Increased anion gap
Causes of increased anion gap include: 

Lactic acidosis
Ketoacidosis (e.g., Diabetic, alcoholic, or starvation)
Chronic kidney failure
Transient 5-oxoprolinemia due to long-term ingestion of high-doses of acetaminophen (often seen with sepsis, liver failure, kidney failure, or malnutrition)
Intoxication:
Salicylates, methanol, ethylene glycol
Organic acids, paraldehyde, ethanol, formaldehyde
Carbon monoxide, cyanide, ibuprofen, metformin
Propylene glycol (metabolized to L and D-lactate and is often found in infusions for certain intravenous medications used in the intensive care unit)
Massive rhabdomyolysis
Isoniazid, iron, phenelzine, tranylcypromine, valproic acid, verapamil
Topiramate
SulfatesNormal anion gap
Causes of normal anion gap include
Inorganic acid addition
Infusion/ingestion of HCl, NH4Cl
Gastrointestinal base loss
Diarrhea
Small bowel fistula/drainage
Surgical diversion of urine into gut loops
Renal base loss/acid retention:
Proximal renal tubular acidosis
Distal renal tubular acidosisHyperalimentation
Addison disease
Acetazolamide
Spironolactone
Saline infusionTo distinguish between the main types of metabolic acidosis, a clinical tool called the anion gap is considered very useful. It is calculated by subtracting the sum of the chloride and bicarbonate levels from the sum of the sodium and potassium levels. As sodium is the main extracellular cation, and chloride and bicarbonate are the main anions, the result should reflect the remaining anions. Normally, this concentration is about 8–16 mmol/L (12±4). An elevated anion gap (i.e. > 16 mmol/L) can indicate particular types of metabolic acidosis, such as types caused by certain poisons, lactate acidosis, and ketoacidosis. It is important to note that the anion gap can be spuriously normal in sampling errors of the sodium level, e.g. in extreme hypertriglyceridemia. The anion gap can also be increased due to relatively low levels of cations other than sodium and potassium (e.g.
At approximately the end of the 7th and the beginning of the 8th week of gestation, the Sertoli cells secretion of AMH occurs, causing male sex differentiation during fetal development. The AMH molecules bind to AMHRII (anti-Müllerian hormone receptor type II) regressing the Müllerian duct. The Leydig cells secrete testosterone to aid the male differentiation process by inducing structures such as the epididymis, vas deferens and seminal vesicles. However, with PMDS individuals, the Müllerian duct persists instead of regressing, either due to AMH secretion (PMDS Type I) or AMH receptors (PMDS Type II). PMDS is usually coincidentally found during surgery for inguinal hernia, or when searching for adult male infertility causes. Other diagnostic tests
Genetic
Another method for the confirmation of PMDS is genetic testing. It is not usually preferred because of its processing period and cost. With image screenings such as ultrasound and MRI, the condition can be efficiently confirmed. Genetic tests can identify those who hold the mutated gene, identify the family members chances and risks, and advise those who are trying to get pregnant. Genetic counseling and further genetic testing is offered to confirm the chances and risks of an individuals offspring obtaining the pair of mutated genes. Further research into the family tree and inheritance is possible as well. ELISA
An ELISA test is a form of immunoassay, a technique which uses an antibody or antigen to identify the presence of particular substances.