Le trafic d’organe, le tourisme de transplantation et le commerce de greffons ont fait l’objet d’un sommet à Istanbul au printemps 2008 aboutissant à la Déclaration d’Istanbul dont le but était de condamner et de faire cesser ces pratiques [1]. En collaboration avec l’Agence de la biomédecine, une enquête nationale auprès des médecins des centres de transplantation rénale avait été réalisée entre 2008 et 2012. Nous avons réactualisé, en 2017, les données médicales de cette cohorte, notamment les complications et la survie des greffons et des patients et évalué le nombre de nouveaux patients transplantés en France dans le cadre du tourisme de transplantation depuis 2012. Nous avons identifié 59 patients dont 41 hommes et 18 femmes, qui ont été transplantés à l’étranger à partir de rein de donneurs rémunérés, entre 1985 et 2017. Onze patients ont été transplantés avant 2000, 38 entre 2000 et 2008 et 10 après 2008. La durée médiane de suivi était de 5,6 années (3,7 ; 12,1). La créatinine moyenne était à 111 ± 49,2 μmol/L à la date du dernier contrôle. Quatre patients ont présenté des complications chirurgicales (deux sténoses de l’artère du greffon, une infection de cicatrice et un hématome). Les infections représentaient la complication la plus fréquente puisqu’elles ont concerné 34 patients. Parmi eux, il y eu une séroconversion VHC, sept réactivations VHC, deux réactivations VHB, une coréactivation VHC et VHB, deux tuberculoses dont une disséminée, trois pneumocystose, une aspergillose, deux infections fongiques. Seize patients ont présenté un rejet dont 7 rejets humoraux et un rejet mixte. Quatorze patients (23,7 %) ont perdu leur greffon. Onze patients (18,6 %) sont décédés. Le tourisme de transplantation en France reste un phénomène marginal. Le nombre de patients transplantés avec un greffon provenant d’un donneur rémunéré est en nette régression depuis la conférence d’Istanbul en 2008. Ces pratiques sont associées à une importante morbi-mortalité [2]. Néanmoins, chez les patients n’ayant pas présenté de complications, la fonction du greffon demeure satisfaisante à long terme.

L’hyperparathyroïdie hypercalcémique post-transplantation (HPTR) est une anomalie métabolique fréquente. Même si des données indirectes semblent indiquer que l’HPTR aurait des conséquences négatives sur l’évolution de la transplantation (FDR de néphrocalcinose microscopique [1], et valeur de PTH pré-greffe prédictive de la perte de greffon [2]), un effet direct du statut parathyroïdien sur la fonction rénale n’a jamais été démontré à ce jour. Quatre cent deux patients ont bénéficié d’une exploration du métabolisme minéral et osseux, et d’une mesure du DFG (clairance du 51-CrEDTA) à 3 et 12 mois post-greffe. L’HPTR était définie à M3 par une PTH > 65 pg/mL et une hypercalcémie ionisée (> 1,29 mM). Trente-deux patients ont été exclus de l’étude (prise de cinalcalcet ou parathyroïdectomie post-greffe). Parmi les 370 patients étudiés, le DFG a été mesuré respectivement à 3 et 12 mois à 50,7 et 48,6 mL/min/1,73 m2, non significativement différents. Quatre-vingt-deux patients présentaient une HPTR à M3 et ont été comparés aux 288 restants (CT). Les seuls facteurs associés à une HPTR sont la prise de cinacalcet en dialyse (57 % groupe HPTR vs 25 %, p < 0,001) et le caractère non préemptif de la greffe (13 % vs 1 %, p 0,006). À la différence du groupe CT, la présence d’une HPTR à M3 est associée à une perte de fonction du greffon rénal (−0,6 mL/min, p = 0,39 vs −3,0 mL/min, p < 0,05) et à un DFG plus bas à M12 (49,9 ± 16,0 mL/min/1,73 m2 vs 44,1 ± 13,8, p = 0,003). En analyse multivariée, les facteurs associés à un DFG du greffon inférieur à 45 mL/min/1,73 m2 à M12 sont l’HPTR (OR 1,9 ; p = 0,03), un donneur décédé (OR 2,6 ; p = 0,01), l’âge du donneur (OR 1,04 ; p = 0,001), la Protéinurie à M3 (OR 1,01 ; p = 0,004), et la survenue d’un rejet (OR 2,2 ; p = 0,06). L’HPTR à M3 constitue donc un FDR de moins bonne fonction du greffon rénal à un an de greffe, indépendamment des facteurs de risque déjà identifiés. Ceci incite à optimiser la prise en charge des troubles minéraux et osseux avant la TR. Les conséquences de l’HPTR sur la fonction du greffon rénal rendent nécessaires des essais thérapeutiques pour évaluer si la prise en charge thérapeutique de l’HPTR annule le risque de déclin accéléré du DFG.

