Compare conditions

Put any two — or three — conditions side by side, adult or pediatric, to spot the look-alike differences fast, row by row.

Kidney type of DI

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In one line

·The kidney cannot hear ADH's command to save water, so it makes huge amounts of watery pee no matter what the body needs.

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Normal physiology

·Your kidneys filter blood and make pee. Normally, a hormone called ADH tells the kidney to pull water back so your pee gets stronger and you stay balanced.

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What goes wrong

·The kidney tubes lose the ability to respond to ADH, so they cannot close the water gates and pee stays dilute no matter what the body needs.

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Hallmark signs

·You pee a huge amount every day — often 3 to 20 liters (like filling a big water jug, or even more than that)
·You feel thirsty all the time and drink water constantly
·You wake up many times at night to pee (nocturia)
·Your pee is very pale or almost clear
·Peeing and drinking keep happening even after you take desmopressin (DDAVP, a medicine that acts like ADH)
·Babies may be fussy, have fevers, vomit, or not gain weight well
·Your blood sodium goes high (hypernatremia — over 145 mEq/L) if you can't drink enough to keep up

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Red flags · escalate now

·Blood sodium above 150 mEq/L (very salty blood — can cause confusion, seizures, or coma)
·A baby who is limp, won't wake up, has sunken eyes or a sunken soft spot, or stops making tears (severe dehydration)
·Sudden confusion, muscle twitching, or seizures in anyone with known diabetes insipidus (sign the brain is being hurt by salt imbalance)
·Not making any pee for hours despite drinking (might mean the kidneys shut down from severe dehydration or another emergency)

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Workup

·Serum sodium
·Urine osmolality
·Serum osmolality
·24-hour urine volume
·Water deprivation test with desmopressin (DDAVP) challenge
·Serum ADH (vasopressin) level
·Serum calcium and potassium
·Genetic testing for AVPR2 or AQP2 mutations (if congenital nephrogenic diabetes insipidus is suspected)

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Treatment

·Stop lithium immediately (if lithium is the cause); correct high calcium (hypercalcemia) (goal calcium < 10.5 mg/dL) with IV fluids, bisphosphonates, or calcitonin; correct low potassium (hypokalemia) (goal potassium > 3.5 mEq/L) with oral or IV potassium
·Low-sodium diet (restrict dietary sodium to < 2–3 grams per day)
·Thiazide diuretic (hydrochlorothiazide 25–50 mg daily) or amiloride (5–10 mg daily, especially if lithium-induced)
·NSAIDs (indomethacin 25–50 mg two to three times daily)
·Ensure unlimited free access to water at all times; educate patient, family, and caregivers to allow drinking to thirst without restriction

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NCLEX trap

·In nephrogenic diabetes insipidus, the kidney's collecting ducts (the final tubes that squeeze water back into blood) cannot hear ADH (the hormone that tells them to save water). DDAVP is fake ADH. If the kidney is deaf to the real signal, the fake version will not work either. You must stop lithium if the patient takes it, bring down high calcium or bring up low potassium, tell the patient to eat less salt, add a thiazide water pill (which, oddly, helps the kidney hold water when ADH is broken), and make sure the patient can drink as much water as they want.
·In nephrogenic diabetes insipidus, the kidney is broken and cannot concentrate pee. The patient is drinking because their body is desperately thirsty and trying to fix the thick, salty blood. This is a real medical emergency, not a psychiatric problem or bad habit.
·You must test the response to DDAVP first (the DDAVP stimulation test or water deprivation test). If pee stays dilute after DDAVP, it is nephrogenic diabetes insipidus — the kidney is not listening. DDAVP will not help. If pee gets more concentrated after DDAVP, then it is central diabetes insipidus (the pituitary gland is not making enough ADH), and DDAVP is the right treatment.
·Nephrogenic diabetes insipidus can be acquired — caused by lithium (the most common drug cause), high calcium (from cancer, overactive parathyroid gland, or too much vitamin D), low potassium (from diuretics or diarrhea), or chronic kidney disease. Stop the drug or fix the mineral problem, and the kidney may start listening to ADH again.
·In nephrogenic diabetes insipidus, IV fluids can make things worse because the kidney will just pee them out as dilute urine, and you can overload the patient with fluid. You must fix the kidney's ability to listen to ADH (stop lithium, fix high calcium or low potassium) and give the patient safe, free access to water by mouth so they can drink when thirsty.
·Seizures happen because of HIGH sodium (hypernatremia — blood salt over 145, often much higher) when the patient cannot get water. The salt in blood gets too thick, water shifts out of brain cells, and the brain shrinks and can seize. The danger is severe dehydration and no access to water, not low sodium.

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