Assessment of urinary cystatin c in TV pel diabetic children

Background: Diabetes is the disease of this century; its incidence had progressively increased in the last few years especially in young ages. Cystatin C is a single chain non glycosylated basic protein produced by all nucleated cells at a constant rate freely filtered by the renal glomernli and almost entirely reabsorbed in the proximal tubule and its level in urine increases in cases with renal tubular dysfunction. Aim: The aim of the present study was to assess the urinary Cystatm C excretion in diabetic children attending the pediatric department of the National Institute of Diabetes and Endocrinology [NIDE] in comparison with apparently healthy children with comparable age and sex

Methods: We studied 60 children and adolescents [38 Females and 22 Males] with type 1 diabetes. They had a mean age of 13.93+/-2.92 years ranging from [10-18] years and a mean duration of 6.67+/- 3.35 years of diabetes. In addition to 30 healthy children and adolescents included as a control group, fourteen of them were females and 16 were males having a mean age of 14.731 2.13 years with the age range of [10- 18] years. All subjects were subjected to full history taking and thorough clinical examination with special emphasis on diabetic details and complications and an investigations including Microalbuminuria detected by measuring the albumin in urine by turbid metric method and urine creatinine by colorimetric measure and represented by [[A/C] ratio] also urinary Cystatin C excretion by ELISA from a morning urine sample was tested

Results and Conclusion: High urinary Cystatin C levels were present in 41 diabetic patients and none of the control group and were positively correlated to HbAlc and microalbuminuria [MA]

Alterations in the ultrastructure of the liver in chronic lead intoxication in the adult albino rats

In the present work, the effect of chronic lead intoxication in two doses [5 mg/kg body weight, as therapeutic dose and 10 mg/kg body weight as sublethal dose] on the ultrastructure of the rat liver was studied. The rats were classified into three groups: one control group [10 rats], experimental group A [20 rats] who received a therapeutic dose of lead acetate orally for six months, and experimental group B [20 rats] who received a sublethal dose of lead acetate orally for six months. Ten rats of both groups A and B were sacrificed one month after the last given dose [recovery rats]. Small slices of the liver of the rats of all groups were processed for electron microscopic examination. The livers of group A rats showed a few pathological changes in the form of proliferation of both rough and smooth endoplasmic reticulum, multiple areas of glycogen depletion with a few lysosomes and fat droplets. The liver of group B rats showed marked pathological changes in both hepatocytes and Van Kuppfer's cells. The cytoplasm of the hepatocytes showed intracytoplasmic vacuoles and a few degenerative granules. The Von Kuppfer's cells showed pale degenerated cytoplasm, intra-cytoplasmic and degenerated electro-dense granules. The recovery animals of group A showed good recovery, while those of group B showed only partial recovery

Ultra-structural changes induced in rat kidney by chronic administration of lead acetate

Lead is a widespread environmental contaminant, found in air, canned food, drinking water and paints, creating environmental pollution. Lead is capable of damaging vital organs especially the kidneys because it is the main route of lead excretion. The purpose of the present work was to determine the ultra-structural effects of lead acetate on the kidneys of albino rats, who are given lead acetate in their drinking water through orogastric intubation in both therapeutic [group A] and sub-lethal [group B] doses for 6 months.The glomerular capillary wall in the kidneys of group A rats showed mild changes in the form of partial fusion of the secondary foot processes of podocytes, while the kidneys of group B rats showed marked changes in the form of diminution of fenestrated endothelia and marked reduction of secondary foot processes of podocytes. The proximal convoluted tubules in the kidneys of group A rats showed mild changes in the form of absence of both basal striations and brush border with disorientation of deep basal infoldings of the cell membrane. The proximal tubules in the kidneys of group B rats showed marked changes in the form of multiple intracytoplasmic vacuoles, multiple lysosomes, multiple degenerated mitochondria and irregular thickened basement membrane. Kidneys of animals left to recover in group A showed complete recovery, while only partial recovery was detected in group B