Le terme de microangiopathie thrombotique (MAT) définit un syndrome regroupant différentes pathologies caractérisées par l'association d'une anémie hémolytique mécanique, d'une thrombopénie périphérique, et de défaillances d'organe de sévérité variable. Parmi ces pathologies, on distingue le purpura thrombotique thrombocytopénique (PTT), forme particulièrement grave pouvant aboutir à une défaillance multiviscérale, et le syndrome hémolytique et urémique (SHU), où l'atteinte rénale est prédominante. Un syndrome de MAT peut également s'observer au cours des situations suivantes : HELLP syndrome (Hemolysis, Elevated Liver enzymes, Low Platelet count), cancers, greffes, infection par le virus de l'immunodéficience humaine, syndrome catastrophique des antiphospholipides, ou coagulation intravasculaire disséminée sévère. De nouveaux mécanismes physiopathologiques des MAT ont été récemment élucidés et ouvrent la voie à une meilleure classification nosologique. Ainsi, le PTT est caractérisé par un déficit héréditaire ou acquis en une enzyme plasmatique (ADAMTS13) qui régule la taille du facteur Willebrand, une protéine indispensable à l'agrégation plaquettaire. Ce déficit aboutit à la formation spontanée de thrombi plaquettaires dans la microcirculation sanguine à l'origine de l'ischémie multiviscérale. Dans le SHU, on distingue des formes associées à une infection par des bactéries entéropathogènes (SHU épidémique ou postdiarrhéique), et des formes associées à des anomalies de certaines protéines du complément (facteur H, facteur I, et CD46/MCP-1) (SHU atypique). Les MAT représentent une urgence diagnostique et thérapeutique. Le traitement de première intention repose sur les échanges plasmatiques. D'autres thérapeutiques (immunosuppresseurs, traitement spécifique d'une pathologie associée, mesures de réanimation) s'avèrent parfois nécessaires selon le contexte. Le pronostic global des MAT reste difficile à établir compte tenu de l'hétérogénéité des différentes entités cliniques concernées.Thrombotic microangiopathies (TMA) consist in a syndrome characterized by a mechanical hemolytic anemia, a consumption thrombocytopenia and multivisceral ischemia. Thrombotic thrombocytopenic purpura (TTP) is a multisystemic form of TMA which prognosis may be severe; hemolytic uremic syndrome (HUS) is a TMA which renal involvement is predominant. A TMA syndrome may also be observed in association with other clinical contexts such as the HELLP (Hemolysis, Elevated Liver enzymes, Low Platelet count) syndrome, cancers, organ transplantations, Human Immunodeficiency Virus infection, catastrophic antiphospholipid syndrome or severe disseminated intravascular coagulation. The pathophysiology for TMA has been recently better elucidated, allowing a more appropriate classification of the various forms of this syndrome. TTP is characterized by a severe enzymatic deficiency of the specific von Willebrand factor (VWF)-cleaving protease named ADAMTS13; this deficiency which is either acquired via autoantibodies or inherited via ADAMTS13 gene mutations, leads to the accumulation of hyperadhesive forms of VWF in plasma inducing the spontaneous formation of platelet thrombi in the microvasculature. Pathophysiology for HUS may involve either verotoxin-producing bacteria (post-diarrheal HUS) or inherited complement proteins deficiencies (factor H, factor I, CD46/MCP-1). Diagnosis and therapeutic management of TMA both remain an emergency. The first intention treatment is plasmatherapy (mainly plasma exchanges) while immunosuppressive drugs, specific treatment for an underlying disease and intensive care procedures may be required as a function of the clinical context. The global prognosis of TMA remains difficult to establish considering the heterogeneity of the different forms of this syndrome.

