Hereditary angiopathy with nephropathy, aneurysms and muscle cramps syndrome is a rare genetic, multisystemic, COL4A1-related disorder, it is characterized by angiopathy, nephropathy, hematuria, development of kidney cysts, intracranial aneurysms (which have the potential to burst), childhood-onset muscle cramps, urinal, heart and ocular problems. Half of the people with this disorder (50%) have leukoencephalopathy, while a very small number of people with this disorder have Raynauds phenomenon. Causes
This syndrome is caused by mutations in the COL4A1 gene, on the chromosome 13q34, this gene provides instructions for making one of the components necessary for the formation of a protein called type IV collagen, this protein is one of the main components for basement membranes throughout the body.The mutations of the gene causes the production of a protein that alters the structure of collagen type IV, because of this, the collagen molecules cant attach themselves to the basement membranes, and, without these networks, they turn unstable and thus weaken surrounding tissues, explaining the weakening of vasculature of ocular, renal, cerebral and muscular tissues.This disorder run in families following an autosomal dominant inheritance pattern

Epidemiology
Although the exact prevalence of this disorder isnt known, only six families affected by this disorder have been recorded in medical literature. == References ==
Cholestatic pruritus is the sensation of itch due to nearly any liver disease, but the most commonly associated entities are primary biliary cholangitis, primary sclerosing cholangitis, obstructive choledocholithiasis, carcinoma of the bile duct, cholestasis (also see drug-induced pruritus), and chronic hepatitis C viral infection and other forms of viral hepatitis. Cause
Cholestasis means "the slowing or stopping of bile flow" which can be caused by any number of diseases of the liver (which produces the bile), the gallbladder (which stores the bile), or biliary tract (also known as the biliary tree, the conduit that allows the bile to leave the liver and gallbladder and enter the small intestine). When this occurs, conjugated bilirubin and the waste products that usually would be cleared in bile reflux back into the bloodstream. This causes a primarily conjugated hyperbilirubinemia and jaundice; the liver conjugates the bile to make it water-soluble and because the bile has already been processed by the liver, when it gets backed up because of a blockage and is refluxed into the blood, the blood will have high levels of conjugated bilirubin. This is in contrast to primarily unconjugated hyperbilirubinemia which is the water-insoluble form that is bound to serum albumin; the liver has not had a chance to conjugate the bilirubin yet and can be caused either because too much unconjugated bilirubin is made (such as in massive hemolysis or ineffective erythropoiesis) or because too little is conjugated (Gilberts disease or Crigler–Najjar syndrome). Unconjugated hyperbilirubinemia does not typically cause pruritus.