Diabetic nephropathy classification

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

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Overview

Classification

The following table distinguishes renal findings in type I vs. type II diabetes mellitus:

Distinguishing Type I vs. Type II Diabetic Nephropathy[1]
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
Adapted from Najafian B, Alpers CE, Fogo AB. Pathology of human diabetic nephropathy. Contrib Nephrol. 2011;170:36-47

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:

Classification of Diabetic Nephropathy According to Histopathological Findings (2010)[6]
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
Adapted from Tervaert TW, Mooyaart AL, Amann K, et al. Pathologic classification of diabetic nephropathy. J Am Soc Nephrol. 2010;21(4):556-63

References

  1. Najafian B, Alpers CE, Fogo AB (2011). "Pathology of human diabetic nephropathy". Contrib Nephrol. 170: 36–47. doi:10.1159/000324942. PMID 21659756.
  2. 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.
  3. 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.
  4. 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.
  5. 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.
  6. 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.

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