Urinary N-Acetyl-Beta-D-Glucosaminidase and Beta-2 Microglobulin Excretion In Primary Nephrotic Children

Abstract

The nephrotic syndrome results from greater than 3.5 gm/d proteinuria and is characterized by oedema , hyperlipidemia , hypoproteinemia and other metabolic disorders . In addition to primary (idiopathic) glomerular diseases , the nephrotic syndrome may be secondary to a large number of identifiable disease states . Despite the differences in these causes , the loss of substantial amounts of protein in the urine results in a shared set of abnormalities that define the nephrotic syndrome .

The great majority of childhood nephrotic syndrome is SSNS and minimal lesion is generally found on histologic examination . In contrast , tubular lesions are more frequent in SRNS . In kidney , N-acetyl-beta-D-glucosaminidase (NAG) is located mainly in lysosomes of proximal tubular cells . Damage of these cells leads to an increase in urinary NAG (U-NAG) excretion . Increased U-NAG levels are shown in proteinuric states as well as in various renal diseases . Low molecular weight (LMW) proteins are freely filtered from the glomerular basement membrane and almost completely reabsorbed by proximal tubular epithelial cells . In proximal tubular dysfunction urinary LMW protein levels increase . Urinary P- 2microglobulins (U-P2M) is the most studied LMW protein and a good parameter of renal tubular function in glomerulonephritis

The study was carried out in pediatric department in El-Minya University Hospital and biochemistry department in Assiut University Hospital . Patients were children admitted with the clinical diagnosis of nephrotic syndrome satisfYing the ISKDC criteria.

A total of 40 patients were enrolled over the peroid from january 2005 to june 2005 , they were subdivided according to their response to corticosteroid therapy into 2 groups ; group I