Cystographie: les bonnes pratiques

How to perform the perfect voiding cystourethrogram.

Agrawalla S, Pearce R, Goodman TR.

Pediatr Radiol. 2004;34:114-9.

The voiding cystourethrogram (VCUG) examination is a difficult investigation toperform and is a stressful experience for patients and their parents, as well asfor the radiologists, technicians and paediatric radiology nurses involved inthe examination. Despite the VCUG being one of the most commonly performedfluoroscopic procedures in paediatric radiology practice, there is no generalconsensus as to the best way to perform this investigation. This is particularlyconcerning when one considers the potentially high gonadal radiation dosechildren may receive. Because of this, we have undertaken a comprehensiveliterature review of various aspects of the test in order to determine the bestway to perform the VCUG in modern paediatric radiology practice.

Premedication during micturating cystourethrogram to achieve sedation and anxiolysis

Akil I, Ozkol M, Ikizoglu OY, Polat M, Tuncyurek OY, Taskin O, Yuksel H.

Pediatr Nephrol. 2005;20:1106-10.

Micturating cystourethrogram (MCUG) is an imaging technique indicated in the diagnosis and follow-up of many diseases. We investigated the reliability and the efficacy of midazolam and chloral hydrate in sedation and anxiolysis during micturating cystourethrogram. Fifty-three children of similar ages (39 girls, 14 boys, mean age of 5.8±3.5 years) were randomized to midazolam (n=17), chloral hydrate (n=18) and control groups (n=18). Oral midazolam 0.6 mg/kg or chloral hydrate 25 mg/kg or saline were administered to the study groups 15–30 min prior to the urinary catheterization. Brietkopf and Buttner, Frankl and Houpt scales and Spielbergers State Anxiety Inventory and parents impressions were used to assess the level of sedation and anxiety. The Brietkopf and Buttner classification of emotional status and Houpt behavior rating scale demonstrated a significantly better emotional status and sedation in the midazolam group when compared to controls (P=0.01 and P=0.018, respectively). The catheterization was described as a more unpleasant and distressing event by the parents of the control and the chloral hydrate groups when compared to the parents of the midazolam group (P<0.05).>0.05). Vital signs did not change significantly in any child. Sedation with midazolam does not have adverse effects on the results of micturating cystourethrogram, while it reduces the discomfort in children undergoing this radiological technique.

Commentaires: quelques suggestions pour améliorer les conditions de cet examen souvent mal vécu par les enfants et leurs parents. Quelles sont les habitudes de vos collègues radiologues ?

Toxicité rénale des AINS

Acute renal failure, associated with non-steroidal anti-inflammatory drugs in healthy children

Irit Krause1 , Roxana Cleper1, Bella Eisenstein1 and Miriam Davidovits1

Pediatric Nephrology. Juillet 2005, online

Seven patients aged 13 to 17.5 years developed acute renal failure after treatment with a variety of non-steroidal anti-inflammatory drugs (NSAID): naproxen, diclofenac, ibuprofen, dipyrone and paracetamol. Six of the patients used more than one kind of NSAID. None of the patients had previous history of renal disease or concomitant treatment with other drugs. The time interval between NSAID administration to the emergence of symptoms ranged from 1 to 4 days. The most common presenting symptoms were flank pain (4 patients), abdominal pain (3 patients) and vomiting (3 patients). All patients had normal urine output. Microscopic hematuria and proteinuria were found in 5 patients and leukocyturia in 2. Serum creatinine ranged from 1.3 to 8.3 mg% at presentation. Kidney biopsy was performed in 3 patients and showed findings consistent with mild interstitial inflammation in 1 patient, and normal renal tissue in 2. All patients were treated with intravenous fluids, 1 received corticosteroids. Renal function completely normalized in all patients within 7 to 16 days.

Commentaires: Un nouveau témoignage sur les effets des AINS sur le rein ...

Les greffés à donneurs vivants grandiraient mieux: rôles des "cytokines rénales" ?