Notre travail a visé à évaluer l’anxiété, la dépression et le trouble de stress post-traumatique post-maladie à coronavirus 2019 (COVID-19) et à identifier les facteurs associés.Nous avons mené une étude transversale durant la période allant du 1er mars 2021 au 15 mai 2021 à l’unité COVID-19 du service de pneumologie à l’hôpital Hédi Chaker Sfax (Tunisie). L’évaluation psychométrique a été réalisée à l’aide des échelles « Hospital Anxiety and Depression Scale », « Impact of Event Scale-Revised » et « Self-Reported Instrument Measuring COVID-19 Related Stigma ».Notre étude a inclus 154 patients. La prévalence de l’anxiété, la dépression et le trouble de stress post-traumatique étaient de 24,7 %, 11 % et 13,6 % respectivement. Nous avons constaté une association entre la dépression et le sexe féminin (p = 0,025), l’atteinte gastro-intestinale (p = 0,002) et la stigmatisation (p = 0,002). Nous avons trouvé une association entre l’anxiété et le niveau scolaire (p = 0,034), ainsi qu’entre l’anxiété et l’asthénie (p = 0,032).L’anxiété, la dépression et le trouble stress post-traumatique étaient indépendants de la majorité des caractéristiques de la maladie, notamment la sévérité de la COVID-19.Our study aimed to assess anxiety, depression, and post-traumatic stress disorder in post coronavirus disease 2019 (COVID-19) and identify associated factors.Our study is a descriptive and analytical cross-sectional study carried out during the period from March 1 to May 15th 2021 on patients who were hospitalized and discharged from the COVID-19 unit in the pneumology department at the Hédi Chaker hospital in Sfax (Tunisia). Patients who met all of the following criteria were included: aged 18 and over; having a diagnosis of COVID-19 by polymerase chain reaction (PCR) and/or by CT scan; monitored at the COVID-19 unit and who their clinical conditions did not require intensive care; survivors after 3 months of discharge; and having given their informed and informal consent to participate in the study.Our study included 154 patients. The prevalence of anxiety, depression and post-traumatic stress disorder was 24.7%, 11% and 13.6% respectively. We found an association between depression and female gender (P = 0.025), gastrointestinal involvement (P = 0.002) and stigma (P = 0.002). We found an association between anxiety and grade level (P = 0.034), and between anxiety and asthenia (P = 0.032).Anxiety, depression, and post-traumatic stress disorder were independent of the majority of disease characteristics including the severity of COVID-19.

L’accès vasculaire pour les épurations extra-rénales aiguës (EER) se fait essentiellement grâce aux cathéters veineux centraux. La plupart des cathéters d’EER actuels sont en poly-uréthane, mais des cathéters en silicone sont également disponibles. Les deux déterminants principaux du débit sanguin autorisé par un cathéter d’EER sont le diamètre du cathéter et la position de son extrémité interne. La voie sous-clavière est fortement déconseillée chez un patient à risque d’insuffisance rénale chronique. La voie fémorale semble associée à un risque de bactériémie plus important que la voie jugulaire interne. Les cathéters fémoraux nécessitent une longueur d’au moins 20 cm pour permettre un débit sanguin régulier sans recirculation excessive. En général, les dysfonctions aiguës sur un cathéter sont liées à une anomalie de positionnement alors que les dysfonctions tardives sont liées à une thrombose interne. La prévention des thromboses internes est fondée sur une injection vigoureuse de sérum salé après chaque utilisation, suivie du placement d’un verrou d’anticoagulant (héparine concentrée ou citrate).Acute catheters for renal replacement therapy (RRT) are used for immediate vascular access in ICU patients with acute renal failure. Most acute catheters are made of poly-urethane, but silicone catheters are also available. The primary determinants of catheter blood flow are the diameter of the catheter and its tip placement. The subclavian insertion site should not be used in a patient who may need permanent vascular access. Femoral catheters seem to be associated with a higher risk of bacteremia than internal jugular catheters. Femoral placement demands a longer length catheter (≥20 cm) for a regular blood flow with limited recirculation. In general, catheter blood flow problems that occur early after placement are related to catheter position while those that occur late are related to thrombosis. Following its use, proper flushing and anticoagulation of the catheter with concentrated heparin or citrate will serve to decrease the risk of internal thrombosis.

