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La nefrocalcinosis, cuyo diagnostico en la actualidad resulta sencillo gracias a la ecografia, no es excepcional en el nino ni en el lactante. Las etiologias son multiples, pero implican casi todas un trastorno metabolico, a menudo de origen genetico, a veces iatrogenico, que aumenta la excrecion urinaria de calcio o de oxalato. Las causas mas frecuentes varian en funcion de la edad. En el recien nacido y en el lactante se habla principalmente de «hipercalciuria del prematuro», cuyo origen, multifactorial, es en gran medida iatrogenico, tubulopatias de aparicion precoz (acidosis tubular distal, sindrome de Bartter) y, afortunadamente muy rara, la hiperoxaluria primaria en su forma de aparicion infantil. En el nino, las principales causas que hay que buscar son: la acidosis tubular distal, la hiperoxaluria primaria y las hipercalciurias de origen genetico conocido (enfermedad de Dent, hipomagnesemia-hipercalciuria familiar) o tambien las causas «idiopaticas». Su evolucion depende de la extension de los depositos calcicos y sobre todo de la causa, es decir, de la posibilidad o no de parar el proceso de calcificacion.

Resume La nephrocalcinose, dont le diagnostic est maintenant facilite par l'echographie, n'est pas exceptionnelle chez l'enfant et meme le nourrisson. Les etiologies en sont multiples, mais impliquent presque toutes un trouble metabolique, souvent d'origine genetique, parfois iatrogene, augmentant l'excretion urinaire du calcium ou de l'oxalate. Les causes les plus frequentes varient suivant l'âge. Chez le nouveau-ne et le nourrisson, on evoque principalement : l'« hypercalciurie du premature », dont l'origine, multifactorielle, est en grande partie iatrogene, les tubulopathies a revelation precoce (acidose tubulaire distale, syndrome de Bartter), et, heureusement tres rare, l'hyperoxalurie primitive dans sa forme a revelation infantile. Chez l'enfant, les principales causes a rechercher sont : l'acidose tubulaire distale, l'hyperoxalurie primitive, et les hypercalciuries, d'origine genetique connue (maladie de Dent, hypomagnesemie-hypercalciurie familiale), ou encore « idiopathiques ». L'evolution depend de l'extension des depots calciques et surtout de la cause, c'est-a-dire de la possibilite ou non d'arreter le processus de calcification.

Resume La lithiase des voies urinaires n'est pas exceptionnelle chez l'enfant et il faut la rechercher par echographie devant toute pyurie, hematurie ou douleur abdominale. Grâce a l'analyse precise du calcul ou, a defaut, des urines, une cause peut etre retrouvee dans 80 % des lithiases de l'enfant. Chez le petit enfant, les deux etiologies principales sont l'infection a germes ureasiques, favorisee ou non par une malformation des voies urinaires, et les perturbations metaboliques induites par la prematurite et le traitement de ses complications (furosemide, corticoides). Chez l'enfant d'âge scolaire, les anomalies metaboliques, en particulier celles dues aux maladies hereditaires, expliquent la majorite des lithiases : hypercalciuries secondaires, iatrogenes, ou idiopathiques, hyperoxaluries primaires genetiques, secondaires ou « moderees » idiopathiques, cystinurie, hyperuricosuries genetiques ou secondaires et autres anomalies de l'excretion des purines. La prevention des recidives, essentielle en cas d'etiologie metabolique, passe toujours par une hydratation abondante (1,5 a 2 l/m 2 /24 h) et par le traitement de la cause si possible. Si un geste chirurgical est necessaire, la lithotritie extracorporelle est le traitement de choix comme chez l'adulte.

Resumen La proteinuria es un signo que puede revelar casi todas las enfermedades nefrologicas infantiles, desde las mas benignas, por ejemplo la proteinuria ortostatica, a las mas graves, como la glomerulonefritis rapidamente progresiva. Por tanto, su deteccion nunca debe omitirse, obligando a practicar un minimo de pruebas complementarias y a establecer un control posterior. En la mayoria de los casos, las proteinurias que no remiten casi por completo en menos de 1 mes justifican la consulta con un especialista para evitar la evolucion de una patologia potencialmente curable. La hematuria pediatrica puede tener multiples causas, pero al contrario que en el adulto, las etiologias «urologicas», y en especial los tumores, no son las mas habituales, de forma que no se justifica iniciar el estudio con una cistoscopia. En realidad, lo mas frecuente es que el contexto clinico y los resultados de algunas pruebas complementarias, siguiendo un arbol de decisiones simple, permitan rapidamente sospechar la causa. Solo dos trastornos, la hematuria microscopica prolongada, sola o asociada con una pequena proteinuria, asi como la hematuria macroscopica recidivante aislada, plantean problemas diagnosticos significativos, y en ambos casos la biopsia renal permite en general encontrar la solucion. No obstante, hay un pequeno porcentaje de hema-turias transitorias cuya etiologia nunca Ilega a demostrarse.

