Diffuse proliferative nephritis

[1] In absence of SLE, DPGN pathology looks more like Membranoproliferative glomerulonephritis[citation needed] In DPGN Most of the glomeruli show endothelial and mesangial proliferation, affecting the entire glomerulus, leading to diffuse hypercellularity of the glomeruli, producing in some cases epithelial crescents that fill Bowman's space.

When extensive, immune complexes create an overall thickening of the capillary wall, resembling rigid "wire loops" on routine light microscopy.

Electron microscopy reveals electron-dense subendothelial immune complexes (between endothelium and basement membrane).

Most of SLE patients with DPGN have hematuria with moderate to severe proteinuria, hypertension, and renal insufficiency.

Many of the symptoms, like edema and hypertension, occur due to the decrease in glomerular filtration rate.

[3] Patients can experience general systemic symptoms including fatigue, vomiting, nausea.

[citation needed] If a patient has DPGN with underlying anti-GBM then they can experience alveolar hemorrhage and respiratory issues.

Usually the deposition of immune-complexes (antigen-antibody complex) that activates the complement system are involved.

Immune-complexes are combinations of DNA, anti-dsDNA ubiquitin, and other proteins in DPGN that are associated with lupus nephritis.

C1q, the first component of the complement system, encounters conformational change that leads to C3 convertase breaking C3 into C3a and C3b.

Interleukins like IL-6, tumor necrosis factor-alpha, and interferon-gamma, that cause cell injury, are released.

This causes proteinuria by damaging the basement membrane and creating a loss of negative charge.

They lead to rupturing of small blood vessels, ultimately causing necrosis and sclerosis.

When working normally they will move the waste, excess electrolytes, and unnecessary fluid from the bloodstream to the urine.

[13][14] There can be adverse side effects; including CYC can cause infertility in both women and men.

[16] ACEIs will decrease hypertension by preventing the body from creating angiotensin II, which narrows the blood vessels.

[4] Aggressive therapy is recommended to avoid progressing to end-stage renal disease (ESRD), which is a strong possibility.

[4] If the biopsy shows the presence of crescents, tubule-interstitial injury with inflammation atrophy and fibrosis, the outcome is worse.

[citation needed] The percentage of glomeruli that show crescents usually correlates to the severity of the renal failure.

[citation needed] Activating complement pathways plays a large role in mediating inflammation.