To characterize the immune defect of patients with end-stage renal disease (ESRD), we performed NK cell subset analysis in 66 patients with ESRD treated by hemodialysis (n = 59) or peritoneal dialysis (n = 7). Compared with healthy blood donors, patients undergoing chronic dialysis showed a profound decrease in NKG2D+ cells within both the CD8+ T cell (58% vs 67%, p = 0.03) and NK cell (39% vs 56%, p = 0.002) populations. CD56dim cells, which comprise the majority of NK cells in the periphery, were more affected in this regard than were CD56bright cells. Uremic serum could decrease NKG2D expression on NK cells from healthy donors. Among factors that could contribute to the decrease in NKG2D expression in ESRD patients, reactive oxygen species (ROS) play a major role. We found that catalase could reverse the effects of uremic serum on NKG2D expression (p < 0.001) and that ROS down-regulated NKG2D at the mRNA level and at the NK cell surface. Additionally, ESRD patients had both increased membrane-bound MHC class I-related chain A (MICA) on monocytes (p = 0.04) and increased soluble MICA (203 pg/ml vs 110 pg/ml; p < 0.001). Both ROS and uremic serum could significantly increase in vitro the expression of the NKG2D ligand MICA on the renal epithelial cell line HK-2. Taken together, these studies suggest for the first time that both low NKG2D expression and up-regulation of its ligand MICA are related to ROS production and may be involved in the immune deficiency of ESRD patients.

Binding polyanionic unfractionated heparin over the modified AN69 polyacrylonitrile membrane, the surface electronegativity of which has been neutralized by polyethyleneimine (AN69-ST), renders the membrane more hemocompatible. This property was tested in two groups of long-term hemodialysis patients. Results were rated as massive or partial clotting of a dialyzer at the end of the session. Group I patients were included in a prospective, cross-over study comparing standard dialysis with hemodialysis without systemic administration of unfractionated heparin (n = 12, 123 sessions). In all instances, priming was made with 2 l saline containing 5,000 IU/l heparin. Only patchy or partial clotting was observed in 11% and 39% of the sessions with standard and heparin-free administration, respectively. Group II patients were included in an open, observational pilot study testing the effects of the heparin-coated membrane, without systemic administration of heparin, in patients at high risk of bleeding (n = 68, 331 sessions). Massive clotting was observed in six sessions only (less than 2%) and normal or slightly patchy dialyzers were found in 88% of the sessions. It is concluded that the dialysis AN69 ST membrane, after adequate priming at bedside, can be used without systemic administration of heparin for hemodialysis in patients at high risk of bleeding.

Background: Binding the polyanionic unfractionated heparin over the modified AN69 polyacrylonitrile membrane, whose surface electronega-tivity has been neutralized by layering polyethyleneimine (AN69-ST), renders the membrane more hemocompatible. Patients, method: in an open, pilot study, 28 patients on chronic hemodialysis prone to systemic bleeding with temporarily contraindication of systemic administration of heparin, were included. AN69-ST dialyzers were primed with heparinired saline and used thereafter, without systemic administration of heparin, nor saline flushing. Results: 331 sessions were performed (mean 11.8 sessions per patient, extreme 1-56) which lasted a mean 240 ± 18 min. At the end of the session the APTT mean was 32 ± 6 sec and the anti-Xa activity mean was 0.1 ± 0.1 IU/ml. Six sessions were stopped because of a massive clotting of the extracorporeal circuit, which was precipitated in 2 instances by undiagnosed mild stenosis of the vascular access. Partial clotting of the dialyser evaluated on a visual scale was quoted in 10 % of the dialyzers. It did not induce a significant blood spoliation. Comments and Conclusion: Regular hemodialysis can he conducted without systemic administration of heparin using a specific priming protocol that leads to heparin coating of the AN69-ST dialyzer. Risk of clotting was less than 2 % and favorably counterbalanced risk of bleeding. As expected, low blood flow rate due to a partial stenosis of the vascular access is, by itself, a risk factor of clotting.

