What drugs can cause nephrogenic diabetes insipidus?

What drugs can cause nephrogenic diabetes insipidus?

Causes of nephrogenic diabetes insipidus in adults include: Lithium, a drug most commonly taken for bipolar disorder; up to 20\% of people taking lithium will develop nephrogenic diabetes insipidus. Other medicines, including demeclocycline (Declomycin), ofloxacin (Floxin), orlistat (alli, Xenical), and others.

What causes NDI?

Genetic NDI occurs due to genetic mutations, which are passed down through families. Mutations are mistakes or damage that cause a change in the genes of a person. These mutations can interfere with the normal functioning of ADH. Genetic NDI is occurs due to a mutation in either AVPR2 or AQP2.

Is nephrogenic diabetes insipidus reversible?

Disordered water channel expression and distribution in acquired nephrogenic diabetes insipidus. Many of the implicated causes are reversible and are caused by isolated effects on the cortical collecting duct without broad damage to the medullary countercurrent system.

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When did nephrogenic diabetes insipidus start?

NDI may also be a temporary complication associated with pregnancy. The term nephrogenic diabetes insipidus was first used in the medical literature in 1947. In the past, the term diabetes insipidus renalis was used to denote this disorder.

How is Nephrogenic DI treated?

Nephrogenic diabetes insipidus. Instead, your doctor may prescribe a low-salt diet to reduce the amount of urine your kidneys make. You’ll also need to drink enough water to avoid dehydration. Treatment with the drug hydrochlorothiazide (Microzide) may improve your symptoms.

How hypercalcemia causes nephrogenic DI?

Hypercalcemia induces targeted autophagic degradation of aquaporin-2 at the onset of nephrogenic diabetes insipidus. Kidney Int.

Why does Aki cause hyperkalemia?

Hyperkalemia is a common complication of AKI when the injury involves the late distal nephron and extends into the collecting duct, causing direct injury of cells responsible for K+ secretion.