Minimal change disease classification

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Yazan Daaboul, Serge Korjian; Vamsikrishna Gunnam M.B.B.S [2]


Minimal change disease can be classified based on the underlying clinical etiology of disease into primary and secondary. Minimal change disease currently has no pathological classification system. Based on the proposed Columbia classification, minimal change disease was considered an entity within the spectrum of focal segmental glomerulonephritis (FSGS).





Clinical Classification


  • In primary (idiopathic) cases, the underlying cause is not known.


Pathological Classification

  • Minimal change disease currently has no classification system.
  • Early observations noted that a small number of patients with minimal change disease have focal tip lesions.[7]
  • Based on the proposed Columbia classification by D’Agati and colleagues in 2004, minimal change disease was considered an entity within the spectrum of focal segmental glomerulonephritis (FSGS) and may have a clinical course similar to those with “tip lesion” subtype of FSGS.[8]
Pathological Classification of Focal Segmental Glomerulosclerosis[8]
Variant Location of Lesion Distribution of Lesion Characteristic Features
Not Otherwise Specified (NOS) Anywhere Segmental Capillary lumen abolished by the segmental increase in matrix.
Perihilar Variant Perihilar Segmental Presence of one or more glomeruli containing hyalinosis in the perihilar regions with or without sclerosis. Within each glomerulus, the segmental lesions must contain > 50% perihilar hyalinosis and/or sclerosis.
Cellular Variant Anywhere Segmental Presence of one or more glomerulus with segmental hypercellularity of the capillary endothelium that blocks the capillary lumen, with or without foam cells and/or karryohexis.
Tip Variant At tip domain Segmental One or more segmental lesions, that include tip domains. Lesions must have adhesions/confluence of podocytes with parietal or tubular cells. Tip domains are defined as 25% of tuft adjacent to the origin of the proximal tubule. Sclerosing lesions shuld be <25% of tuft, while cellular lesions should be < 50% of tuft. No perihilar sclerosis should be observed.
Collapsing Variant Anywhere Segmental or global One or more glomeruli with collapse with evidence of podocyte hypertrophy and hyperplasia.


  1. Sagel I, Treser G, Ty A, Yoshizawa N, Kleinberger H, Yuceoglu AM, Wasserman E, Lange K (October 1973). "Occurrence and nature of glomerular lesions after group A streptococci infections in children". Ann. Intern. Med. 79 (4): 492–9. PMID 4795879.
  2. O'Donoghue DJ, Lawler W, Hunt LP, Acheson EJ, Mallick NP (April 1991). "IgM-associated primary diffuse mesangial proliferative glomerulonephritis: natural history and prognostic indicators". Q. J. Med. 79 (288): 333–50. PMID 1852859.
  3. Kersnik Levart T, Kenda RB, Avgustin Cavić M, Ferluga D, Hvala A, Vizjak A (December 2005). "C1Q nephropathy in children". Pediatr. Nephrol. 20 (12): 1756–61. doi:10.1007/s00467-005-2040-4. PMID 16247648.
  4. Jennette JC, Hipp CG (August 1985). "C1q nephropathy: a distinct pathologic entity usually causing nephrotic syndrome". Am. J. Kidney Dis. 6 (2): 103–10. PMID 3875286.
  5. Iskandar SS, Browning MC, Lorentz WB (October 1991). "C1q nephropathy: a pediatric clinicopathologic study". Am. J. Kidney Dis. 18 (4): 459–65. PMID 1928065.
  6. Habib GS, Saliba W, Nashashibi M, Armali Z (August 2006). "Penicillamine and nephrotic syndrome". Eur. J. Intern. Med. 17 (5): 343–8. doi:10.1016/j.ejim.2006.03.001. PMID 16864010.
  7. Haas M, Yousefzadeh N (2002). "Glomerular tip lesion in minimal change nephropathy: a study of autopsies before 1950". Am J Kidney Dis. 39 (6): 1168–75. doi:10.1053/ajkd.2002.33386. PMID 12046027.
  8. 8.0 8.1 D'Agati VD, Fogo AB, Bruijn JA, Jennette JC (2004). "Pathologic classification of focal segmental glomerulosclerosis: a working proposal". Am J Kidney Dis. 43 (2): 368–82. PMID 14750104.

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