Diabetic nephropathy classification: Difference between revisions
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==Classification== | ==Classification== | ||
The following table distinguishes renal findings in type I vs. type II diabetes mellitus: | |||
{| border="1" style="border-collapse:collapse; text-align:left;" cellpadding="5" align="center" | |||
|+ '''''Distinguishing Type I vs. Type II Diabetic Nephropathy<ref name="pmid21659756">{{cite journal| author=Najafian B, Alpers CE, Fogo AB| title=Pathology of human diabetic nephropathy. | journal=Contrib Nephrol | year= 2011 | volume= 170 | issue= | pages= 36-47 | pmid=21659756 | doi=10.1159/000324942 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21659756 }} </ref>''''' | |||
| bgcolor="#d9ff54"|'''Type of Diabetes ''' || bgcolor="#d9ff54"|'''Frequency'''||bgcolor="#d9ff54"|'''Heterogeneity'''||bgcolor="#d9ff54"|'''Severity of Glomerulopathy''' | |||
|- | |||
| bgcolor="#ececec"|'''Type I''' || *20% of diabetes-related ESRD<br>*Renal lesions more frequently attributed to diabetes || Usually less heterogenous lesions || *More severe <br>*Clinical severity associated with renal findings | |||
|- | |||
| bgcolor="#ececec"|'''Type II''' ||*80% of diabetes-related ESRD<br>*Renal lesions may often be non-diabetic || Usually more heterogeneous lesions || *Less severe<br>*Clinical severity and association with renal findings is variable | |||
|} | |||
<sup><center>Adapted from Najafian B, Alpers CE, Fogo AB. Pathology of human diabetic nephropathy. ''Contrib Nephrol''. 2011;170:36-47</center></sup> | |||
Histopathological findings directly correlate with clinical signs and symptoms. The extent of mesangial expansion is inversely associated with the estiamted glomerular filtration rate (GFR) and albumin excretion rate (AER).<ref name="pmid6480821">{{cite journal| author=Mauer SM, Steffes MW, Ellis EN, Sutherland DE, Brown DM, Goetz FC| title=Structural-functional relationships in diabetic nephropathy. | journal=J Clin Invest | year= 1984 | volume= 74 | issue= 4 | pages= 1143-55 | pmid=6480821 | doi=10.1172/JCI111523 | pmc=PMC425280 |url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=6480821 }} </ref><ref name="pmid3712971">{{cite journal| author=Ellis EN, Steffes MW, Goetz FC, Sutherland DE, Mauer SM|title=Glomerular filtration surface in type I diabetes mellitus. | journal=Kidney Int | year= 1986| volume= 29 | issue= 4 | pages= 889-94 | pmid=3712971 | doi= | pmc= |url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3712971 }} </ref><ref name="pmid11812762">{{cite journal| author=Caramori ML, Kim Y, Huang C, Fish AJ, Rich SS, Miller ME et al.| title=Cellular basis of diabetic nephropathy: 1. Study design and renal structural-functional relationships in patients with long-standing type 1 diabetes. | journal=Diabetes |year= 2002 | volume= 51 | issue= 2 | pages= 506-13 | pmid=11812762 | doi= | pmc= |url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11812762 }} </ref> Podocyte injury is also correlated with the degree of proteinuria in diabetic patients; proteinuria is frequently seen when more than 20% of podocytes are denuded from the GBM.<ref name="pmid17536064">{{cite journal| author=Toyoda M, Najafian B, Kim Y, Caramori ML, Mauer M| title=Podocyte detachment and reduced glomerular capillary endothelial fenestration in human type 1 diabetic nephropathy. | journal=Diabetes | year= 2007 | volume= 56 | issue= 8 | pages= 2155-60 |pmid=17536064 | doi=10.2337/db07-0019 | pmc= |url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17536064 }} </ref> | |||
The following table summarizes a classification system proposed in 2010 that correlates histopathological findings with severity of diabetic nephropathy: | |||
{| border="1" style="border-collapse:collapse; text-align:left;" cellpadding="5" align="center" | |||
|+ '''''Classification of Diabetic Nephropathy According to Histopathological Findings (2010)<ref name="pmid20167701">{{cite journal| author=Tervaert TW, Mooyaart AL, Amann K, Cohen AH, Cook HT, Drachenberg CB et al.| title=Pathologic classification of diabetic nephropathy. | journal=J Am Soc Nephrol | year= 2010 | volume= 21 | issue= 4 | pages= 556-63 | pmid=20167701 | doi=10.1681/ASN.2010010010 | pmc= |url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20167701 }}</ref>''''' | |||
| bgcolor="#d9ff54"|'''Class''' || bgcolor="#d9ff54"|'''Findings'''|| bgcolor="#d9ff54"|'''Inclusion Criteria''' | |||
|- | |||
