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Acute kidney injury is known as an acute reversible insult to the kidney but its definition and classification is not uniform. Earlier classification of acute renal failure was according to pre-renal, renal, and post renal by using history, the time of response to fluid therapy, and some blood and urinary parameters and markers. Recently, efforts have been made to present a uniform definition of acute kidney injury for earlier disease detection in order to decrease the rate of morbidity, mortality, length of hospital stay, and even death. However, it is clear that serum creatinine is a late marker of renal injury and many new investigations have tried to find more sensitive biomarkers to recognize earlier stages of AKI, its exact underlying mechanism, and outcome. Here we provide the first section of a series about new concepts on AKI with focus on pediatrics.

 Keywords: Acute Kidney Injury; Pediatrics; Biological Markers; Classification.

Introduction: Early rehydration with bolus fluid can be life saving. We compared isotonic saline with a hypotonic fluid which was composed of saline 0.9%, dextrose, and bicarbonate in our clinical setting.

Materials and Methods: 71 children entered to this study , 41 cases received isotonic saline and the remaining 30 cases received hypotonic fluid which was composed of 750 cc saline 0.9%, 28 cc bicarbonate 7.5%, and 222cc dextrose 5% for resuscitation fluid challenge at a dose of 20ml/kg over 20 minutes that could be repeated up to 3 times as needed. Serum sodium (Na), potassium (K), blood sugar (BS) and bicarbonate (HCo3) were measured before initiating rehydration and after 3 hours. T independent test was used to compare the values between the two groups and T paired test in each group in SPSS 16. The level of significance was set at 0.05.

Results: Serum Na, K, BS, and HCo3 were 134±5, 3.8 ±0.6, 90±16, and 11.6±3.6 before and 135±4, 3.7±0.5, 73±13, and 15±3 three hours after rehydration in the isotonic group, respectively.

In the isotonic rehydrated group, BS drop and HCo3 rise significantly (p<0.001). Serum Na, K, BS, and HCo3 were 134±6, 3.6±0.6, 91±15, and 10.1±1.9 before and 136±3, 3.6±0.4, 94±10, and 15±2 three hours after rehydration in the hypotonic saline group, respectively. Serum sodium increased 2meq/dl (p<0.04) and bicarbonate increased 4.9 meq/l (P< 0.001).

Conclusions: The hypotonic serum containing 115meq/l of sodium chloride combined with 25meq/l of sodium bicarbonate and dextrose 1.1% is not associated with a decrease in BS or hyponatremia. It also increases serum HCo3 prominently.

Keywords: Hypotonic Solutions; Isotonic Solutions; Dehydration; Child.

Introduction: To evaluate the response to low dose oxybutynin in children with nocturnal enuresis.

Materials and Methods: Forty-one neurologically normal enuretic children who were visited in our nephrology clinic in a 3-year period (2007-2009) received low dose oxybutynin (2.5-10 mg/day depending on the weight) to define response to the drug in one and 3- month periods. No, partial, and full response were defined as 0-49%, 50-89% and ≥90% decrease in bed wetting, respectively.

Results: In the first month of treatment, full, partial, and no response were reported in 3 (7.3%), 14 (34.1%), and 24 (58.6%) patients, respectively. In the non-responder patients, 6 (25%) and 5 (20.8 %) patients showed full and partial response in the 3-month period whereas 13 (54.2%) had no response. The side effects of the drug were reported in 5 (12.2%) patients. Children with non-mono symptomatic nocturnal enuresis (NMNE) showed a better response to the drug than those with mono symptomatic nocturnal enuresis (MNE) (75% versus 25%). There was no significant differences in age, gender, family history of enuresis, and the presence or absence of daytime urinary or bowel symptoms between responder and non-responder groups (P>0.05 for all).

Conclusions: In this clinical report study, there was 68.3% treatment benefit and 12% risk (side effects of the drug) with low dose oxybutynin. Therefore, it may have a role in treating nocturnal enuresis, especially in patients with NMNE who experience adverse effects of standard treatment (Higher doses of the drug).

 Keywords: Nocturnal Enuresis; Child; Oxybutynin; Risks and Benefits; Adverse effects.

