Dense Deposit Disease

Watchlist

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Retrieved

2022-04-26

Source

Gard

Trials

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Genes

CFH, ALB, C1QA, CFHR1, PON1, TSLP, CFHR5, C3, KRT5, IGAN1

Drugs

(2S,4R)-1-(2-(3-acetyl-5-(2-methylpyrimidine-5-yl)-1H-indazol-1-yl)acetyl)-N-(6-bromopyridine-2-yl)-4-fluoropyrrolidine-2-carboxamide, 4-{(2S,4S)-4-ethoxy-1-[(5-methoxy-7-methyl-1H-indol-4-yl)methyl]piperidin-2-yl}benzoic acid-hydrogen chloride(1/1), Avacopan, PEGylated peptide inhibitor of complement C3, Recombinant human minibody against complement component C5, S3,S13-cyclo(D-tyrolsyl-L-isoleucyl-L-cysteinyl-L-valyl-1-methyl-L-tryptophyl-L-glutaminyl-L-aspartyl-L-tryptophyl-N-methyl-L-glycyl-L-alanyl-L-histidyl-L-arginyl-L-cysteinyl-N-methyl-L-isoleucinamide)

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Dense deposit disease (DDD) is a condition that primarily affects kidney function. Signs and symptoms usually start between the ages of 5 and 15 but may also begin in adulthood. The major features of DDD are due to kidney malfunction, and often include proteinuria; hematuria; reduced amounts of urine; low levels of protein in the blood; and swelling in many areas of the body. About half of affected people develop end-stage renal disease (ESRD) within 10 years after symptoms start. DDD can have genetic or non-genetic causes. It can be caused by mutations in the C3 and CFH genes; it may develop as a result of both genetic risk factors and environmental triggers; or it can result from the presence of autoantibodies that block the activity of proteins needed for the body's immune response. Most cases are sporadic (occurring by chance in people with no history of the disorder in their family).