Diabetic nephropathy classification: Difference between revisions
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==Overview== | ==Overview== | ||
Diabetic nephropathy can be classified according to the type of underlying diabetes mellitus or the histopathological findings of the disease. | |||
==Classification== | ==Classification== | ||
Diabetic nephropathy can be classified according to the type of diabetes which resulted in the disease process. Another method of classification is based on the histopathological findings in diabetic nephropathy. | Diabetic nephropathy can be classified according to the type of [[Diabetes mellitus|diabetes]] which resulted in the disease process. Another method of classification is based on the histopathological findings in diabetic nephropathy. | ||
===Type of Diabetes=== | ===Type of Diabetes=== | ||
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|+ '''''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>''''' | |+ '''''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="#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 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 | | 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><center>Adapted from Najafian B, Alpers CE, Fogo AB. Pathology of human diabetic nephropathy. ''Contrib Nephrol''. 2011;170:36-47</center> | ||
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> | Histopathological findings directly correlate with clinical signs and symptoms. The extent of [[Mesangial cell|mesangial]] expansion is inversely associated with the estiamted [[Glomerular filtration rate|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> [[Podocytes|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> | ||
===Histopathological Findings of Diabetic Nephropathy=== | ===Histopathological Findings of Diabetic Nephropathy=== | ||
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|+ '''''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>''''' | |+ '''''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="#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" |'''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" |'''IIa''' ||Mild [[Mesangial cell|mesangial]] expansion || *Biopsy does not meet criteria for class III or IV<br>*Mild [[Mesangial cell|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" |'''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" |'''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 | | 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><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> | ||
==References== | ==References== | ||
Latest revision as of 15:42, 16 July 2018
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Dima Nimri, M.D. [2]
Overview
Diabetic nephropathy can be classified according to the type of underlying diabetes mellitus or the histopathological findings of the disease.
Classification
Diabetic nephropathy can be classified according to the type of diabetes which resulted in the disease process. Another method of classification is based on the histopathological findings in diabetic nephropathy.
Type of Diabetes
| 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]
Histopathological Findings of Diabetic Nephropathy
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.