When a person receives one changed form of the gene AGU from one of the parents, the individual is then classified as a carrier. Diagnosis
In order to be diagnosed with AGU an individual takes a urine test, which will show indication of an increased amount of aspartylglucosamin being secreted. The confirmation of the diagnosis of aspartylglucosaminuria requires a blood test. This helps show if the enzyme aspartylglucosaminidase is present or partially absent. A skin simple will also show the amount of aspartylglucosaminidase present. Pre-natal diagnosis
When families have a child who has already been diagnosed with AGU, they have the option to observe the enzymes activity that codes for AGU in future pregnancy, to help determine if the next child will also have a positive diagnosis for aspartylglucosaminuria. Treatment
No treatment is available to cure or slow down the progression of aspartylglucosaminuria. Bone marrow transplants have been conducted in hope that the bone marrow will produce the missing enzyme. The results of the tests thus far have shown to be inconclusive.
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).