'hépatite virale B par vaccin recombinant chez une transplantée rénale.

BACKGROUND: Cutaneous vasculitis is a known complication of hepatitis B vaccination with recombinant vaccine. CASE REPORT: A renal transplant recipient with the HLD-DR4 susceptibility antigen developed histologically proven cutaneous vasculitis with serum antibodies after vaccination with anti-hepatitis B recombinant vaccine. The skin manifestation, evolved favorably after discontinuation of the immunization and bed rest. DISCUSSION: This case suggests that anti-hepatitis B vaccination with recombinant vaccine can produce cutaneous vasculitis in renal transplant recipients. The vaccination strategy in this population should be revisited.

Renal osteodystrophy in dialysis patients: diagnosis and treatment.

This article reviews the clinical, biological, radiological, and pathological procedures and their respective indications for the practical diagnosis of the following various histological patterns of renal osteodystrophy: osteitis fibrosa due to parathyroid hormone (PTH) hypersecretion: osteomalacia or rickets due to native vitamin D deficiency and/or aluminum overload; and adynamic bone disease (ABD) due to aluminum overload and/or PTH secretion oversuppression. Our advice regarding bone biopsy is to restrict it to patients with symptoms and hypercalcemia, especially those who have been previously exposed to aluminum. In other cases, we propose relying merely on the determination of the plasma concentrations of calcium, protide, phosphate, bicarbonate, intact PTH, aluminum, 25(OH)D3, and alkaline phosphatase (total and bony if hepatic disease is associated) to choose the appropriate treatment. Because of the danger of the desferrioxamine treatment necessary to chelate and remove aluminum, the suspicion of aluminic bone disease (osteomalacia or ABD) will always be confirmed by a bone biopsy. In the case of nonaluminic osteomalacia, correction of the vitamin D deficiency by native vitamin D or 25(OH)D3, and of the calcium deficiency and acidosis by alkaline salts of calcium and if necessary sodium bicarbonate are sufficient to cure the disease. In the case of nonaluminic ABD, the stimulation of PTH secretion by the discontinuation of 1alpha hydroxylated vitamin D and the induction of a negative calcium balance during dialysis by decreasing the calcium concentration in the dialysate will allow an increase of the CaCO3 dose to correct for hyperphosphatemia without inducing hypercalcemia. For hyperparathyroidism, i.e., plasma intact PTH levels greater than two- or four-fold the upper limit of normal levels (according to the absence or presence of previous aluminum exposure), the treatment will consist in increasing the CaCO3 dose to correct for hyperphosphatemia together with a decrease of the calcium concentration in the dialysate if the dose of CaCO3 is so high that it induces hypercalcemia. When the hyperphosphatemia has been corrected and there is still a low or normal corrected plasma calcium level, 1alpha(OH)D3 in an oral bolus 2 or 3 times a week should be given at the minimal dose of 1 microg. When the PTH level stays above 400 pg while hypercalcemia occurs and hyperphosphatemia persists, surgical subtotal parathyroidectomy is recommended or the injection of calcitriol into the big nodular hyperplastic parathyroid glands under sonography control in high surgical risk patients. Special recommendations are given for children.

Inhibition of gastric secretion by omeprazole and efficiency of calcium carbonate on the control of hyperphosphatemia in patients on chronic hemodialysis.

Contradictions exist in the literature regarding the effect of gastric secretion inhibition on phosphate absorption. In healthy controls, omeprazole would decrease the hyperphosphatemia or the hyperphosphaturia induced by an acute phosphate load, suggesting an inhibition of phosphate absorption. In chronic hemodialysis patients, gastric hypersecretion is associated with hyperphosphatemia, but inhibition of gastric hypersecretion by ranitidine in those receiving calcium carbonate (CaCO3) as a phosphate binder would paradoxically exacerbate their hyperphosphatemia. Because of these conflicting observations, we performed an open crossover study on 16 chronic stable hemodialyzed patients with a daily mean intake of 9.4+/-4 g of CaCO3, and we compared the plasmatic predialysis levels of phosphate, calcium, protides, bicarbonates, intact parathyroid hormone (PTH), urea, and creatininemia during 2 successive periods of 2 months, the first one without omeprazole and the second one with 20 mg omeprazole intake in the morning. Phosphatemia increased with omeprazole but not significantly from 1.80+/-0.38 to 1.89+/-0.42 mM whereas corrected calcemia decreased significantly (p = 0.04) from 2.41+/-0.18 to 2.36+/-0.16 mM as did bicarbonatemia from 26.7+/-3.5 to 25.7+/-3.1 mM (p < 0.05). No change in creatininemia or in blood urea was observed, suggesting the stable efficiency of dialysis as well as the stable intakes of protein and therefore of phosphate during the two study periods. In conclusion, inhibition of gastric secretion by omeprazole increases the plasmatic phosphate predialytic level but in a nonsignificant way. This increase may be explained by a slight but significant concomitant decrease of calcemia and bicarbonatemia. These results do not support the phosphate binding efficiency of CaCO3 being decreased by the inhibition of gastric acid secretion.

Role of calcium carbonate administration timing in relation to food intake on its efficiency in controlling hyperphosphatemia in patients on maintenance dialysis.

A study has claimed that at an equal elemental calcium dose, CaCO3 was not less but equally as efficient in controlling predialysis hyperphosphatemia as calcium acetate, provided both calcium salts were ingested 5 min before meals instead of during meals because the higher acidity of the fasting gastric juice would allow for better dissociation of CaCO3. However, this study did not directly demonstrate that the efficiency of CaCO3 in controlling hyperphosphatemia was actually greater when it was administered before a meal than during a meal. To examine this point, we performed a 3 month randomized crossover trial in 12 reliable and stable patients maintained on chronic hemodialysis. Their plasma concentrations of calcium, protein, phosphate, bicarbonate, urea, and creatinine were measured before the first dialysis of each week and the amount of intact parathyroid hormone (PTH) at the beginning and at the end of each of the 3 months. Comparison of the plasma concentrations measured during the 2 modes of administration showed no significant differences in creatinine, urea, bicarbonate, or intact PTH. The mean (+/-SD) plasma concentration of PO4 was not significantly lower (1.88+/-0.50 vs. 1.74+/-0.41 mM) whereas the corrected level of plasma Ca was significantly lower (2.30+/-0.17 vs. 2.38+/-0.16 mM; p < 0.04) when CaCO3 was given before meals than during meals. In conclusion, the administration of CaCO3 before a meal does not increase its efficiency in controlling hyperphosphatemia because the level of plasma PO4 was actually slightly higher with this timing of administration whereas the comparison of the creatinine and urea levels suggested a stability of phosphate intake and the comparison of the PTH and bicarbonate levels suggested the stability of osteolysis and of the transcellular membrane shift of phosphate. Also, administration of CaCO3 before a meal is associated with significantly lower plasma corrected calcium, suggesting less absorption of calcium, which may be an advantage but only in hypercalcemic patients. There is no reason other than the prevention of its hypercalcemic effect to recommend the administration of CaCO3 just before meals rather than during meals.

Invasive versus non-invasive diagnosis of renal bone disease.

At present, bone histomorphometry remains the gold standard for the diagnosis of the various types of renal bone disease. In the search for a non-invasive method of diagnosis, biochemical serum markers of bone remodelling, in addition to serum intact parathyroid hormone and aluminium determinations, have been proposed as the most reliable tools and are at present widely used in clinical practice. Their respective diagnostic values, as separate items and in combined analysis, are thoroughly discussed in the present review.