Master Rapidly Progressive Glomerulonephritis with Picmonic for Medicine

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Rapidly Progressive Glomerulonephritis

Rapids Glow-mare
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Rapidly progressive glomerulonephritis (RPGN) is a type of nephritic syndrome associated with severe glomerular injury with rapid and progressive loss of renal function. 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. 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. RPGN can be caused by a several different diseases including Goodpasture syndrome, Wegener’s granulomatosis, and microscopic polyangiitis. While some forms respond to plasmapheresis, steroids, and cytotoxic agents, some patients eventually require chronic dialysis or transplantation despite therapy. 
8 KEY FACTS
Nephritic
Nerd-cricket

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.

Crescent Shape
Crescent kayak

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 C3b
Fiber-optic-cables and computer (3) Tree

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.

With Macrophages
Mac-men

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's Syndrome
Gold-pastor

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
Wagon

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
Microscope Poly-angel

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.

Poor Prognosis
Gravestone

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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