Background. Binding of polycationic unfractionated heparin onto the modified AN69 polyacrylonitrile membrane, whose surface electronegativity has been neutralized by layering polyethyleneimine (AN69ST), produces stable coating. We investigated whether the heparin-coated membrane was suitable for regular haemodialysis with low heparin doses.Methods. Sheep were instrumented for extracorporeal circulation perfusing a dialyser equipped with either the AN69ST or the original AN69 membrane. Dialysis sessions were performed after priming the dialyser with heparinized saline. The session was conducted without systemic administration of heparin. In chronic haemodialysis patients, the AN69ST membrane was tested for safety, clotting and thrombin generation according to protocols of 4-h haemodialysis sessions with tapered heparin doses. The goal was to define optimal heparin requirements with the heparin-coated membrane in the setting of continuous or intermittent administration of heparin. Both unfractionated and low molecular weight heparin (LMWH) (enoxaparin) were tested.Results. In sheep, systemic heparin-free haemodialysis was conducted for 6 h without clotting using the heparin-coated dialyser. In the same conditions, massive clotting was observed within 90 min of dialysis with the native AN69 membrane. In man, through kinetic measurements of activated partial thromboplastin time (APTT), heparin anti-Xa concentration and thrombin-anti-thrombin complexes levels (TAT), significant dialyser clotting was avoided when APTT and anti-Xa concentration at 180 min of dialysis, were maintained at >40 s and >0.2 IU/ml, respectively. With the AN69ST heparin-coated membrane, thrombin generation was reduced then suppressed, as compared with the original AN69, primed in the same conditions. Safety of haemodialysis conducted with the AN69ST heparin-coated membrane and low doses of unfractionated heparin (50% reduction of the reference dose) was validated by a survey of 2590 sessions in 32 patients. Doses of LMWH were also safely reduced by 50%. In addition, haemodialysis without systemic administration of heparin was possible with minor risk of clotting.Conclusion. During the rinsing phase, the ionic interactions between the new AN69ST polyacrylonitrile membrane and unfractionated heparin induce stable heparin coating. This allows a significant reduction of systemic anticoagulant requirements without increasing the risk of clotting, both in the experimental setting and in the chronic haemodialysis patients. Further studies are required to assess this advantage in patients with acute renal failure and at risk of bleeding and to reduce the metabolic consequences of long-term treatment with heparin.

BACKGROUND It has been postulated that protein glycation and formation of advanced glycation end products (AGE) are among toxic factors in chronic uremia, whether the renal disease is of diabetic or nondiabetic origin. In this setting, AGE-modified beta2-microglobulin (beta2m) may favor dialysis beta2m-related dialysis amyloidosis. Consequently, efficient removal of modified beta2m by highly permeable dialysis membranes is as important as removal of native beta2m to postpone the development of dialysis amyloidosis. METHODS To define the role of dialysis membrane surface electronegativity on plasma protein transfer, an in vitro model was used to test the interactions of native and glycated beta2m with various highly permeable dialysis membranes. An experimental circuit with minidialyzers was used. The neutral high-flux polysulfone membrane (PS), the electronegative polymethylmetacrylate membrane (PMMA), the electronegative AN69 membrane and a modified AN69 membrane, the surface of which was neutralized with polyethyleneimine (AN69-PEI), were tested using both native beta2m and the more acidic glycated beta2m. Protein mass transfer and binding to the membrane were measured. RESULTS Mass transfer of glycated beta2m was significantly decreased through all membranes tested when compared with native beta2m. This result was due to the increased molecular weight of beta2m, which became less permeable to porous membranes, whereas adsorption of both native and glycated beta2m to membranes, due to ionic interactions, decreased similarly with AN69 and AN69-PEI, but remained unchanged with PS and PMMA. Moreover, surface neutralization of AN69 membrane did not alter its core binding capacity, since beta2m absorption accounted for 98 and 97% and glycated beta2m for 83.7 and 81.4% of the protein removed with AN69 and AN69-PEI, respectively. CONCLUSION Clearance of glycated beta2m through highly permeable neutral and negatively charged membranes was lower than that of native beta2m, reflecting a decreased sieving coefficient for the neoformed higher molecular weight and conformationally altered molecule. The binding capacity of the neutral PS was roughly half that of the charged membranes. Neutralizing surface electronegativity of the AN69 membrane with PEI did not alter its binding capacity. These results suggest that it would be useful for dialysis protocols to include comparative studies of both serum native and modified beta2m in order to prevent beta2m-amyloidosis.

