Many concepts you will learn in nursing school are related, but different enough that it can often be confusing to keep all the key elements distinct from one another. A great example of these are the two related-but-different conditions DI and SIADH. 

Diabetes insipidus (DI) and syndrome of inappropriate antidiuretic hormone (SIADH) are essentially opposite of one another. It’s important you understand how to differentiate between the two in clinical and on your exams. 

What is antidiuretic hormone?

Before we dive into DI and SIADH, let’s talk about the key hormone involved, which is antidiuretic hormone (ADH), which you may also see referenced as vasopressin. The role of ADH is to maintain blood pressure by holding on to water and maintaining fluid balance. It is produced in the hypothalamus and released into the bloodstream by the pituitary in response to a variety of factors. The key ones are: 

  • Decreases in blood volume/pressure (sensed by baroreceptors). 
  • Increased serum osmolality (sensed by osmoreceptors)

When ADH levels are elevated, this causes the body to hold on to fluid…there’s essentially more antidiuretic action happening. When the levels of ADH are too low, the body loses more water than it should.

Diabetes insipidus overview

Diabetes insipidus results from a deficiency of antidiuretic hormone (ADH). Without the appropriate levels of ADH, the body will excrete more fluid than is being reabsorbed. This leads to a net loss of total body water. There are four types of DI:

  • Central (neurogenic) – The most common type is central or neurogenic DI. In this condition, there are disruptions in ADH synthesis, transportation or release. The disruptions are typically caused by brain tumors, head injuries, neurosurgery or CNS infections. 
  • Nephrogenic DI – In this condition, the kidneys are not responding to ADH appropriately. Common causes are lithium, hypercalcemia, and acute or chronic renal disease.
  • Primary DI (also called dipsogenic DI) – This condition occurs with excess water intake when the individual’s thirst mechanism is malfunctioning. This can be a consequence of a psychological disorder or damage to the hypothalamus or pituitary.
  • Gestational DI – This form of diabetes insipidus occurs when enzymes produced in the placenta interfere with the kidney’s ability to properly process the ADH. It is usually transient and self-corrects once the pregnancy ends.

Regardless of the type of DI present, the lack of ADH or (or inability to respond to ADH appropriately) means the kidneys are unable to reabsorb fluid. This causes large quantities of diluted urine to be voided. 

SIADH overview

Syndrome of inappropriate antidiuretic hormone is a condition in which there is too much ADH. The end result is the body holds on to more water than it should. 

SIADH occurs due to a variety of factors as well. One of the most common causes is small cell carcinoma, a type of lung cancer. It can also be related to CNS disorders such as infection, injury, lupus and guillain-barré . Additionally, SIADH occurs with administration of certain medications. These include SSRIs, TCAs, anesthesia, thiazide diuretics and chemotherapy. Lastly, SIADH can be related to other conditions such as adrenal insufficiency, COPD, hypothyroidism, HIV, lung infections and even positive pressure ventilation.

Now that you have a little background on these two conditions, let’s compare and contrast them using the Straight A Nursing LATTE method. I’m going to keep it very streamlined here, but if you want to go into greater detail, I will be adding a comprehensive lesson complete with a downloadable study guide to my Med Surg program, which you can learn more about here.

L: How does the patient LOOK?

DI vs SIADH How the patient looks

A: How do you ASSESS the patient?

For both conditions, monitor I/Os, weight, level of consciousness, and for the presence of other neurological symptoms such as headache, nausea/vomiting, irritability and confusion. Specific interventions for each are:

How to assess DI vs SIADH patients

T: What TESTS will be ordered?

For both DI and SIADH, you will be monitoring urine specific gravity, urine osmolality, serum sodium and serum osmolality. The patient may also receive testing to determine if the cause of the disorder is related to an underlying condition.

Normal reference ranges can vary widely, so always go by your facility or school’s reference.

  • Urine specific gravity: 1.010 – 1.020, but you may see 1.005 to 1.030
  • Urine osmolality: 300 – 800 mOsm/kg (reference ranges for this vary widely)
  • Serum sodium: 135-145 mEq/L
  • Serum osmolality: 275-295 mOsm/kg

What tests to expect for DI vs SIADH patients

To determine if the cause of the DI is neurogenic vs nephrogenic, the patient may undergo a water deprivation test. In this test, the patient’s weight is measured along with urine osmolality, specific gravity and volume. The patient is then deprived of water for 8 to 12 hours and then given desmopressin (which acts on vasopressin receptors in the body). Patients with neurogenic DI will show an increase in urine osmolality and a decrease in urine output. If the cause of the DI is nephrogenic in nature, there will be no change in urine output or osmolality.

