Urinary tract infection (UTI) is one of the most common community-acquired infections. Different organisms can be the cause of UTI in children, with resistance to antibiotics becoming a significant problem in the choice of treatment. Worldwide studies have documented the prevalence of uropathogens in different countries. However, there is no previous study documenting the incidence of different uropathogens in Oman. We aim to report the most common uropathogens and their antibiotic sensitivity patterns in children presenting with documented, single episode UTI at a tertiary hospital in Oman. A retrospective analysis of all Omani children below 14 years who presented with a case of first documented UTI to SQUH between September 2008 and August 2012 was conducted. Data were obtained from the patients' electronic records in the hospital information system. Data were then analyzed using SSPS (Statistical Package for Social Sciences program, Version 20, IBM, Chicago, IL, USA). In the retrospective review of all urine cultures, 438 positive urine cultures were identified. Out of those, 208 (47.5%) belonged to children with their first episode of UTI. Thirty-three patients were excluded and 75 patients were included in the final analysis. Escherichia coli was the most frequently encountered uropathogen in our cohort (69%), followed by Klebsiella pneumoniae infection (17%). Nearly half (46.6%) of these two common organism were resistant to Cotrimoxazole, while 31% of them were resistant to Augmentin. Twenty-four percent of the E. coli and K. pneumoniae strains were resistant to Cefuroxime, and only 10% were resistant to nitrofurantoin. Both Augmentin and Cotrimoxazole should not be the first line antibiotics to treat UTI.

Consanguineous marriage is quite prevalent in the Sultanate of Oman, with up to 45% of marriages being consanguineous. The aim of this study was to determine demographic, clinical and serological characteristics between familial and non-familial cases of juvenile systemic lupus erythematosus (SLE) in a highly consanguineous region such as Oman. Hospital medical records were retrospectively reviewed for 44 consecutive children with juvenile SLE seen at Sultan Qaboos University Hospital, 16 with familial SLE and 28 with non-familial SLE. All the children included in the study were Omani, diagnosed before 13 years of age, and fulfilled the 1982 revised ACR criteria. Analyses were performed using descriptive statistics. There were largely no significant differences in the clinical and serological manifestations between the two cohorts. However, the familial SLE group was associated with worse SLEDAI score at onset of diagnosis compared with the non-familial cohort (12 vs. 17; p = 0.003) suggesting a greater severity of disease in the familial group. Even though the rate of familial SLE is higher in Oman (36%) compared with the Western world (10-12%), it appears that familial and non-familial SLE cases are in fact similar disease entities in both the West and the Middle Eastern countries.

Nocardia asteroides is a rare pathogen in peritoneal dialysis-related peritonitis. We report on a 13-year-old female with Nocardia asteroides peritonitis complicated by an intra-abdominal abscess. Linezolid was administered intravenously for 3 months and followed by oral therapy for an additional 5 months with close monitoring for adverse effects. The patient was discharged after 3 months of hospitalization on hemodialysis. The diagnosis and management of such cases can be problematic due to the slow growth and difficulty of identifying Nocardia species. The optimal duration of treatment for Nocardia peritonitis is not known. Linezolid can be used for prolonged periods in cases of trimethoprim/sulfamethoxazole-resistant cases with close monitoring for adverse effects.

Very few studies have been published on how to treat children with membranoproliferative glomerulonephritis type I (MPGN I), and as yet there is only one report on the use of mycophenolate mofetil (MMF) in children with MPGN I. We report a 12-year-old boy who presented with edema, hypertension, nephrotic range proteinuria, and microscopic hematuria following an upper respiratory tract infection. Laboratory tests revealed a serum creatinine of 90 micromol/l, albumin of 20 g/l, and a C3 of 0.11 g/l (normal range: 0.7-1.4). Renal biopsy showed the presence of MPGN I. Upon failure to induce remission with prednisone, we started the patient on MMF at 500 mg/day (300 mg/m(2)), increasing up to a final dose of 2 g/day (1200 mg/m(2)), with a MMF metabolite mycophenolic acid (MPA) target range of 2-5 mg/l. Prednisone was subsequently reduced to alternate day therapy and gradually weaned to 7.5 mg on alternate days over 9 months. Within 4 months of starting MMF therapy, there was significant improvement in serum creatinine (decrease from 156 to 64 micromol/l), serum albumin (increase from 23 to 40 g/l), and proteinuria (decrease from 13 g/day to 40 mg/day). Twelve months following the introduction of MMF into his therapeutic regimen, he remains in remission with no further relapses. In summary, this case suggests that there may be potential benefit for use of MMF in children with refractory MPGN I, which supports the rationale for prospectively evaluating MMF treatment in a treatment trial of refractory MPGN I.

Introduction Imerslund‐Gräsbeck syndrome (IGS) is a rare autosomal‐recessive disorder characterized by selective vitamin B12 malabsorption, megaloblastic anemia, and proteinuria. The precise incidence of this disorder is unknown in the Middle East and Arab countries. The disease is caused by a homozygous variant in either AMN or CUBN genes. In addition, some compound heterozygous variants are reported. Methods Clinical and laboratory data of patients diagnosed with IGS in Oman were retrospectively collected. Mutation analysis for all genes involved in vitamin B12/folic acid metabolism and megaloblastic anemia was conducted using next‐generation sequencing (NGS). Results Three siblings (2 girls and a boy) have been diagnosed with the condition. They exhibit a phenotypic variability with different age of presentation and different spectrum of disease. All patients harbor a novel biallelic frameshift mutation in exon 11 of AMN gene (p.Pro409Glyfs*), which was not reported previously in the literature. Both parents are heterozygotes for the same variant. All patients responded well to vitamin B12 parenteral therapy, but proteinuria persisted. Conclusion In communities with high incidence of consanguinity, cases of early‐onset vitamin B12 deficiency should be thoroughly investigated to explore the possibility of Imerslund‐Gräsbeck syndrome and other vitamin B12–related hereditary disorders. Further local and regional studies are highly recommended.