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Biomedical subjects

G Pillion

Publications and source records attributed to G Pillion.

30 records · Page 2Linked to original sources

Urokinase treatment of pulmonary artery thrombosis complicating the pediatric nephrotic syndrome.

Two pediatric patients with severe pulmonary thrombosis complicating a lipoid nephrosis were treated with urokinase administered either as a continuous infusion or in massive bolus doses. Both patients recovered but one died suddenly 2 yr later after recurrence of the nephrotic syndrome and probably new massive pulmonary thrombosis. These patients had severe abnormalities of hemostasis and fibrinolysis, which favored thrombosis and complicated fibrinolytic treatment.

Child↗

Hemolytic-uremic syndrome: an analysis of the natural history and prognostic features.

Sixty-seven children with hemolytic-uremic syndrome (HUS) were admitted between 1974 and 1981. Of these, 52 (78%) were aged less than 3 years. All children had acute renal failure and 48 (72%) required peritoneal dialysis. The etiology in twenty cases varied from bacterial and viral infections (7 and 5 cases, respectively) to renal irradiation with chemotherapy (2) and preexisting glomerulopathy (1). 5 (7%) children died during the acute phase of the illness. Long-term follow-up (mean 3 years 3 months) of 56 cases showed that 37 children (60%) had so far experienced no functional sequelae and 8 (13%) only mild sequelae while 3 (5%) were on iterative hemodialysis, 3 had severe chronic renal failure and high blood pressure (HBP) and 5 (8%) had HBP and normal kidney function. While the recovery rate was approximately 60% in all age groups, the mortality rate and serious after-effects were twice as frequent (42%) in children over 3 years of age as in those less than 3. Renal histology (total of 37) showed 12 cases of cortical necrosis, 22 of glomerular thrombotic microangiopathy (TMA) and 3 arterial TMA. Prognosis was poor for all cases of arterial TMA and 58% of those exhibiting cortical necrosis.

Acute Kidney Injury↗

[Treatment of childhood hemolytic-uremic syndrome with urokinase. Cooperative controlled trial].

The results of a controlled therapeutic trial comparing 2 groups of patients presenting with hemolytic-uremic syndrome (HUS) are reported. Group A (15 children) was given urokinase (UK) and heparin; group B (18 children) received no treatment. Ages of patients, the delay before admission, the severity of anemia, thrombocytopenia and initial renal failure were similar in both groups. UK was responsible for bleedings in 12 children, minimal in 8, severe in 4. No child died in group A, 3 children died in group B (n.s.). Durations of hemolysis, thrombocytopenia and anuria were similar in both groups. Long-term evolutions of renal function and arterial pressure were comparable in both groups. Needle kidney biopsy (26 cases) showed cortical necrosis in 3 children of group A and in 2 of group B, and glomerular thrombotic microangiopathy in 10 children of group A and in 11 of group B. The average ratio of injured glomeruli was 40 (19 to 80) in group A, and 38 (21 to 75) in group B. Two children in group A and 3 children in group B presented with 50 to 80% of glomerular lesions. This trial suggests that UK is of no significant value in the treatment of HUS.

Adolescent↗

[Rhabdomyolysis and acute encephalitis in coxsackievirus infection].

We report the case of a 6 year-old boy with rhabdomyolysis involving only the inferior limbs. It was complicated by renal failure with anuria and intravenous coagulopathy and associated with encephalitis. Virologic investigations showed a recent infection due to Coxsackie B5 virus. Full recovery was observed after symptomatic treatment with peritoneal dialysis, exchange transfusion and heparin therapy.

Acute Disease↗

["Renal dwarfism". Its impact on dental development and on maxillary growth].

Children with terminal renal failure require iterative dialysis while awaiting kidney graft, and these have to be repeated over a period of years until a suitable graft presenting histocompatibility with the receiver is found. This has a considerable growth retardation effect (-3 to -6 SD, according to the age at onset of terminal failure). Two features appear to be paradoxical in these children. 1) In spite of a high carbohydrate diet and generally poor oral hygiene, they present a low prevalence of caries, probably related to modified salivary components. The only objective finding is an increase in salivary urea levels. 2) In spite of harmonious hypotrophy, no particular encumbrance of the dental arch is observed. Alveolar growth, contemporary with dental eruption, is sufficient to compensate possible hypotrophy of maxillary bone bases.

