Diabetic nephropathy classification
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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
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.