Prenatal ultrasonographic detection of autosomal recessive polycystic kidney disease (ARPKD) is of poor reliability, especially in early pregnancy. Molecular genetics allows earlier diagnosis, from 11 weeks of gestation; however, since only indirect diagnosis is possible--the ARPKD gene being localized on chromosome 6 but not identified--the feasibility of molecular diagnosis requires several conditions: definitive diagnosis in the index case, availability of index case and parents' DNA, genetic informativity of the family at the ARPKD locus. Results and limits of this method are analyzed, using a series of 56 requests for prenatal diagnosis.In eight of the 56 families ARPKD was excluded on the basis of histological (seven cases) and/or genetic (two cases) criteria. Molecular study was impossible in three families due to the lack of index case's DNA, and two other families were non-informative. Among the 43 families in which prenatal diagnosis was feasible, analysis of the haplotype of 35 fetuses issued from 29 families showed that 11 fetuses with the same haplotypes as that of the index case were affected, while 24 were not. No false positive or false negative result was reported.Early and reliable prenatal diagnosis of recessive polycystic kidney disease is possible in nearly 80% of affected families.

The exact reasons for the high incidence of Kaposi's sarcoma (KS) after kidney transplantation are still unknown. Immunosuppression is classically considered as the main risk factor, but the relative risk contributed by the patient's geographic origin and by human herpes virus (HHV)-8 infection still has to be determined.We carried out a retrospective and a prospective study among kidney transplant recipients (TP) to identify the risk factors for posttransplantation KS. Each of 30 KS patients was matched with two controls to investigate the association with geographic origin, immunosuppressive regimen, HHV-8 antibodies before and after transplantation, and other infections. Among TP with new onset of KS, we prospectively evaluated HHV-8 serology and viremia in response to decreased immunosuppression.African and Middle East origins, past infection with hepatitis B, hemoglobin level12 g/dl, lymphocyte count750/mm3 at the time of diagnosis and initial use of polyclonal antilymphocyte sera were risk factors for KS. After multivariate analysis, origin in Africa or Middle East and use of antilymphocyte sera for induction remained as independent risk factors. Sixty-eight percent (17/25) of TP with HHV-8 antibodies before or after transplantation developed KS compared with 3% (1/33) of seronegative TP (P0.00001). HHV-8 DNA was detectable in seven of nine peripheral blood mononuclear cells (PBMC) and in six of six KS lesions at diagnosis; it became negative in PBMC in three of five patients in parallel with tumor regression.African and Middle East geographic origins, HHV-8 infection before and after kidney transplantation, and initial use of polyclonal antilymphocyte sera were independent risk factors for KS. The presence of HHV-8 antibodies before or after transplantation was highly predictive of the emergence of posttransplantation KS and conferred a 28-fold increased risk of KS (odds ratio=28.4; 95% confidence interval: 4.9-279). Detection of HHV-8 DNA within PBMC and KS lesions seems related to tumor burden and evolution.

Primary hyperoxaluria type I (PH I) is a congenital error of metabolism that can be manifested by an increased oxalate production, and ultimately result in kidney failure. After a combined liver/kidney transplantation, children with PH I have persistent excretion of oxalate that causes crystal formation in the urinary tract, and could result in systemic oxalosis and eventual graft failure. We speculated that crystalluria may be predictive of this nephrolithogenic tendency and thus investigated the effect of an intensive therapeutic strategy to prevent crystal formation in 13 children at our hospital. Oxalate crystal volume (OCV) measurements were performed at regular intervals for 36 months, and compared with urine supersaturation measurements. We found that crystalluria with the OCV measurement is non-invasive, easily performed, and gives feedback on the efficacy of PH I therapy within one hour. Further study is needed to determine whether this method is a better predictor of nephrocalcinosis than is supersaturation alone.

