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IgG Subclass Expression in Diabetic Nephropathy
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Abstract
Background: This study aimed to analyze the distribution of IgG subclasses in diabetic nephropathy (DN) and its association with clinico-pathological features. Methods: Forty DN cases were analyzed to identify IgG subclasses, as well as collagen IV α5, CD34, and KIM-1.Results: Both IgG and its subclasses showed a linear expression and overlapped with collagen IV α5 on glomerular basement membrane (GBM) and some of tubular basement membrane (TBM), without complement deposition. Eleven cases of IgG subclass deposition along both GBM and TBM were associated with more proteinuria. Five cases of TBM-only IgG subclass deposition were accompanied with less KIM-1 positivity and more arteriosclerosis. The major IgG subclasses expressed on GBM were IgG1 and IgG2, while TBM expression was mainly IgG1 and IgG3. Glomerular IgG1-positive status was associated with less CD34 expression, while IgG2-positive status was associated with thicker GBM. Expression of multiple IgG subclasses along TBM showed less KIM-1 positivity and interstitial inflammation than those with isotype or no IgG subclass expression.Conclusions: IgG subclasses were selectively deposited along GBM and TBM in DN, which was determined by their profiles and severity of glomerular/tubular injury. IgG and its subclass deposition is not causal, but the consequence of renal injury and these positive statuses are associated with different DN injuries.
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Title: IgG Subclass Expression in Diabetic Nephropathy
Description:
Abstract
Background: This study aimed to analyze the distribution of IgG subclasses in diabetic nephropathy (DN) and its association with clinico-pathological features.
Methods: Forty DN cases were analyzed to identify IgG subclasses, as well as collagen IV α5, CD34, and KIM-1.
Results: Both IgG and its subclasses showed a linear expression and overlapped with collagen IV α5 on glomerular basement membrane (GBM) and some of tubular basement membrane (TBM), without complement deposition.
Eleven cases of IgG subclass deposition along both GBM and TBM were associated with more proteinuria.
Five cases of TBM-only IgG subclass deposition were accompanied with less KIM-1 positivity and more arteriosclerosis.
The major IgG subclasses expressed on GBM were IgG1 and IgG2, while TBM expression was mainly IgG1 and IgG3.
Glomerular IgG1-positive status was associated with less CD34 expression, while IgG2-positive status was associated with thicker GBM.
Expression of multiple IgG subclasses along TBM showed less KIM-1 positivity and interstitial inflammation than those with isotype or no IgG subclass expression.
Conclusions: IgG subclasses were selectively deposited along GBM and TBM in DN, which was determined by their profiles and severity of glomerular/tubular injury.
IgG and its subclass deposition is not causal, but the consequence of renal injury and these positive statuses are associated with different DN injuries.
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