| bgcolor="#ececec"|'''I''' || *Thickening of GBM on electron microscopy<br>*Mild or no changes on light microscopy || *Biopsy does not meet criterial mentioned for class II, III, or IV<br>*GB width by electron microscopy measuring > 395 nm in female and > 430 nm in male patients aged 9 years and above | |||
|- | |||
| bgcolor="#ececec"|'''IIa''' ||Mild mesangial expansion || *Biopsy does not meet criteria for class III or IV<br>*Mild mesangial expansion in > 25% of observed mesangium | |||
|- | |||
| bgcolor="#ececec"|'''IIb''' || *Severe mesangial expansion || *Biopsy does not meet criteria for class III or IV<br>*Severe mesangial expansion in > 25% of observed mesangium | |||
|- | |||
| bgcolor="#ececec"|'''III''' || Nodular sclerosis (Kimmelstiel-Wilson nodules) || *Biopsy does not meet criteria for class IV<br>*At least one Kimmelstiel-Wilson nodule | |||
|- | |||
|bgcolor="#ececec"|'''IV''' || Advanced diabetic glomerulosclerosis || *Global glomerular slerosis in > 50% of glomeruli<br>*Lesions from classes I through III | |||
|} | |||
<sup><center>Adapted from Tervaert TW, Mooyaart AL, Amann K, et al. Pathologic classification of diabetic nephropathy. ''J Am Soc Nephrol''. 2010;21(4):556-63</center></sup> | |||
==References== | ==References== |
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Overview
Classification
The following table distinguishes renal findings in type I vs. type II diabetes mellitus:
Type of Diabetes | Frequency | Heterogeneity | Severity of Glomerulopathy |
Type I | *20% of diabetes-related ESRD *Renal lesions more frequently attributed to diabetes |
Usually less heterogenous lesions | *More severe *Clinical severity associated with renal findings |
Type II | *80% of diabetes-related ESRD *Renal lesions may often be non-diabetic |
Usually more heterogeneous lesions | *Less severe *Clinical severity and association with renal findings is variable |
Histopathological findings directly correlate with clinical signs and symptoms. The extent of mesangial expansion is inversely associated with the estiamted glomerular filtration rate (GFR) and albumin excretion rate (AER).[2][3][4] Podocyte injury is also correlated with the degree of proteinuria in diabetic patients; proteinuria is frequently seen when more than 20% of podocytes are denuded from the GBM.[5]
The following table summarizes a classification system proposed in 2010 that correlates histopathological findings with severity of diabetic nephropathy:
Class | Findings | Inclusion Criteria |
I | *Thickening of GBM on electron microscopy *Mild or no changes on light microscopy |
*Biopsy does not meet criterial mentioned for class II, III, or IV *GB width by electron microscopy measuring > 395 nm in female and > 430 nm in male patients aged 9 years and above |
IIa | Mild mesangial expansion | *Biopsy does not meet criteria for class III or IV *Mild mesangial expansion in > 25% of observed mesangium |
IIb | *Severe mesangial expansion | *Biopsy does not meet criteria for class III or IV *Severe mesangial expansion in > 25% of observed mesangium |
III | Nodular sclerosis (Kimmelstiel-Wilson nodules) | *Biopsy does not meet criteria for class IV *At least one Kimmelstiel-Wilson nodule |
IV | Advanced diabetic glomerulosclerosis | *Global glomerular slerosis in > 50% of glomeruli *Lesions from classes I through III |
References
- ↑ Najafian B, Alpers CE, Fogo AB (2011). "Pathology of human diabetic nephropathy". Contrib Nephrol. 170: 36–47. doi:10.1159/000324942. PMID 21659756.
- ↑ Mauer SM, Steffes MW, Ellis EN, Sutherland DE, Brown DM, Goetz FC (1984). "Structural-functional relationships in diabetic nephropathy". J Clin Invest. 74 (4): 1143–55. doi:10.1172/JCI111523. PMC 425280. PMID 6480821.
- ↑ Ellis EN, Steffes MW, Goetz FC, Sutherland DE, Mauer SM (1986). "Glomerular filtration surface in type I diabetes mellitus". Kidney Int. 29 (4): 889–94. PMID 3712971.
- ↑ Caramori ML, Kim Y, Huang C, Fish AJ, Rich SS, Miller ME; et al. (2002). "Cellular basis of diabetic nephropathy: 1. Study design and renal structural-functional relationships in patients with long-standing type 1 diabetes". Diabetes. 51 (2): 506–13. PMID 11812762.
- ↑ Toyoda M, Najafian B, Kim Y, Caramori ML, Mauer M (2007). "Podocyte detachment and reduced glomerular capillary endothelial fenestration in human type 1 diabetic nephropathy". Diabetes. 56 (8): 2155–60. doi:10.2337/db07-0019. PMID 17536064.
- ↑ Tervaert TW, Mooyaart AL, Amann K, Cohen AH, Cook HT, Drachenberg CB; et al. (2010). "Pathologic classification of diabetic nephropathy". J Am Soc Nephrol. 21 (4): 556–63. doi:10.1681/ASN.2010010010. PMID 20167701.