Systemic Lupus Erythematosus is an autoimmune disease involving multiple

organs, characterized by a vast array of autoantibodies, particularly antinuclear

antibodies (ANAs), in which injury is caused mainly by deposition of immune
complexes and binding of antibodies to various cells and tissues.

Injury to the skin, joints, kidney, and serosal membranes is prominent, but virtually every
organ in the body may be affected.

Kidney. Up to 50% of SLE patients have clinically significant renal involvement, and the
kidney virtually always shows evidence of abnormality if examined by electron
microscopy and immunofluorescence.

Picture:- Schematic representation of the pathogenesis of lupus nephritis.

six patterns of glomerular disease are recognized

A. Minimal mesangial lupus nephritis (class I)

B. Mesangial proliferative lupus nephritis (class II)
C. Focal lupus nephritis (class III)
D. Diffuse lupus nephritis (class IV)
E. Membranous lupus nephritis (class V)
F. Advanced sclerosing lupus nephritis (class VI)

Picture:-Characteristics and specificity of the histopathology of lupus nephritis.

 A. Minimal mesangial lupus nephritis (class I)
1. It is very uncommon, and is characterized by immune complex deposition in the
mesangium,
2. Identified by immunofluorescence and by electron microscopy, but without
structural changes by light microscopy.

B. Mesangial proliferative lupus nephritis (class II)

1. It is characterized by mesangial cell proliferation, often accompanied by
accumulation of mesangial matrix, and granular mesangial deposits of
immunoglobulin and complement without involvement of glomerular capillaries.

C. Focal lupus nephritis (class III)

1. It is defined by involvement of fewer than 50% of all glomeruli.
2. The lesions may be segmental (affecting only a portion of the glomerulus) or
global (involving the entire glomerulus).
3. Affected glomeruli may exhibit swelling and proliferation of endothelial and
mesangial cells associated with leukocyte accumulation, capillary necrosis, and
hyaline thrombi.
4. Often, there also is extra capillary proliferation associated with focal necrosis and
crescent formation (Fig.A).

Focal proliferative glomerulonephritis, with two focal necrotizing lesions at the 11 o’clock and 2 o’clock positions
(H&E stain). Extra capillary proliferation is not prominent in this case.
5. The clinical presentation ranges from mild hematuria and proteinuria to acute
renal insufficiency. Red blood cell casts in the urine are common when the
disease is active.
6. Some patients progress to diffuse glomerulonephritis.
7. The active (or proliferative) inflammatory lesions can heal completely or lead to
chronic global or segmental glomerular scarring.

D. Diffuse lupus nephritis (class IV)

1. is the most common and severe form of lupus nephritis.
2. The lesions are identical to those in class III, but differ in extent; in diffuse
lupus nephritis, half or more of the glomeruli are affected.
3. Involved glomeruli show proliferation of endothelial, mesangial, and epithelial
cells (see fig. B), with the latter producing cellular crescents that fill Bowman’s
space.
4. Subendothelial immune complex deposits may create a circumferential
thickening of the capillary wall, forming “wire-loop” structures on light
microscopy (see Fig.C).
5. Immune complexes can be readily detected by electron microscopy (see Fig.
D) and immunofluorescence (see Fig. E).
6. Lesions may progress to scarring of glomeruli. Patients with diffuse
glomerulonephritis are usually symptomatic, showing hematuria as well as
proteinuria. Hypertension and mild to severe renal insufficiency also are
common.
(E) Deposition of IgG antibody in a granular pattern, detected by immunofluorescence . (B) Diffuse proliferative
glomerulonephritis. Note the marked increase in cellularity throughout the glomerulus (H&E stain). (C) Lupus nephritis
showing a glomerulus with several “wire-loop” lesions representing extensive subendothelial deposits of immune complexes
(periodic acid-Schiff stain). (D) Electron micrograph of a renal glomerular capillary loop from a patient with SLE nephritis.
Subendothelial dense deposits (arrowheads) on basement membrane (arrow) correspond to “wire loops” seen by light
microscopy

E. Membranous lupus nephritis (class V)

1. It is characterized by diffuse thickening of the capillary walls due to deposition
of subepithelial immune complexes, similar to idiopathic membranous
nephropathy.
2. The immune complexes are usually accompanied by increased production of
basement membrane-like material, resulting in “holes” and “spikes” on silver
stain.
3. This lesion is usually accompanied by severe proteinuria or nephrotic syndrome,
and may occur concurrently with focal or diffuse lupus nephritis.
F. Advanced sclerosing lupus nephritis (class VI)
1. is characterized by sclerosis of more than 90% of the glomeruli, and
represents end-stage renal disease.
2. Changes in the interstitium and tubules are frequently present.
3. Rarely, tubulointerstitial lesions may be the dominant abnormality.
4. Discrete immune complexes similar to those in glomeruli are present in the
tubular or peritubular capillary basement membranes in many lupus nephritis
patients.
5. Sometimes, there are well-organized B-cell follicles in the interstitium, associated
with plasma cells that may be sources of autoantibodies.