No abstract available.
Ependymoma*

No abstract available.
Extremities* ; Gangrene* ; Haemophilus influenzae type b* ; Haemophilus influenzae* ; Haemophilus*

No abstract available.
Drug Therapy*

The detection of even microscopic amounts of blood in a child's urine, whether accompanied by symptoms or asymptomatic, alarms the patient, parents, and physician, and often prompts the performance of many laboratory studies. Hematuria is one of the most important signs of renal or bladder disease, but proteinuria is a more important diagnostic and prognostic finding, except in the case of calculi or malignancies. Hematuria is almost never a cause of anemia. Primary care physicians frequently encounter children with hematuria. Among children presenting to a pediatric emergency clinic, gross hematuria was found an incidence of 1.3 per 1000. Microscopic hematuria in children is much more common, with a prevalence rate between 1 and 4%. The pediatricians should ensure that serious conditions are not overlooked, while avoiding the performance of unnecessary and often expensive laboratory studies, and provide guidelines for additional studies if there is a change in the child's course. This article provides a stepwise approach to the evaluation and management of hematuria in a child.
Anemia ; Calculi ; Child* ; Emergencies ; Hematuria* ; Humans ; Incidence ; Parents ; Physicians, Primary Care ; Prevalence ; Proteinuria ; Urinary Bladder Diseases

Tubulointerstitial (TI) fibrosis is a final common pathway to progressive renal injury of all forms of renal disease. However, once renal damage reaches a certain threshold, progression of renal disease is consistent, irreversible, and largely independent of the initial injury. Angiotensin (AT) II is the main effector of the renin angiotensin system (RAS) and effects that may contribute to the onset and progression of renal damage. AT II may also directly contribute to accelerate renal damage by sustaining cell growth, inflammation, and fibrosis. Interventions that inhibit the activity of the RAS are renoprotective and may retard or even halt the progression of chronic nephropathies. Unilateral ureteral obstruction suggested as a well-established experimental model of progressive interstitial expansion and fibrosis. Although technically challenging, some investigators have successfully relieved the obstruction and reported significant reduction in interstitial fibrosis severity. Drugs that modulate the RAS, such as ACE inhibitors and angiotensin type 1 (AT1) receptor antagonists, have demonstrated protective renal effects and can ameliorate fibrosis. However, neither ACE inhibitor nor AT1 receptor blockade completely suppresses progression of renal disease. Dual blockade of the RAS with ACE inhibitors and AT1 receptor blockers may provide renal benefit beyond therapy with either drug alone, due to their potential additive beneficial effect.
Angiotensin-Converting Enzyme Inhibitors ; Angiotensins* ; Fibrosis* ; Humans ; Inflammation ; Models, Theoretical ; Renin-Angiotensin System ; Research Personnel ; Ureteral Obstruction

PURPOSE: Vesicoureteral reflux(VUR) is defined as a retrograde flow of urine from the bladder into the upper urinary tract. It has been shown to predispose patients to hypertension, renal scarring, and end-stage renal failure if not recognized and treated. The observation that VUR occurs in siblings of children with reflux at a significantly higher rate than the general pediatric population has been recognized for many years and VUR was detected in 26% to 51% of siblings of patients with VUR. The purpose of this study is to determine the incidence of VUR in asymptomatic siblings of children with VUR and to see if this form of screening would be practical. METHODS: We retrospectively reviewed the records of 28 patients with VUR and their siblings. The total number of asymptomatic siblings investigating VUR were 28 persons. All patients and siblings were evaluated for VUR by a voiding cystourethrography and all patients and siblings with VUR were performed 99mTc 2,3-dimercaptosuccinic acid renal scan. RESULTS: A total of 28 patients(14 boys, 14 girls) with VUR were studied; the mean patient age was 2.7 years(range 1 month to 8.4 years). The total number of asymptomatic siblings investigating VUR were 28 persons(17 boys, 11 girls) and the mean age was 3.3 years(range 2 months to 7.4 years). Renal scar was detected in 20 of 28(71.4%) patients with VUR. VUR was noted in three of 28(10.7%) siblings and renal scar was detected in one of three siblings with VUR. CONCLUSIONS: In this study, the predictive value of a positive family history alone in identifying VUR was 10.7%. This incidence suggests more investigation of asymptomatic siblings and continued study of this group of patients at risk is needed for clarifying the family screening of patients with VUR.
Child ; Cicatrix ; Humans ; Hypertension, Renal ; Incidence* ; Kidney Failure, Chronic ; Mass Screening ; Retrospective Studies ; Siblings* ; Succimer ; Urinary Bladder ; Urinary Tract ; Urinary Tract Infections ; Vesico-Ureteral Reflux*

No abstract available.
Nephritis, Interstitial*

No abstract available.
Fibrosis* ; Renin* ; Renin-Angiotensin System*

No abstract available.
Biomarkers* ; Carcinoma, Hepatocellular* ; Hepatitis B* ; Hepatitis* ; Humans ; Korea* ; Prevalence*

Serum alkaline phosphatase (AP) activity is elevated in hepatobiliary disease, bone disease, pregnancy and certain neoplasms. Recently we experienced marked elevation of serum AP activity after administration of albumin preparation in nephrotic patients who suffered from hypovolemic symptoms. So serum AP activity and the isoenzymes in the albumin preparations & patient's serum after the administration of albumin preparation were studied. Serum AP activity was significantly higher after administration of albumin preparation (318+/-101 IU/L) then before (123+/-43 IU/L). The predominant isoenzyme after administration of albumin was placental type, while liver and bone type was predominant before administration. AP activity in albumin preparation was high (2,133+/-1,410 IU/L) and the isoenzyme was mostly placental type. So we concluded that marked elevation of serum AP activity after administration of albumin was traced to the placental type AP isoenzyme in some albumin preparations which was manufactured from the plasma of placental origin. Elevated serum AP activity like these may lead to erroneous interpretation. Manufactures should notify alkaline phosphatase activity in albumin preparations of placental origin.
Administration, Intravenous* ; Alkaline Phosphatase* ; Bone Diseases ; Humans ; Hypovolemia ; Isoenzymes ; Liver ; Plasma ; Pregnancy