Among all inherited cystic kidney diseases, the commonest are polycystic kidney diseases, which include 2 diseases characterized by their pathological characteristics and their mode of inheritance, namely autosomal dominant or recessive. Autosomal dominant polycystic kidney disease is usually diagnosed in adulthood and is related at least to 2 different genes; PKD1 gene on chromosome 16 accounts for 85% of cases. This frequent disease (1 in 1,000 people) leads to end-stage renal failure in most patients at a mean age of 55 years. Renal ultrasonography allows its detection at an early stage, during childhood or adolescence, and even in utero in some cases. Autosomal recessive polycystic kidney disease, related to a single gene mapped to chromosome 6, is a rare disease, usually diagnosed during infancy because of enlarged kidneys and hypertension. The early occurrence of advanced renal failure is uncommon and only 1/3 of patients require renal replacement therapy during childhood. The term "polycystic kidney disease" should be limited to these 2 diseases; however there are many other inherited conditions including renal cysts like tuberous sclerosis or Hippel-Lindau's disease in adults, and several malformative syndromes in children.

Steroid-resistant nephrotic syndrome with either minimal changes or focal and segmental glomerular sclerosis on initial biopsy is a severe condition as more than 50% of patients with the disease progress to end-stage renal failure within 10 years. We recently identified a distinct form of idiopathic nephrotic syndrome with an autosomal recessive mode of inheritance and were able to map the gene on the long arm of chromosome 1. The absence of recurrence of the disease after renal transplantation suggest a primary defect in a glomerular basement membrane protein. Several reports suggest that cyclosporine is effective in a proportion of patients with steroid-resistant idiopathic nephrotic syndrome, particularly when used in combination with corticosteroids. There are also data suggesting that high doses of cyclosporine may be necessary in patients with severe hypercholesterolemia. However, cyclosporine treatment should be carefully monitored in view of the high risk of nephrotoxicity, as shown by the results of repeat renal biopsies. The beneficial role of cyclosporine in recurrent steroid-resistant nephrotic syndrome is still debated. Preliminary observations suggest that the early use of intravenous cyclosporine may be effective in these patients.

Oxalosis is the systemic deposition of calcium oxalate crystals, caused by primary hyperoxaluria type I (PH I), an autosomal recessive peroxisomal defect involving glyoxylate metabolism in the liver and leading to an excesssive synthesis of oxalate. Primary hyperoxaluria type II (or L-glyceric aciduria) is a much rarer disease caused by a different enzymatic defect and does not seem to induce oxalosis [1].

In a series of 715 renal transplantations performed between 1973 and 1989, 72 cases of renal artery stenosis (RAS) in 69 children (9.7%) were managed at Hôpital Necker Enfants Malades. Forty cases of RAS were treated exclusively by antihypertensive drugs. A good result was obtained in 82.5% of cases. Thirty three transluminal angioplasties (TLA) were performed in 23 children with 26 RAS. A good clinical result was obtained in 15 children with a total of 17 stenoses, corresponding to a success rate of 65%. Transluminal dilatation of anastomotic stenoses always failed. There were no cases of transplant thrombosis. Eleven RAS were operated, including 5 after failure of TLA. Eight patients (73%) obtained a clinical improvement. There were 2 postoperative thromboses. Antihypertensive treatment must be administered in every case. If medical treatment fails, and with the exception of anastomotic stenoses, TLA should be the first-line procedure, while surgery is reserved for failures of TLA and for anastomotic stenoses.

In a series of 859 transplantations performed in children and adolescents from January 1973 to December 1992, vascular thrombosis accounted for 18% of all graft losses (2nd cause of graft failure), and 57% of early failures (within 2 months). Renal veins and arteries were equally affected. The young age of the donors and recipients constituted the main risk factor, thrombosis accounting for 40 and 37% respectively of all graft losses in donors and recipients5 years old. This explained the lower survival rate of these age groups after grafting, as reported in most published pediatric series. The prophylactic use of a low molecular weight heparin in high-risk grafts may help to decrease its incidence. A renal artery stenosis, located a few cm beyond the anastomosis in 2/3 of cases, was observed in 10% of grafts. Often severe hypertension (HBP) with cerebral complications, responsible for permanent sequelae in some cases, was the prominent symptom. Anti-hypertensive drug therapy was sufficient to control HBP in 40 cases out of 72, and in 10 of these, a spontaneous regression of the stenosis was remarked within a few months after repeated angiography. Transluminal angioplasty was used on 26 stenosis and was effective in 2/3 of cases; the recurrence rate, however, was 27%.