Introduction: This study was done in Children’s Medical Center Hospital affiliated with Tehran University of medical science, Tehran, Iran.

Materials and Methods: The patients were 140 children who were admitted for gastroenteritis and we detected acute kidney injury in them. All of the patients were admitted and managed in the Emergency Department, and were evaluated for symptoms of AKI including dehydration, renal function tests, electrolytes, and urine output.

Results: The median age of the children with gastroenteritis and AKI was 2.5 years (ranging from 2 months to 12 years) and 78.6% of them were male. Acute kidney injury (AKI) was present in 116 (82.9%) patients at admission with 53 (37.8%) patients in the “failure” category (RIFLE). Twelve children had anuria and 54 patients had oliguria. At presentation, 24 patients (15%) had serum BUN levels between 30-75 and creatinine levels in the range of 0.9-2.1mg/dl. One patient had HUS that was excluded from this study. Seventy-six children had symptoms of severe dehydration and metabolic acidosis. After adequate fluid therapy, 30 children had polyuria of 6.4 (range 4-9) cc/kg/min. Twenty-three patients (16.4%) had hyponatremia and 41 patients (29.2%) had hypernatremia. Nine children (6.4%) suffered from hypokalemia. Some children had received ORS at home. All of them were managed in the emergency ward and discharged with normal GFR without any electrolyte abnormalities. The patients were fallowed for 3-6 months and all of them had normal renal function at the end of the study.

Conclusions: Early diagnosis and urgent management of gastroenteritis and dehydration can prevent AKI.

Keywords: Acute Kidney Injury; Child; Gastroenteritis.

The association of idiopathic nephrotic syndrome with some malignancies has been reported. We hereunder report a child with focal segmental sclerosis who presented with brain tumor eleven years after renal presentation. A 16- year-old boy presented with nephrotic syndrome since was 5 years old. He was a steroid responder at first but became steroid dependent after subsequent relapses. He received cyclosporine for two years and then mycophenolate mofetil was added for three years. After that, he received losartan and enalapril. Four years later, he developed glioblastoma multiforme.  He passed away two years after surgical resection and chemo-radiotherapy. The occurrence of brain tumor after immunosuppressive therapy in this child might be a late sequel or a coincidence. This might be an alarm for using immunosuppressive agents more cautiously.

Keywords: Glioblastoma; Immunosuppression; Mycophenolate Mofetil; Cyclosporine; Losartan; Enalapri; Nephrotic Syndrome. 

Ureteropelvic junction (UPJ) stenosis occurs in 13% of children. Antenatally, the diagnosis is possible by showing renal pelvis dilatation by obstetric ultrasonography. Giant hydronephrosis (GH) is a rare condition. There are different etiologies for GH which are mostly congenital and occur during infancy and childhood. GH was confirmed by complementary evaluations in a 2-month-old female infant with poor feeding, lethargy, and vomiting together with an antenatal sonography in favor of hydronephrosis, and a 5-year-old boy with an abdominal mass diagnosed by sonography following 2 weeks of progressive abdominal distention. Pyeloplasty was associated with an excellent result in both of them.

Keywords: Hydronephrosis; Ureteral Obstruction; Congenital; Urologic Diseases.

Renal tubular acidosis (RTA) is a rare genetic disorder. It has four clinical types, and type 3 demonstrates a mixed pattern of tubular dysfunction. The causative gene for type 3 RTA (CAII) is located on the 8q22 locus and encodes a protein called carbonic anhydrase II. In this study, we analyzed the entire exons and flanking regions of the CAII gene in a child suffering renal tubular acidosis with an autosomal recessive pattern that was diagnosed with type3 RTA. DNA was extracted from the blood sample of the patient and his parents by the salting out extraction method. The exons and flanking regions of the CAII gene were amplified using polymerase chain reaction (PCR). We performed exon direct sequencing by forward and reverse primers, which were designed by primer3 program. No mutation was found following the screening of the entire coding sequence of the CAII gene. It is likely that another gene might be involved in this case. In other words, other types of RTA have to be considered.

Keywords: Renal Tubular Acidosis, distal, type 3; Gene; Polymerase Chain Reaction; Sequence Analysis, DNA.

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