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. Author manuscript; available in PMC: 2012 Mar 1.
Published in final edited form as: Am J Kidney Dis. 2011 Jan 15;57(3):498–507. doi: 10.1053/j.ajkd.2010.10.052

Table 2.

A comparison of characteristics of LN in humans and mice

Features of human LN Spontaneous disease in lupus mice*

Female predominance NZB/W F1, NZM2328

Serum autoantibodies
   anti-nuclear, anti-dsDNA All strains
   anti-Sm MRL/lpr

Kidney Pathology

   Glomerular Immune complexes All strains

   Proliferative GN All strains

   Type V membranous nephropathy None**

   Glomerulosclerosis All strains

   Tubulointerstitial inflammation All strains

Cellular infiltrates

   Neutrophils NZM2328

   Macrophages All strains

   Dendritic cells All strains

   NK cells MRL/lpr

   T cells (CD4/CD8) MRL/lpr, NZM2328, NZB/W F1

   B cells NZB/W F1

   Plasma cells NZB/W F1

Kidney failure*** All strains

Other clinical features

   Hypertension None reported

   Systemic involvement skin, MRL/lpr; salivary glands, NZB/W F1

Abbreviations: dsDNA, double-stranded DNA; LN, lupus nephritis; NZB, New Zealand Black; NZW, NZ White; NZM, NZ Mixed; NK, natural killer; GN, glomerulonephritis.

*

includes NZB/W F1, NZM2410, NZM2328, MRL/lpr, BXSB strains

**

can be induced by immuno-modulation

***

elevated serum creatinine, serum urea nitrogen, proteinuria