Increased carbamylated hemoglobin formed in erythrocytes during uremia may interfere with HbA1c assays, but few studies compared directly both parameters. We measured carbamylated hemoglobin by HPLC in 45 non-diabetic uremic patients (16 with acute and two with chronic renal failure, 27 with transplant recipients) as 57.8 +/- 22.3 microg carbamylvaline/g Hb (mean +/- standard deviation) vs. 31.6 +/- 5.1 in 15 controls (+83%, p < 0.001). In these samples, HbA1c was evaluated by three ion-exchange HPLC methods, 1: Diamat (BioRad), 2: A1c2.2 (Tosoh) and 3: HA8140 (Menarini), and one immunoassay method (Tinaquant II Roche). Whichever the method, mean HbA1c values obtained increased in patients with high (> 60 microg carbamylvaline/g Hb) vs. low (< 45) carbamylated hemoglobin values (+0.08 to 0.25% of total Hb), but differences were not significant. Minor peaks on the chromatograms were however increased in parallel to carbamylated hemoglobin. HbA1c values over 6% were found in 4, 1, 2 and 0 samples, with HPLC 1, 2, 3 and immunoassay, respectively. Fructosamine values were not significantly altered. Our results show that Hb adducts, whether due to carbamylation or to other chemical reactions, interfere to a variable extent with different HbA1c assay methods, and confirm that HbA1c values should be interpreted with caution in uremic patients.

BACKGROUND:Carbamylation of proteins by isocyanic acid, the reactive form of cyanate derived from urea, is increased in uraemia and may contribute to uraemic toxicity. Kinetics of carbamylation that may reflect uraemic toxicity is not clearly defined in acute renal failure (ARF).METHODS:Twenty-eight patients with ARF and 13 with chronic renal failure (CRF) were included in the study in order to determine changes in carbamylated haemoglobin concentration (CarHb) in ARF. The usefulness of this parameter for differentiating ARF from CRF was also investigated. CarHb was measured by high-performance liquid chromatography after acid hydrolysis.RESULTS:Mean CarHb level (expressed as microg carbamyl valine per gram (CV/g) Hb) was significantly higher in ARF (54.3+/-5.2) than in normal subjects (31.6+/-1.3). On admission, CarHb level was correlated with duration of ARF prior to hospitalization in the intensive care unit (r(2)=0.723, P<0.001). CarHb was significantly higher at recovery in the subgroup of patients requiring haemodialysis than in the subgroup not requiring haemodialysis (82. 4+/-11.3 vs 46.7+/-5.2, P<0.01). Similarly dialysis patients lost more weight (8.6+/-1.4 vs 2.7+/-0.5 kg, P<0.005) and had higher averaged blood urea levels in the 20 days prior to recovery (17. 6+/-1.9 vs 11.3+/-1.8 mol/l, P<0.05). After recovery, CarHb level decreased at a rate of 0.219 microg CV/g Hb per day in patients with reversible renal insufficiency. CarHb concentration was higher in patients with CRF. A cut-off CarHb value of 100 microg CV/g Hb had a sensitivity of 94% and a positive predictive value of 94% for differentiating ARF from CRF.CONCLUSIONS:Kinetics of CarHb showed a near normal red blood cell life span in ARF. Changes in CarHb enabled, with a good sensitivity, the distinction to be made between patients who recovered from ARF and those with sustained renal impairment, whether due to prior CRF or resulting from parenchymal sequelae. Measurement of CarHb is valuable at clinical presentation of ARF in patients with an unknown medical history of renal disease.

