Vaginal depth varies widely for CAIS women, but is typically shorter than unaffected women; one study of eight women with CAIS measured the average vaginal depth to be 5.9 cm  (vs. 11.1 ± 1.0 cm for unaffected women ). In some extreme cases, the vagina has been reported to be aplastic (resembling a "dimple"), though the exact incidence of this is unknown.The gonads in these women are not ovaries, but instead, are testes; during the embryonic stage of development, testes form in an androgen-independent process that occurs due to the influence of the SRY gene on the Y chromosome. They may be located intra-abdominally, at the internal inguinal ring, or may herniate into the labia majora, often leading to the discovery of the condition. Testes in affected women have been found to be atrophic upon gonadectomy.Testosterone produced by the testes cannot be directly used due to the mutant androgen receptor that characterizes CAIS; instead, it is aromatized into estrogen, which effectively feminizes the body and accounts for the normal female phenotype observed in CAIS. However, up to 5% of individuals with CAIS do not have an AR mutation. The receptor in question is encoded by the AR gene located on the X chromosome at Xq11–12. At least 15 different mutations were known in 2003, and they are all recessive, which makes the disease to follow X-linked recessive inheritance.Immature sperm cells in the testes do not mature past an early stage, as sensitivity to androgens is required in order for spermatogenesis to complete.
People who excessively consume alcohol are usually also malnourished with regard to minerals. In addition, alcohol treatment is associated with refeeding, which further depletes phosphate, and the stress of alcohol withdrawal may create respiratory alkalosis, which exacerbates hypophosphatemia (see above). Malabsorption – This includes gastrointestinal damage, and also failure to absorb phosphate due to lack of vitamin D, or chronic use of phosphate binders such as sucralfate, aluminum-containing antacids, and (more rarely) calcium-containing antacids. Intravenous iron (usually for anemia) may cause hypophosphatemia. The loss of phosphate is predominantly the result of renal wasting.Primary hypophosphatemia is the most common cause of non-nutritional rickets. Laboratory findings include low-normal serum calcium, moderately low serum phosphate, elevated serum alkaline phosphatase, and low serum 1,25 dihydroxy-vitamin D levels, hyperphosphaturia, and no evidence of hyperparathyroidism.Hypophosphatemia decreases 2,3-bisphosphoglycerate (2,3-BPG) causing a left shift in the oxyhemoglobin curve.Other rarer causes include:

Certain blood cancers such as lymphoma or leukemia
Hereditary causes
Liver failure
Tumor-induced osteomalacia

Pathophysiology
Hypophosphatemia is caused by the following three mechanisms:

Inadequate intake (often unmasked in refeeding after long-term low phosphate intake)
Increased excretion (e.g. in hyperparathyroidism, hypophosphatemic rickets)
Shift of phosphorus from the extracellular to the intracellular space. This can be seen in treatment of diabetic ketoacidosis, refeeding, short-term increases in cellular demand (e.g. hungry bone syndrome) and acute respiratory alkalosis. Diagnosis
Hypophosphatemia is diagnosed by measuring the concentration of phosphate in the blood. Concentrations of phosphate less than 0.81 mmol/L (2.5 mg/dL) are considered diagnostic of hypophosphatemia, though additional tests may be needed to identify the underlying cause of the disorder.