Intravenous recombinant human erythropoietin (Eprex Cilag) was used in 28 hemodialyzed children, treated in 3 French paediatric centers, from November 1989 to November 1990. Transfusion dependency disappeared in all cases: the number of transfusions decreased from 7.3 unit/patient/year to 0.6 unit/pt/year. The mean haemoglobin concentration for the whole group increased from 6.6 +/- 0.8 g/dl, to 9.2 +/- 1.2 at 6 months and 9.7 +/- 0.7 g/dl at 1 year. Twenty-two out of 28 children reached the target haemoglobin value of 9.6 g/dl (6 mmol/dL) within a mean time of 16.5 weeks. Poor responses were due to either a premature withdrawal of treatment because of renal transplantation, or too low a dosage for the age. The study showed indeed that the dose requirement was significantly dependent on physical development: the mean dosage required to maintain haemoglobin concentration at the target value was 300 U/kg/week in children weighing less than 20 kg, 222 U/kg/week in 20-30 kg children, and 135 U/kg/week in those weighing more than 30 kg (p = 0.02). The only complication was an increase in blood pressure, observed in 43% of cases. The increase of anti-hypertensive medication was always successful in controlling blood pressure, and hospitalization was required in only one case. The improvement in general condition was obvious, and in several cases, the cognitive abilities seemed to improve. The growth deficit remained unchanged.

In primary hyperoxaluria type I (PHI) after hepatic and renal transplantation (HRT), the oxalate pool is slowly removed by urine excretion. To minimize the amount of oxalate deposition in the graft during the first weeks, haemodialysis (HD), hyperdiuresis and diuretics have been suggested. Crystallization risk is usually evaluated by calcium oxalate product (pCaOx) but in PHI it can be inappropriate, so we measured total volume of oxalate crystals.

The renal ultrasonography (US) scans of 23 children who had recently undergone kidney transplantation were reviewed; the studies included Doppler US scanning of the arterial vessels at several levels. There were 43 studies for children whose postoperative course was normal; 16 studies were obtained during episodes of acute tubular necrosis and 21 during episodes of acute rejection. The upper limit of normal for the resistive index (RI) at the arcuate artery is higher (up to 0.79) for a pediatric renal transplant patient than for adults with normal kidneys, regardless of the age of the kidney donor. Therefore, elevation of the RI to 0.80 or higher or complete loss of diastolic flow always indicates a complication of transplantation. Abnormally high RI values were seen in patients with both acute tubular necrosis and acute rejection; however, the RI value as determined by US did not distinguish these two entities. In addition, in 7 cases of acute tubular necrosis and 12 of acute rejection the RI was normal (0.58 to 0.79).

Ultrasound is the first imaging modality used to evaluate acute renal disease in neonates. Normal findings and abnormalities seen in venous or arterial thrombosis, hemodynamic shock, or sepsis are reviewed. Transient changes due to intoxications, tubular disorders, or congenital nephrotic syndrome are considerably less common.

Twenty-four ultrasonography (US) studies of 21 renal transplants that had been in place for 1 to 19 (median 3) years were evaluated. The absolute resistive indices (RIs) determined during Doppler US at various arterial levels and the differences in RI between the levels did not correlate with the clinical diagnosis of chronic rejection. This study suggests that measuring RI values with Doppler US in people who received renal grafts as children does not currently contribute additional information for diagnosis or management.

From 1976 through 1991, 50 renal transplants (with 7 kidneys from living related donors and 43 cadaver kidneys) were performed in 47 children under five years of age (range 11 to 59 months) at the Enfants-Malades Hospital, Paris, France. Donor age ranged from 3 months to 53 years. Six of the seven kidneys from living related donors are currently functioning after a follow-up of 6 months to 8 years, whereas actuarial survival of cadaver kidneys was 70% at one year and 66% at five years. The main cause of graft loss was vascular thrombosis (40% of lost kidneys). In the most recent years of the study period, graft survival was substantially improved by routine prophylactic anticoagulant therapy with low-molecular weight heparin: one-year graft survival rate was 83% in the 23 children grafted between 1989 and 1991. Posttransplantation growth was closely related to quality of graft function: among the 29 children with sufficiently long follow-up the 19 patients with normal renal function exhibited normal or catch-up growth, whereas the ten patients with chronic renal failure or recent rejection had poor growth. Complications were uncommon with the exception of hypertension. Mortality rate was 12%, i.e., only slightly higher than in older pediatric kidney recipients. Achievement at school was normal in most cases (with a lag in only five patients). Provided effective therapy is given to prevent the main adverse outcome (i.e., vascular thrombosis), renal transplantation does not involve excessive risks even in infants as young as one year of age.

