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Heavy Proteinuria May Speed Progression Of Diabetic Nephropathy
A DGReview of :"Association of monocyte chemoattractant protein-1 with renal tubular damage in diabetic nephropathy."
Journal of Diabetes and its Complications
01/13/2003
By David Loshak
Heavy proteinuria may quicken the progression of diabetic nephropathy, say researchers.
The process may be a result of the increase in the expression of monocyte chemoattractant protein-1 in renal tubuli, say investigators at Akita University School of Medicine, Akita, Japan.
Monocyte chemoattractant protein-1 is a chemokine which mediates renal interstitial inflammation, tubular atrophy and interstitial fibrosis. It does so by recruiting monocytes and macrophages into renal tubulointerstitium.
The investigators noted that recent studies had shown that protein overload in renal tubular cells up-regulated monocyte chemoattractant protein-1 gene and its protein expression.
They then put forward the idea that increased expression of monocyte chemoattractant protein-1 in renal tubuli, probably triggered by increased leakage of plasma protein from glomerular capillary to tubular fluid, might contribute to renal tubular damage and accelerate diabetic nephropathy.
The investigators examined urinary excretion levels of monocyte chemoattractant protein-1and N-acetylglucosaminidase, a sensitive marker of renal tubular damage, in 72 Japanese Type II diabetic patients. Twenty nine had normoalbuminuria, 25 had microalbuminuria and 18 had macroalbuminuria.
The median urinary excretion level of monocyte chemoattractant protein-1 in patients with macroalbuminuria was 394.4 ng/g creatinine, significantly higher than the levels in patients with normoalbuminuria (159.6 ng/g creatinine) and microalbuminuria (193.9 ng/g creatinine). Moreover, urinary monocyte chemoattractant protein-1 excretion level was positively correlated with urinary excretion levels of albumin and N-acetylglucosaminidase in all patients.
The investigators said that these findings suggested that monocyte chemoattractant protein-1 was produced in renal tubular cells and released into urine in proportion to the degree of proteinuria (albuminuria).
Journal of Diabetes and its Complications 2003;17(1):11-15.
"Association of monocyte chemoattractant protein-1 with renal tubular damage in diabetic nephropathy."
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