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| Nephrogenic Diabetes Insipidus |  Nephrogenic diabetes insipidus is a disorder that characterized by the passage of great volumes of urine because of a defect of the kidney tubules. This disorder is also called Nephrogenic diabetes insipidus; or Acquired nephrogenic diabetes insipidus.
Nephrogenic Diabetes Insipidus Causes
Antidiuretic hormone (ADH; vasopressin) is a hormone made in the hypothalamus of the brain. It concentrates the urine by triggering the kidneys to reabsorb water into the blood stream rather than throwing out water into the urine.
Nephrogenic diabetes insipidus involves a shortcoming in the kidney tubules (the portion of the kidneys that encourages water to be excreted or reabsorbed).
As a rule, the particular kidney shortcoming is a partial or complete failure of special receptors placed on or within the kidney tubules to act in response to ADH, the hormone that passes the instruction to focus the urine to the inside of the cells.
Extreme amounts of water are excreted with the urine, creating a large amount of very dilute urine. There is little or no reaction to vasopressin, even though the blood level of this hormone is higher than normal.
If thirst mechanisms are normal and adequate fluids are consumed, there are no significant effects on the fluid and/or electrolyte balance of the body. If inadequate fluids are consumed, the high urine output may lead to dehydration and high blood sodium.
Nephrogenic DI is an atypical disorder. It may be present at birth as a result of a sex-linked defect (congenital nephrogenic DI) that usually affects men, while women can transmit the gene on to their children.
As a rule, nephrogenic diabetes insipidus is an acquired disorder. Such factors as drugs (lithium, demeclocycline, amphotericin B), electrolyte disorders (high calcium or low potassium levels), and urinary obstruction can bring on the disorder.
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