Diabetes insipidus

● due to low levels of ADH (or, rarely, renal insensitivity to ADH)

● high output of dilute urine (< 200 mOsmol/kg or SG < 1.003) with normal or high plasma osmolality and high serum sodium.

● often accompanied by a craving for water, especially ice-water

● danger of severe dehydration if not managed carefully

Although they have a common name, diabetes mellitus and diabetes insipidus are two entirely separate conditions with unrelated mechanisms. Both cause large amounts of urine to be produced (polyuria), and the term “diabetes” is derived from the Greek word meaning siphon. However, diabetes insipidus is either a problem with the production of antidiuretic hormone (central diabetes insipidus) or kidney's response to antidiuretic hormone (nephrogenic diabetes insipidus), whereas diabetes mellitus causes polyuria via a process called osmotic diuresis, due to the high blood sugar leaking into the urine and taking excess water along with it.

Diabetes insipidus (DI) is a condition characterized by excessive thirst and excretion of large amounts of severely diluted urine, with a reduction of fluid intake having no effect on the concentration of the urine.

see Central diabetes insipidus.

see Nephrogenic diabetes insipidus.

Diabetes insipidus is either a problem with the production of antidiuretic hormone (central diabetes insipidus) or kidney's response to antidiuretic hormone (nephrogenic diabetes insipidus).

The most common type in humans is the neurological form, called (central diabetes insipidus) (CDI), which involves a deficiency of arginine vasopressin (AVP), also known as antidiuretic hormone (ADH).

The second common type of DI is nephrogenic diabetes insipidus (NDI), which is due to kidney or nephron dysfunction caused by an insensitivity of the kidneys or nephrons to ADH. DI can also be gestational, or caused by alcohol or some types of drug abuse. DI should not be confused with nocturia.

see Adipsic diabetes insipidus.

The incidence of diabetes insipidus in the general population is 3 in 100,000.

Central diabetes insipidus etiology.

Nephrogenic diabetes insipidus etiology.

see Diabetes insipidus diagnosis.

The scarcity of studies comparing different treatment and monitoring strategies for these disorders and the lack of prior clinical guidelines makes it difficult to provide recommendations following a methodology based on grades of evidence ¹⁾.

Most patients with diabetes insipidus (DI) can drink enough fluid to replace their urine losses. When oral intake is inadequate and hypernatremia is present, replace losses with dextrose and water or an intravenous (IV) fluid that is hypo-osmolar with respect to the patient’s serum. Do not administer sterile water without dextrose intravenously, as it can cause hemolysis.

To avoid hyperglycemia, volume overload, and overly rapid correction of hypernatremia, fluid replacement should be provided at a rate no greater than 500-750 mL/h. A good rule of thumb is to reduce serum sodium by 0.5 mmol/L (0.5 mEq/L) every hour. The water deficit may be calculated on the basis of the assumption that body water is approximately 60% of body weight.

Diabetes insipidus case series.

A 42-Year-Old Male with Diabetes Insipidus ²⁾.

MRI of the Pituitary Gland By Jean-François Bonneville, Fabrice Bonneville, Françoise Cattin, Sonia Nagi

This clinically oriented book will familiarize the reader with all aspects of the diagnosis of tumors and other disorders of the pituitary gland by means of magnetic resonance imaging (MRI). The coverage includes acromegaly, Cushing’s disease, Rathke cleft cysts, prolactinomas, incidentalomas, Clinically non-functioning pituitary adenomas, other lesions of the sellar region, hypophysitis, and central diabetes insipidus. Normal radiologic anatomy and the numerous normal variants are described, and guidance is also provided on difficulties, artifacts, and other pitfalls. The book combines concise text and high-quality images with a question and answer format geared toward the needs of the practitioner. MRI is today considered the cornerstone in the diagnosis of diseases of the hypophyseal-hypothalamic region but the relatively small size of the pituitary gland, its deep location, the many normal anatomic variants, and the often tiny size of lesions can hinder precise evaluation of the anatomic structures and particularly the pituitary gland itself. Radiologists and endocrinologists will find MRI of the Pituitary Gland to be full of helpful information on this essential examination, and the book will also be of interest to internists and neurosurgeons.