Growth in children after kidney transplantation with living related donor graft or cadaveric graft
DrL Pape MDa, , ProfJHH Ehrich MDa, M Zivicnjak PhDa and ProfG Offner MDa

Lancet. 2005;366:151-153

The extent to which growth after renal transplantation differs between children with a living related donor graft (LRD) and those with a cadaveric donor graft (CAD) is unclear. We retrospectively studied growth in the 5 years after transplantation in 30 boys who received LRD and 21 who received CAD. Height was similar in both groups after transplantation but was greater in LRD than in CAD recipients during follow-up. LRD recipients were taller at all ages, and had greater growth velocity in infancy and during puberty. Glomerular filtration rate (GFR) was higher immediately after transplantation in LRD than in CAD recipients, but did not differ between the groups during follow-up. GFR and other factors did not affect height 5 years after transplantation. These findings support use of LRD as the preferred option in children.

Commentaires: Cette étude par le groupe de Hanovre compare la vitesse de croissance après greffe rénale avec donneur vivant ou cadavérique. L'analyse montre une meilleure vitesse de croissance dans le groupe "donneur vivant", qui ne semble pas être le fait d'une meilleure filtration glomérulaitre ni même d'une épargne cortisonique. Les auteurs font l'hypothèse d'une pertubation de l'expression des gènes codant pour certaines cytokines dans les reins après ischémie froide. Cette idée est intéressante mais reste purement spéculative, aucun dosage ou étude d'expression génique n'est ici réalisée. De plus, il faut noter que le nombre de patients étudiés est relativement faible (30 et 21 dans chaque groupe) et la taille des parents n'est pas prise en compte ce qui doit rendre prudent quant à l'interprétation des résutats. Une étude sur un plus grand nombre de greffes s'impose.

RS

Système kallikréine-kinine et paroi artérielle: modulation diététique et génétique

Arterial and renal consequences of partial genetic deficiency in tissue kallikrein activity in humans.

Azizi M, Boutouyrie P, Bissery A, Agharazii M, Verbeke F, Stern N, Bura-RiviereA, Laurent S, Alhenc-Gelas F, Jeunemaitre X.

J Clin Invest. 2005;115:780-7.

Tissue kallikrein (TK), the major kinin-forming enzyme, is synthesized in several organs, including the kidney and arteries. A loss-of-function polymorphism of the human TK gene (R53H) induces a substantial decrease in enzyme activity. As inactivation of the TK gene in the mouse induces endothelial dysfunction, we investigated the vascular, hormonal, and renal phenotypes of carriers of the 53H allele. In a crossover study, 30 R53R-homozygous and 10 R53H-heterozygous young normotensive white males were randomly assigned to receive both a low sodium-high potassium diet to stimulate TK synthesis and a high sodium-low potassium diet to suppress TK synthesis, each for 1 week. Urinary kallikrein activity was 50-60% lower in R53H subjects than in R53R subjects. Acute flow-dependent vasodilatation and endothelium-independent vasodilatation of the brachial artery were both unaffected in R53H subjects. In contrast, R53H subjects consistently exhibited an increase in wall shear stress and a paradoxical reduction in artery diameter and lumen compared with R53R subjects. Renal and hormonal adaptation to diets was unaffected in R53H subjects. The partial genetic deficiency in TK activity is associated with an inward remodeling of the brachial artery, which is not adapted to a chronic increase in wall shear stress, indicating a new form of arterial dysfunction affecting 5-7% of white people.

Commentaires: Ce travail fort intéressant de l'équipe de Xavier Jeunemaitre montre qu'un polymorphisme dans le gène codant pour la kallikréine présent dans 5 à 7% de la population à peau blanche est associé à une réduction de l'activité de cette enzyme et à une modification des propriétés mécaniques de la paroi artérielle. A coté des facteurs diététiques (Na et K) qui modulent le système kallikréine-kinine, un facteur génétique est donc clairement identifié qui pourrait rendre compte d'une part de l'héritabilité de l'hypertension artérielle.

RS