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Renal tubular acidosis
Minimal change disease
Focal segmental glomerulosclerosis (NORD)
Rapidly progressive glomerulonephritis
IgA nephropathy (NORD)
Acute tubular necrosis
Renal papillary necrosis
Renal cortical necrosis
Chronic kidney disease
Polycystic kidney disease
Multicystic dysplastic kidney
Medullary cystic kidney disease
Medullary sponge kidney
Renal artery stenosis
Renal cell carcinoma
Nephroblastoma (Wilms tumor)
Posterior urethral valves
Hypospadias and epispadias
Lower urinary tract infection
Transitional cell carcinoma
Non-urothelial bladder cancers
Congenital renal disorders: Pathology review
Renal tubular defects: Pathology review
Renal tubular acidosis: Pathology review
Acid-base disturbances: Pathology review
Electrolyte disturbances: Pathology review
Renal failure: Pathology review
Nephrotic syndromes: Pathology review
Nephritic syndromes: Pathology review
Urinary incontinence: Pathology review
Urinary tract infections: Pathology review
Kidney stones: Pathology review
Renal and urinary tract masses: Pathology review
Rapidly progressive glomerulonephritis
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rapidly progressive glomerulonephritis p. 622
Tanner Marshall, MS
Crescentic glomerulonephritis, which is sometimes called rapidly progressive glomerulonephritis, is a type of nephritic syndrome, meaning it involves inflammation of the kidney’s glomeruli.
This inflammation ultimately causes a proliferation of cells in the Bowman’s space, which forms a crescent shape and this change leads to renal failure relatively quickly—within weeks to months.
The development of crescents in Bowman’s space can happen in several ways.
In some cases it’s the idiopathic, meaning there’s no identifiable cause.
When the cause is identifiable, though, it can be split into several types.
Type I is caused by anti-glomerular basement membrane, or GBM, antibodies, antibodies that target the GBM.
Type I is associated with Goodpasture syndrome, which also involves pulmonary hemorrhages.
Type II is immune-complex-mediated, meaning caused by immune complexes, composed of antigens and antibodies.
This might be the case with poststreptococcal glomerulonephritis, systemic lupus erythematosus, IgA nephropathy, and Henoch-Schonlein purpura.
And finally type III is known as pauci-immune, meaning little or no anti-GBM antibodies or immune-complex deposits.
In these cases, often anti-neutrophilic cytoplasmic antibodies or ANCAs are in the blood, which are autoantibodies against the body’s own neutrophils.
Furthermore, you can break it down into the type of ANCA. C-ANCAs, or cytoplasmic ANCAs, are associated with Wegener granulomatosis.
P-ANCAs or perinuclear ANCAs on the other hand are associated with microscopic polyangiitis and Churg-Strauss syndrome, the latter of which can be distinguished by having granulomatous inflammation, which is when immune cells attempt to wall off a substance perceived as foreign, asthma, and eosinophilia
Whatever the underlying cause is, the common feature is severe glomerular injury and the development of a crescent shape.
Rapidly progressive glomerulonephritis (RPGN) is a type of kidney disease characterized by a rapid loss of renal function, with characteristic glomerular crescent-shaped scars seen on renal biopsies. It is caused by inflammation and damage to the glomeruli, which can result from conditions like infections, immune disorders, and vasculitis.
Symptoms of RPGN can include blood in the urine, swelling in the legs and face, high blood pressure, and decreased urine output. The condition can progress rapidly, leading to kidney failure if left untreated. Treatment options may include immunosuppressive drugs to reduce inflammation, as well as a specific treatment for the underlying cause of the condition. If the renal failure becomes irreversible, dialysis or a kidney transplant are required.
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