Key points:

1. Up to 50% patients with SLE develop renal disease (>550 mg/ day of proteinuria, and/or active urine sediment) within the first year from SLE diagnosis. But renal disease can present years before or after the development of systemic SLE.
2. Lupus nephritis (LN) is defined by the presence of immune deposits by light (LM), immunofluorescence (IF) and/or electron microscopy (EM). The location, nature, and chronicity of the immune deposits primarily determine the type of lesion observed by LM (Class I-VI).
3. Other renal lesions lacking immune deposits might also be seen in patients with SLE (e.g. lupus podocytopathy, ANCA overlap, cryoglobulinemic GN, or antiphospholipid antibody associated thrombotic microangiopathy) = lupus-associated renal disease rather than lupus nephritis.
4. Immunofluorescence shows full house positive for : C3, C1q, IgG, IgA, IgM.
5. Different patterns of injury are as follow:

• Mesangial pattern of injury. Mesangial deposits are hallmark of LN-Clinically: microscopic hematuria, sub-nephrotic proteinuria, normal eGFR-LM: mesangial hypercellularity and proliferation-EM: mesangial EDD, with no cell membrane surrounding them i.e. extra-cellular deposits.
• Epithelial pattern of injury. Clinically: significant proteinuria with nephrotic syndrome, normal to mild decrease in GFR. On LM: Thick GBM spikes (Jones stain). On EM: Discrete subepithelial deposits with varying degrees of lucency (implies chronicity). Over time, intramembranous deposits eventually become lucent and resolve. Also, foot process effacement together with mesangial and sub-endothelial deposits, is strongly suggestive of LN.
• Membrano-proliferative pattern of injury. On LM: Double contours of GBM (outer contour is original GBM, inner contour is new GBM made by endothelial cells, clear space in middle is artifact of staining). On EM: Sub-endothelial deposits.
• Endothelial pattern of injury (Most destructive). Clinical: nephritic , decreased GFR, hematuria, mild to moderate proteinuria. On LM: endocapillary proliferation/ leukocytosis, endothelial injury. On EM: subendothelial immune complex deposits.
• Other findings. Segmental necrosis: Mediated by inflammation. Segmental sclerosis: scarring from prior segmental necrosis. Karryorhectic debris, segmental necrosis, fibrinoid necrosis, leading to cellular crescent, eventually>> fibrocellular>>fibrous crescent.