الفهرس 
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Abstract
Diabetic nephropathy (DN) is a common complication of diabetes mellitus which has a major impact on patient morbidity and mortality, and therefore a profound impact on the delivery of health care. It is now the commonest cause of renal failure requiring renal replacement therapy worldwide. It affects more than one-third of patients with type 1 diabetes and an ever-increasing proportion of patients with type 2 diabetes, such that it is the single most common cause of end-stage renal failure.
Diabetic kidney disease is complex and multifactorial. The structural alterations related to diabetes mellitus (DM) may be divided into early adaptive alterations and the later pathologic changes associated with progression of nephropathy. Although diabetic nephropathy was traditionally considered a primary glomerular disease, it is now widely accepted that the rate of deterioration of function correlate best with the degree of renal tubulointerstitial fibrosis. Recently, tubular involvement has been proved to precede glomerular involvement because several tubular proteins and enzymes are detectable even before the appearance of microalbuminuria and rise in serum urea and creatinine, such as kidney injury molecule-1(KIM-1), B- N-acetylglucosaminidase (B- NAG), β2-microglobulin, and Retinol binding protein (RBP). If tubular lesion is early detected, diabetic nephropathy could be probably controlled by good glycemic control.
KIM-1 is a type 1 membrane glycoprotein that is not present in urine normally. The soluble KIM-1 protein that appears in the urine of humans is about 90KDa and was markedly up regulated as early as 6 hours after an ischemic insult and remain elevated for a period of 48 hours post-injury.
KIM-1 helps to remove the apoptotic cells in a timely fashion way forming professional phagocytes and also to avoid the undesirable attachment of exfoliated cells to one another or fibronectin so as to reduce cast formation and tubular obstruction.
KIM-1 was believed to be an ideal biomarker of kidney injury; due to its marked up regulation and insertion into the apical membrane of the proximal tubule; its persistence in the epithelial cell until the cell has completely recovered and the urinary levels of KIM-1 increased prior to the appearance of casts in the urine making it more sensitive and specific than the measurement of blood urea nitrogen, creatinine and urinary albumin.
The present work aimed at determining Kidney injury molecule (KIM-1) level in the urine of patients with type 2 diabetes mellitus in order to evaluate it as an early diagnostic parameter for nephropathy in comparison to urinary albumin excretion.
The present study was performed on eighty subjects divided into two main categories. The Control group (Group I) included twenty apparently healthy subjects. The patients group included sixty diabetic patients. These patients were divided into 3 groups according to their urinary albumin- creatinine ratio according to American Diabetes Association: Group II included twenty normoalbuminuric diabetics with albumin to creatinine ratio (ACR) less than 30 mg/g. Group III included twenty microalbuminuric diabetics with albumin to creatinine ratio (ACR) ranging from 30 – 299 mg/g and Group IV included twenty macroalbuminuric diabetics with albumin to creatinine ratio (ACR) equal to or more than300 mg/g.