Renal cortical necrosis (RCN) is a rare cause of acute kidney failure. The condition is "usually caused by significantly diminished arterial perfusion of the kidneys due to spasms of the feeding arteries, microvascular injury, or disseminated intravascular coagulation" and is the pathological progression of acute tubular necrosis. It is frequently associated with obstetric catastrophes such as abruptio placentae and septic shock, and is three times more common in developing nations versus industrialized nations (2% versus 6% in causes of acute kidney failure). Causes
Adults
Pregnancy related (>50% of cases)
Placental abruption
Infected abortion
Prolonged intrauterine fetal death
Severe eclampsia
HIV
Snake bites
Binge drinking
Shock
Trauma
Sickle cell disease
Systemic lupus erythematosus (SLE)
Sepsis
SLE-associated antiphospholipid syndrome
Vitamin deficiency
Pancreatitis
Malaria
Meningococcemia
Drug-induced toxicity (e.g. NSAIDs, Contrast Media, Quinine, or ATRA)

Babies
Congenital heart disease
Fetal-maternal transfusion
Dehydration
Perinatal asphyxia
Anemia
Placental hemorrhage
Severe hemolytic disease
Sepsis

Pathophysiology
The exact pathologic mechanism for RCN is unclear, however the onset of small vessel pathology is likely an important aspect in the cause of this condition. In general the renal cortex is under greater oxygen tension and more prone to ischemic injury, especially at the level of the proximal collecting tubule, leading to its preferential damage in a sudden drop in perfusion. Rapidly corrected acute renal ischemia leads to acute tubular necrosis, from which complete recovery is possible, while more prolonged ischemia may lead to RCN. Pathologically, the cortex of the kidney is grossly atrophied with relative preservation of the gross structure of the medulla. The damage is usually bilateral owing to its underlying systemic causes, and is most frequently associated with pregnancy (>50% of cases).
For another member of the gene family, mutations in the Notch1 gene are associated with bicuspid aortic valve, a valve with two leaflets instead of three. Notch1 is also associated with calcification of the aortic valve, the third most common cause of heart disease in adults.Mutations of a cell regulatory mechanism, the Ras/MAPK pathway are responsible for a variety of syndromes, including Noonan syndrome, LEOPARD syndrome, Costello syndrome and cardiofaciocutaneous syndrome in which there is cardiac involvement. While the conditions listed are known genetic causes, there are likely many other genes which are more subtle. It is known that the risk for congenital heart defects is higher when there is a close relative with one. Environmental
Known environmental factors include certain infections during pregnancy such as rubella, drugs (alcohol, hydantoin, lithium and thalidomide) and maternal illness (diabetes mellitus, phenylketonuria, and systemic lupus erythematosus). Alcohol exposure in the father also appears to increase the risk of congenital heart defects.Being overweight or obese increases the risk of congenital heart disease. Additionally, as maternal obesity increases, the risk of heart defects also increases. A distinct physiological mechanism has not been identified to explain the link between maternal obesity and CHD, but both pre-pregnancy folate deficiency and diabetes have been implicated in some studies. Mechanism
There is a complex sequence of events that result in a well formed heart at birth and disruption of any portion may result in a defect.