Central diabetes insipidus, also called neurogenic diabetes insipidus, is a type of diabetes insipidus due to a lack of vasopressin (ADH) production in the brain. Vasopressin acts to increase the volume of blood (intravascularly), and decrease the volume of urine produced. Therefore, a lack of it causes increased urine production and volume depletion. It is also known as neurohypophyseal diabetes insipidus, referring to the posterior pituitary (neurohypophysis), which is supplied by the hypothalamus in the brain. This condition has only polyuria in common with diabetes. Although not mutually exclusive, with most typical cases, the name diabetes insipidus is a misleading misnomer. A better name might be "hypothalamic-neurohypophyseal ADH deficiency". Signs and symptoms
Increased thirst, polyuria and dehydration with metabolic encephalopathy. Causes
Unknown
In at least 25% of cases (the most commonly occurring classification), neurogenic diabetes insipidus is of unknown cause, meaning that the lack of vasopressin production arose from an unknown cause. It is also due to damage of the hypothalamus, pituitary stalk, posterior pituitary, and can arise from head trauma. Acquired
The lack of vasopressin production usually results from some sort of damage to the pituitary gland. It may be due to damage to the brain caused by:

Benign suprasellar tumors (20% of cases)
Infections (encephalitis, tuberculosis, etc.) Trauma (17% of cases) or neurosurgery (9% of cases)
Non-infectious granuloma (sarcoidosis, Langerhans cell histiocytosis etc.) Leukaemia
Autoimmune - associated with thyroiditis
Other rare causes which include hemochromatosis and histiocytosis.Vasopressin is released by the posterior pituitary, but unlike most other pituitary hormones, vasopressin is produced in the hypothalamus.
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).