This study investigated the incidence of subclinical abdominal hernia in patients starting peritoneal dialysis (PD). From April 1995 to August 1999, every new patient without clinical evidence of abdominal leakage underwent peritoneal scintigraphy. A total of 59 patients were enrolled in the study. Imaging of the peritoneal cavity was performed by mixing 74 MBq (2 mCi) of 99 m technetium sulfur colloid with 2 L of 1.36% dextrose peritoneal dialysis solution. Sequential gamma camera static images were obtained at 0 minutes, 60 minutes, and after drainage. Ten abdominal hernias (2 diaphragmatic leaks, 8 inguinal hernias) were observed in ten patients (6 males, 4 females; mean age: 65.1 years). One patient with diaphragmatic leak recovered partial renal function and stopped continuous ambulatory peritoneal dialysis (CAPD); the other was switched to automated peritoneal dialysis (APD). Among the eight patients with inguinal hernia, six had no clinical manifestations within eight months of follow-up. Two patients became symptomatic at 15 months and 25 months respectively. They underwent surgical repair. In CAPD patients without obvious abdominal hernias, peritoneal scintigraphy at onset of dialysis discovered 17% positive cases. The technique of scintigraphy is safe, with a low radiation exposure. Surgical repair for maintenance on CAPD is not always necessary, and a change in the PD strategy may be useful.

In the past few years, alpha-1-microglobulin (α1m) has been copurified from human urine with bikunin, a potent inhibitor of calcium oxalate (CaOx) crystallization in vitro. In this study, we have purified α1m without bikunin contamination and investigated its possible role in CaOx crystallization by in vitro and in vivo studies. Alpha-1m was purified with an anti-α1m antibodies CNBr-activated sepharose column. Two molecular species of α1m of respectively 30 and 60 kDa were purified. For each protein, two blots of 30 and 60 kDa cross-reacted with anti-α1m antibodies, suggesting that these two forms were derived one from the other. Both protein species inhibited CaOx crystallization in a dose-dependent manner in two in vitro tests. In the first test, the presence of α1m of 30 kDa (8 μg/ml) in a medium containing 0.76 mM CaCl2 (with 45Ca) and 0.76 mM Ox(NH4)2 inhibited CaOx crystallization by 38% as estimated by supernatant radioactivity after 1 h of agitation. In the second test, CaOx kinetics were examined for 3 to 10 min in a turbidimetric model at 620 nm. The presence of α1m of 30 kDa in a medium containing 4 mM CaCl2 and 0.5 mM Na2Ox inhibited CaOx crystallization by 41.5%, as estimated by the slope modification of turbidimetric curve. Alpha-1m can be considered as another inhibitor of urinary CaOx crystal formation, as shown by the present in vitro studies. Using an ELISA assay, we found that urinary α1m concentration was significantly lower in 31 CaOx stone formers than in 18 healthy subjects (2.95 ± 0.29 vs 5.34 ± 1.08 mg/l respectively, P = 0.01). The decreased concentration of α1m in CaOx stone formers could be responsible in these patients, at least in part, for an increased risk of CaOx crystalluria.

Among the limitations of continuous renal replacement therapy (CRRT) in patients with severe acute renal failure (ARF) and cardiovascular instability is the use of acetate in the substitution fluid. Acetate is required to maintain acidity of the polyelectrolytic solution to avoid calcium carbonate precipitation in the presence of bicarbonate. In addition, in patients with cardiovascular instability, acetate metabolism is impaired and further compromises hemodynamics. A new CRRT technique is proposed in which bicarbonate is used as a buffer, but the acetate requirements are cancelled: acetate free veno-venous hemofiltration (AF-CVVH). This technique allows control of acid-base disturbances independent of urea removal. This preliminary report describes the feasibility of the technique based on separate infusion of water and electrolytes administered prefiltration, and isotonic sodium bicarbonate administered post filtration. The setting of the technique, adapted to the PRISMA device (Hospal, Lyon, France), was based on a model predicting the bicarbonate infusion rate for a target plasma bicarbonate level. The AF-CVVH was compared with conventional, continuous veno-venous hemofiltration (CVVH) in a crossover study that showed AF-CVVH allowed fastest control of acidosis, avoiding 70 to 80 mmol/d of acetate transfer to the patient. Urea removal was similar with both techniques. It was concluded that AF-CVVH, when compared with CVVH, has the main advantage of separately controlling urea retention and metabolic acidosis in patients with severe ARF and cardiovascular instability.