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Glomerulocystic kidney disease can be inherited by autosomal dominant inheritance, develop due to urinary tract obstruction, [3] manifest in cell proliferation during organogenesis, [8] and develop through other related kidney diseases. Familial heritable GCKD can be inherited by offspring through adults which can cause GCKD in children or babies.
Membranoproliferative glomerulonephritis (MPGN) is a type of glomerulonephritis caused by deposits in the kidney glomerular mesangium and basement membrane thickening, [2] activating the complement system and damaging the glomeruli. MPGN accounts for approximately 4% of primary renal causes of nephrotic syndrome in children and 7% in adults. [3]
[2] [3] This process damages the filtration function of the kidney, resulting in protein presence in the urine due to protein loss. [3] FSGS is a leading cause of excess protein loss—nephrotic syndrome—in children and adults in the US. [4] Signs and symptoms include proteinuria and edema.
Both children and adults can develop glomerulosclerosis, which can result in different types of kidney conditions. One frequently encountered type of glomerulosclerosis is caused by diabetes. Drug use or infections may cause focal segmental glomerulosclerosis (FSGS), a very chronic kidney condition.
IgA nephropathy (IgAN), also known as Berger's disease (/ b ɛər ˈ ʒ eɪ /) (and variations), or synpharyngitic glomerulonephritis, is a disease of the kidney (or nephropathy) and the immune system; specifically it is a form of glomerulonephritis or an inflammation of the glomeruli of the kidney.
IgM nephropathy or immunoglobulin M nephropathy (IgMN) is a kind of idiopathic glomerulonephritis that is marked by IgM diffuse deposits in the glomerular mesangium. [1] IgM nephropathy was initially documented in 1978 by two separate teams of researchers.
Rapidly progressive glomerulonephritis (RPGN) is a syndrome of the kidney that is characterized by a rapid loss of kidney function, [4] [5] (usually a 50% decline in the glomerular filtration rate (GFR) within 3 months) [5] with glomerular crescent formation seen in at least 50% [5] or 75% [4] of glomeruli seen on kidney biopsies.
Acute proliferative glomerulonephritis is a disorder of the small blood vessels of the kidney.It is a common complication of bacterial infections, typically skin infection by Streptococcus bacteria types 12, 4 and 1 but also after streptococcal pharyngitis, for which it is also known as postinfectious glomerulonephritis (PIGN) or poststreptococcal glomerulonephritis (PSGN). [4]