Among 149 kidneys transplanted in 141 children and teenagers aged 4 1/2 to 20 years, from November 1972 through December 1979, 70 (47%) were still functioning after ten years (67/145 cadaver donor grafts and 3/4 living related donor grafts). Medical and social status at the last follow-up visit (10 to 16 1/2 years after transplantation; m = 12 years) was analyzed. Patients were divided into five groups on the basis of glomerular filtration rate (GFR; ml/min/1.73 m2) and blood pressure (BP): 1) GFR greater than 80 ml and normal BP: 23 patients (33%); 2) GFR in the 60-80 ml range and/or high BP: 24 patients (34%/3) GFR in the 40-60 range: 6 patients; 4) GFR in the 15-40 range: 7 patients; and 5) hemodialysis restarted 10 1/2 to 13 years after transplantation. Mean adult stature was 155.7 +/- 10.4 cm in males and 149.8 +/- 10 cm in females. Osteoporosis was found in 88% of patients who underwent bone density quantitation. Twenty-four per cent of patients had aseptic osteonecrosis with variable degrees of impairment as a result. Chronic HBsAg carrier status was found in 37% of patients and was accompanied with persistent cytolysis in half the cases. Only one malignancy was seen (carcinoma of the urinary bladder in a child under cyclophosphamide). Six deaths were recorded between 10 and 13 years after transplantation; causes included septicemia (2 cases), cancer (1 case), hepatitis B (1 case), cerebral cystinosis (1 case), and unexplained sudden death (1 case).(ABSTRACT TRUNCATED AT 250 WORDS)

Vascular thrombosis is one of the main causes of early transplant failure in pediatric patients. This paper reports the results of an open trial of the low molecular weight heparin (Enoxaparine) used to prevent renal graft thrombosis in pediatric recipients with risk factors including donor or recipient age under 5 years, multiple arteries supplying the transplant, and positive history for recurrent thrombosis. During 1989, 42 of 67 children given a renal transplant were prophylactically treated with Enoxaparin. Only one transplant was lost to thrombosis among treated patients (1.5%), versus 9 transplants among 73 (12%) children who received their kidney in 1988 without prophylactic Enoxaparin. Risk factors were comparable in both groups of recipients. Enoxaparine therapy was associated with an increased rate of bleeding (12/42) without severe consequences. In conclusion, Enoxaparin is effective in preventing renal graft thrombosis. Availability of this prophylactic therapy makes it possible to use transplants removed from the youngest donors considered as inadequate by some groups.

A clinicopathologic study of 41 biopsy specimens from renal grafts transplanted at least ten years earlier showed normal findings or only mild tubulointerstitial lesions in 63% of cases. Results confirmed the good prognostic value of renal graft biopsy performed ten years after transplantation. A very close correlation was demonstrated between histologic evidence of chronic rejection (interstitial fibrosis, tubular atrophy, and fibrous endarteritis) and long-term graft outcome. Severity of interstitial fibrosis was apparently a more reliable indicator of prognosis than severity of fibrous endarteritis. Among 16 patients with a history of acute rejection, none had residual parenchymatous lesions. In contrast, among patients with major tubulointerstitial and/or vascular lesions, most had previously experienced one or several episodes of acute rejection. Evidence of allograft glomerulopathy was seen in approximately one case in four (11 patients). Among these patients, only eight had proteinuria and only four lost their graft. Among the four patients who developed recurrent membranoproliferative glomerulonephritis (type I in three cases and type II in one case), three lost the deposits previously detected by immunofluorescence, probably as a result of immunosuppressive therapy.

