Abstract
We investigated the effect of aminoguanidine (AG) administration on GBM thickness, glomerular heparan sulfate (HS) content, and urinary albumin and HS excretion in diabetic rats. After induction of diabetes, female Wistar rats were divided into 2 groups: Group AGDM (n=11) received 1g/L aminoguanidine bicarbonate in drinking water, group DC (n=12) was given only tap water. Control rats received AG (group AGH, n=8) or tap water (group HC, n=8). At the end of a period of 8 weeks, urinary albumin and glycosaminoglycan (GAG) excretion was detected. GBM heparan sulfate distribution and count was determined under the electron microscope. The AGDM group had lower urinary albumin and GAG excretion than diabetic controls. GBM thickness was increased in diabetic rats compared to groups of AGDM and HC. In AGDM group alcian blue stained particle distribution and count in the GBM was similar to healthy controls. In conclusion AG prevents the decrease of anionic charged molecules in the GBM and GBM thickening. This can be one of the mechanisms by which AG decreases albuminuria in diabetic rats.
Highlights
Thickening of the glomerular basement membrane (GBM) and albuminuria are the characteristic features of diabetic nephropathy.I1-31 Biochemical alterations of GBM subsequent to increased non-enzymatic glycation of structural proteins and formation of advanced glycosylation end products (AGE) have been invoked in the genesis of an altered size and charge-selective barrier.I4-61 Aminoguanidine, a hydrazine compound that inhibits glycosylation, prevents diabetic complications
Tel.: +90 216 4490347, Fax: +90 216 4280013, e-mail: dyavuz@turk.net parameters: albuminuria, which reflects the defect in glomerular permeability,I131 red blood cell anionic charge (RBCCh) that mirrors the electrostatic charge on the glomerular basement membrane,I141 urine glycosaminoglycan, which is the major elements of glomerular anionic barrier, as an marker of GAG loss from GBM,[5,6,7,8,9,10,11,12,13,14,15,16,17] and the glomerular basement membrane heparan sulfate particles distribution and count that represent the charge selective barrier.Il
RBCCh was found to be lower in had higher GBM thickness than healthy groups diabetic control rats than in the other 3 groups (p
Summary
Thickening of the glomerular basement membrane (GBM) and albuminuria are the characteristic features of diabetic nephropathy.I1-31 Biochemical alterations of GBM subsequent to increased non-enzymatic glycation of structural proteins and formation of advanced glycosylation end products (AGE) have been invoked in the genesis of an altered size and charge-selective barrier.I4-61 Aminoguanidine, a hydrazine compound that inhibits glycosylation, prevents diabetic complications. We do not yet understand the exact mechanism of action of this compound, our hypothesis is that the benefical effects of AG on diabetic kidney could be by preventing the loss of glomerular anionic charge. The aim of this study is to evaluate the effects of AG on glomerular basement membrane charge selectivity. For the determination of glomerular anionic change, we have measured the following parameters: albuminuria, which reflects the defect in glomerular permeability,I131 red blood cell anionic charge (RBCCh) that mirrors the electrostatic charge on the glomerular basement membrane,I141 urine glycosaminoglycan, which is the major elements of glomerular anionic barrier, as an marker of GAG loss from GBM,[5,6,7,8,9,10,11,12,13,14,15,16,17] and the glomerular basement membrane heparan sulfate particles distribution and count that represent the charge selective barrier.Il
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