Assessment of early kidney injury caused by asymptomatic bacteriuria in children with type 1 diabetes.

INTRODUCTION: Infection is one of the most frequent causes of morbidity and mortality in diabetic patients. Some microorganisms become more virulent in a high glucose concentration. Diabetics are more likely to have asymptomatic and symptomatic bacteriuria. NGAL is secreted in high concentrations into the blood and urine within two hours of AKI. OBJECTIVES: The aim of the study is early detection of UTI in type1diabetic children through screening of their urine samples, and measurement of NGAL urinary levels in cases with asymptomatic bacteriuria for early detection of AKI to prevent serious complications. PATIENTS AND METHODS: One thousand twenty-two known diabetic children on regular follow up in endocrine outpatient clinic at Minia Children University hospital were screened for UTI. From them only 52 diabetic children were diagnosed as asymptomatic bacteriuria (group I), 52 diabetic children with normal urine analysis (group II) and 52 apparently healthy children, age and sex matched, served as controls (group III). CBC, Renal function test, HbA1c, hs- CRP, Albumin/creatinine ratio, urine examination, urine culture, GFR and urinary NGAL were done to all children. RESULTS: Thirty-seven females (71.2%) had asymptomatic bacteriuria, Hs CRP and urinary NGAL were significantly higher, while GFR was significantly lower in diabetic children with bacteriuria than the other two groups. For diabetic children with bacteriuria, (AUC) for NGAL was 1 with optimal cutoff value of > 44.1 (Sensitivity 100% and Specificity 100%) while AUC for hsCRP was 0.887 with optimal cutoff value of > 1 (Sensitivity 82.69% and Specificity 90.38%). CONCLUSION: Routine urine analysis should be done for all diabetic children even if they are asymptomatic. NGAL and hsCRP are non-invasive methods that could detect early renal injury in these patients thus, early, and proper management of UTI should be started to prevent renal injury.

Effect of acute and chronic liver diseases on the thyroid function in children.

BACKGROUND: Thyroid hormones modulate hepatic function through regulation of basal metabolic rate in addition; the liver metabolizes the thyroid hormones and regulates their endocrine effects. OBJECTIVES: To assess thyroid functions in children with acute and chronic liver diseases. METHODS: 85 studied children were divided into 4 groups; group 1 (20 children) with acute hepatitis (AH), group 2 (20 children) chronic liver disease1 (CLD1; relatively preserved liver functions including Child-Pugh stage A), group 3 (20 children) chronic liver disease2 (CLD2; includes Child-Pugh stage B or C), group 4 (25 children) controls. All groups were subjected to detailed history, physical examination, Complete blood count, liver, renal function tests, viral markers, and thyroid functions (FT3, FT4, TSH). RESULTS: Free T3 levels were lower in children with AH, CLD1 and CLD2. There was significant increase in TSH serum levels in CLD2.In acute hepatitis a negative correlation between serum free T4 and AST (r = -0.991), positive correlation between serum TSH and AST, VLDL, and cholesterol levels (r= 0.503, 0.533 and 0.498). A positive correlation between free T3 levels and prothrombin concentration (r= 0.991). Negative correlations between free T3 levels and PT, serum bilirubin and LDL serum levels in children with CLD2 (r= -0.992) (r= -0.902) and (r= -0.946) CONCLUSION: Acute and chronic liver diseases affect thyroid function in children and is correlated with the disease severity.

Assessment of Preptin peptide level in the sera of rachitic children and in breast milk of their mothers.

BACKGROUND: Preptin is a 34-residue pancreatic hormone that stimulates osteoblast proliferation and reduces osteoblast apoptosis. RESEARCH AIMS: To measure levels of serum Preptin in rachitic children and in breastmilk of their mothers and to compare with levels in healthy non-rachitic children. METHODS: Thirty children with rickets and another 30 non-rachitic age and sex matched controls were subjected to detailed history, physical examination including anthropometric measurements, assessment of signs of rickets and laboratory measurement of serum vitamin D, calcium, phosphorus, alkaline phosphatase and Preptin. Mothers' breast milk Preptin were also measured. RESULTS: Significantly lower serum Preptin (p < 0.001) in rachitic children with a significant negative correlation between serum Preptin and alkaline phosphatase (P < 0.0001). Lower breastmilk Preptin levels in mothers of rachitic children (P < 0.001) with a negative correlation between breastmilk Preptin and both maternal weight and BMI(P < 0.01&P < 0.02). Mothers' milk Preptin is positively correlated with serum Preptin and calcium in non-rachitic children(P < 0.001&0.04), but negatively correlated with their mothers' age (P < 0.01). CONCLUSION: Preptin may play a role in the etiology of rickets in children. Further studies are recommended to evaluate Preptin role in treatment of rickets in children.