Nephritic syndrome is characterized by inflammation of the glomeruli and is a set of symptoms which include hematuria, hypertension, oliguria, and less than 3.5 grams per day of proteinuria. Patients with nephritic syndrome also commonly present with red cell casts in the urine and azotemia. Nephritic syndrome can be caused by several diseases including Berger's disease, poststreptococcal glomerulonephritis and rapidly progressive glomerulonephritis.
Crescents are formed by proliferation of parietal cells and by migration of monocytes and macrophages. Fibrin strands are frequently prominent.
Crescents consist of fibrin and plasma proteins including C3b. The fibrin is a product of blood clotting and hemorrhage while the plasma protein C3b is a component of the complement cascade responsible for the inflammatory response. Crescents are formed by proliferation of parietal cells and by migration of monocytes and macrophages.
The disease is commony called crescentic glomerulonephritis due to the most common histologic picture with the presence of crescents in most glomeruli, caused by proliferation of the parietal epithelial cells that line Bowman's capsule along with the infiltration of fibrin and plasma proteins like C3b. Monocytes and macrophages are also known to infiltrate causing crescent formation.
Goodpasture syndrome is a cause of rapidly progressive crescentic glomerulonephritis. Goodpasture syndrome is characterized by the presence of anti-glomerular basement membrane antibodies (GBM) that cross react with pulmonary alveolar basement membranes to produce a clinical picture of pulmonary hemorrhage associated with renal failure. The goodpasture antigen is a peptide within type IV collagen.
Wegener's granulomatosis, more recently termed granulomatosis with polyangiitis, is a small and medium vessel necrotizing vasculitis that typically affects the nose, lungs, and kidneys. Kidney involvement can cause a rapidly progressive glomerulonephritic pattern with crescent formation.
Microscopic Polyangiitis is an autoimmune small vessel vasculitis affecting multiple organs in the body. The small vessel inflammation leads to disease manifestation in the brain, lungs, intestines and kidneys. Kidney involvement can lead to a rapidly progressive glomerulonephritic pattern with crescent formation.
This form of glomerulonephritis typically presents with severe oliguria and other signs of nephritic syndrome including hematuria, hypertension, and mild proteinuria. If untreated, this form can cause death from renal failure within several weeks to months. While some forms respond to plasmapheresis, steroids, and cytotoxic agents, some patients eventually require chronic dialysis or transplantation despite therapy.
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