After its description in adult patients by Oreopoulos in 1978 continuous ambulatory peritoneal dialysis (CAPD) appeared rapidly as a method of choice for the treatment of children with ESRD ([1],[2]). For that reason there was a rapid increase in the proportion of children on renal replacement therapy (RRT) surviving by the means of CAPD between 1980 and 1987, as it was reported in the EDTA registry. By the end of 1987 28% of the european children on dialysis were treated by CAPD versus 5% in 1980, but there were also considerable differences between countries. For example in 1987 in UK 67% of uremic children on dialysis were on CAPD versus 13% in France, and one can wander about the reasons of these differences. Were they due to differences in the availability of different modes of treatment that is to say to financial constraints, or are they related to different perception in the quality of the results, already questioned by Potter et al. ([3]). Since CAPD is less expansive than hemodialysis (HD), we are proposing the hypothesis that financial constraint was one of the reason explaining the development of CAPD in children in spite of the fact that hemodialysis is a more valuable mode of treatment. This hypothesis is supported by the evolution of CAPD in the Enfants Malades unit where this method was started in 1979–80, developed rapidly till 1984–86 and then decreased as a mode of long term RRT. The aim of this study is to analyze and compare the data of children who received RRT at least 3 months by the means of each mode of treatment, in order to understand the progressive loss of popularity of CAPD in the last years in our unit.

We report our experience with endoluminal angioplasty for the treatment of arterial stenosis involving transplanted kidneys in children. Four anatomic groups were individualized: stenosis of the iliac artery proximal to or at the level ot the anastomosis, single stenosis of the main renal artery, double stenosis of the main renal artery and/or a branch of the renal artery, and multiple arterial lesions. Angioplasty is performed under general anesthesia using balloon catheters appropriate for pediatric patients. Prevention of spasm and heparin therapy are essential. Results depended on the distal vascular bed. Good results were achieved in those patients with a dilatation distal to the stenosis and no multiple arterial lesions (type IV) that actually reflect vascular rejection. The overall success rate was estimated at 66% and the recurrence rate at 22%.

To study the accuracy of renal function quantification with 99Tcm-DMSA we compared DMSA renal uptake and creatinine clearance in 16 cases of children with single kidney. The age of the patients ranged from two months to fourteen years. Creatinine clearance was normalized to 1.73 m2. DMSA uptake was measured 7 h after intravenous injection. Background subtraction was used and soft tissue attenuation was taken into account. The uptake was normalized in percentage of the injected activity. A significant correlation was found between creatinine clearance and DMSA uptake (rt = 0.866, p less than 0.01). Normal creatinine clearance range in children (80 to 120 ml min-1/1.73 m2) allowed determination of normal uptake range (36 to 60%). This study indicates that in case of asymmetrical renal impairment renal uptake will reflect split renal creatinine clearance. Since the former is much easier to measure, DMSA should play an important role in the evaluation of differential renal function.

Infantile cystinosis is an autosomal recessive lysosomal disorder of aminoacid metabolism leading to a storage of cystine crystals in the cells of many tissues, but mainly in the kidney and the eye. The ocular symptoms and long term evolution were studied in a series of 25 patients at the Enfants Malades Hospital. The follow-up over 26 years demonstrated that infantile cystinosis affected mainly corneal and retinal epithelium just as it affected the kidney epithelium. Corneal involvement was a constant finding after one year of age. It induced photophobia, which appeared between three and four years when a superficial punctate keratopathy appeared. A characteristic retinopathy was observed as early as three years of age. It was constantly present at seven years of age and caused loss of vision. When ERG results were compared to the most recent measurement of visual acuity, a correlation was observed between retinopathy and visual defect. For this reason, no corneal grafts were performed. The use of topic cysteamine appeared promising but no definitive conclusions could be made.

The apparition of cyclosporine, immunodepressive drug, has largely improved the organ transplantations. However, the range of blood concentrations must be defined to allow the efficacity of cyclosporine therapy and to avoid toxic reactions, because there are very important variations for a same dosage according to the individuals and the diseases. Relative to the low concentrations to be determined (about one hundred ng/ml), the most useful methods for cyclosporine measurement are based on immunochemical assays. This work compare the two methods: radioimmunoassay (RIA) and fluorescence polarization immunoassay (FPIA) simultaneously performed on several hundred samples. A very significant correlation exists between the two techniques (r = 0,80). The advantages of immunofluorescent assay consists in rapidity, sensibility and facility to realize emergency analysis.