Adolescent↗

[Coagulation and fibrinolysis proteins in nephrotic syndromes in children].

The main coagulation and fibrinolysis proteins have been studied in 22 children with nephrotic syndrome. Some anomalies such as the increase of fibrinogen and of Factors II, V, VII + X concentrations and the decrease of antithrombin III concentration could induce an hypercoagulability. Other anomalies such as the high alpha 2 macroglobulin concentration and the frequently low plasminogen concentrations could induce a decrease of the plasma fibrinolytic activity. The consequences of the low alpha 1 antitrypsin levels are probably less important. The fast alpha 2 antiplasmin levels have been found variable in the different patients. Practically, it appears that most children with plasma albumin levels less than 15-17 g/l have antithrombin III levels less than 23 mg/dl (70% of normal), which appears to result in a high risk of thrombosis (11).

Adolescent↗

[Value of chlormethine in children with corticoid-dependent or partially corticoid-sensitive nephrosis, in steroid poisoning].

Mechlorethamine was administered at a low dose (0.8 mg/kg) to 27 children presenting with steroid dependent or partially responsive nephrotic syndrome, with signs of steroid toxicity. This drug induced a fast decrease of proteinuria (average delay: 7 days). It led to long lasting remission (average follow-up 34 months) in 16 cases (59%). Relapse occurred in 11 children (41%) most often (9 of 11 cases) in the first 7 months. However the evolutive pattern was clearly improved in 5 of these cases. Altogether, mechlorethamine allowed to stop corticosteroid therapy or, at least, to reduce the given dose, with a decrease of the signs of steroid toxicity, in 78% of the cases. In 6 cases (22%) evolution was almost not improved. One may hope that this dosage of mechlorethamine will not be gonadotoxic. This should be checked later on.

Adolescent↗

[Chronic renal insufficiency in the child. Etiology, development and prognosis].

Our study concerned 147 children with chronic renal failure (CRF) (creatinine clearance less than 50 ml/min/1.73 m2). Its goal was to analyse the distribution of primary renal diseases, natural history of renal failure (RF) according to etiology, and long term survival. Renal diseases responsible for RF were: malformations of the urinary tract (38%), glomerular pathology (26%), hereditary renal diseases (20%), isolated renal hypoplasias (11%), and miscellaneous (5%). Corticoresistant nephrosis accounted for 34% of glomerular diseases and nephronophtisis 63% of hereditary renal diseases. On the whole, RF was related with an uropathy or renal hypoplasia in half of cases and with congenital renal disease in almost 3/4 of cases. The natural history varied according to primary renal disease: slow deterioration after a period of relative stability for uropathy or renal hypoplasias, slow and regular deterioration for nephronophtisis, rapid deterioration for glomerular diseases.

Adolescent↗

Long-term outcome of children with malformative uropathies.

125 cases of severe malformative uropathies, 42 urethral valves (V), 52 degree III vesicoureteral refluxes (VUR), 18 ureterovesical junction stenoses (UVJ), 13 pyeloureteral junction stenoses (PUJ), were studied for a period of 12 years. Based on the hypothesis that prognosis depends on the number of residual nephrons, we used the glomerular filtration rate (GFR) as our basic reference. 62% of our cases had an initial GFR below 50 ml/min/1.73 m2 and 30% had GFR's below 25. Early diagnosis and intervention are important for improvement of GFR. Of the 32% who improved, most were diagnosed in the first year of life, and the exceptional few after 2 years. The extent of initial renal damage is also a limiting factor. Improvement was rarely seen when the initial GFR was below 30 ml/min/1.73 m2. There was a correlation between the initial and final GFR levels. Renal degradation (28% of cases) is most influenced by follow up time. The average age of end stage renal failure (ESRF) onset was 11 years 4 months, but is earlier for V than for VUR. Onset is even earlier when initial damage is more severe. As normal GFR does not exclude later degradation of renal function, another indicator of the risk of this type of evolution should be adopted.

Child↗