If the patient has SIADH, or is suspected of having SIADH, the MD may order an ADH level and assess for other contributing factors such as infection or small cell carcinoma.

T: What TREATMENTS are provided for DI and SIADH?

Treatments for DI vary depending on the cause. The main goals are to maintain fluid and electrolyte balance. 

  • For central or neurogenic DI, the patient will receive fluid replacement to achieve euvolemia along with hormone therapy in the form of DDAVP (desmopressin). The goal of this therapy is for the body to have more ADH to retain water and stop the fluid losses. Desmopressin can be given IV, PO, sub Q or via a nasal spray. 
  • In cases of nephrogenic DI, additional ADH will not help as the kidneys are not responding appropriately to this hormone. Instead, we try to identify the offending agent if one is present, such as lithium toxicity. Thiazide diuretics may be administered to help reduce flow to the more ADH-sensitive distal nephrons of the kidneys. If ineffective, indomethacin may be utilized to increase the kidney’s responsiveness to ADH. Patients with nephrogenic DI will likely be instructed to follow a low-salt diet.
  • Gestational DI is usually treated with desmopressin.
  • Primary or dipsogenic DI is treated by decreasing fluid intake and addressing any underlying mental illness or neurological condition that is contributing.
  • If the cause is a tumor or CNS infection, we treat the underlying cause.

Treatments for SIADH center on addressing the underlying cause while promoting fluid and electrolyte balance. For example, if a tumor is causing the SIADH, surgical removal may be necessary. If the SIADH is caused by a medication such as a thiazide diuretic, the patient’s prescription may be changed. 

  • Mild cases without neurological compromise (serum sodium not less than ~125 mEq/L): 
    • Treatment may simply start with fluid restriction. A common fluid restriction is less than 800 ml/day. 
    • The patient may also be prescribed salt tablets or may be advised to increase sodium intake through their diet. 
    • If these measures do not produce the desired result, a vasopressor receptor antagonist such as conivaptan may be used. Conivaptan causes diuresis without affecting sodium or potassium excretion. The result is removal of excess fluid and normalization of sodium levels. 
    • Patients taking conivaptan will have increased thirst that can be quite uncomfortable. Teach them to space their fluids throughout the day and utilize things like sugarless gum and hard candies to help with the discomfort.
  • Severe cases with neurological compromise:  
    • Treatment will likely be aimed at slowly increasing the serum sodium level by using 3% NaCl (a type of hypertonic saline) alone or with a vasopressin receptor antagonist. 
    • Note that hypertonic saline is a HIGH ALERT medication that must be given slowly to avoid cerebral osmotic demyelination (locked-in syndrome). The general rule of thumb is to infuse hypertonic saline at a rate not to exceed 30ml/hr. Always carefully check the medication administration instructions.
    • The general recommended rate of sodium correction is to increase serum sodium by less than 8mEq/L in a 24-hour period. However, in cases of severe hyponatremia with significant symptoms (such as seizures) the MD may correct the sodium level a little more quickly at a rate of 4 to 6 mEq/L in the first two to four hours. Always follow the MD specifications and ensure routine lab testing is done on time. This is generally a serum sodium and serum osmolality level drawn every four to six hours, but this can vary based on the patient and MD orders.
  • Loop diuretics: Furosemide may also be utilized to promote diuresis, with or without concurrent replacement of sodium with hypertonic saline. 
  • Urea may also be utilized for diuresis, though it’s not as commonly used as other modalities. This medication will cause the patient to excrete water without losing sodium.
  • Lithium and demeclocycline: Though not widely used, these medications diminish the collecting tubule cells response to ADH, which increases water excretion.

Specific nursing interventions for a patient with DI or SIADH will center on patient safety and preventing complications. Initiate seizure precautions anytime sodium levels are abnormal or when your patient’s neurological status is unpredictable.

E: How do you EDUCATE the patient/family?

Patient education for both conditions involves teaching about the importance of daily weights and how to recognize signs of fluid imbalance. If the cause of the disorder is related to an underlying condition, teaching should focus on how that condition is being addressed (such as surgery, treating infection or changing medications). 

How to educate DI vs SIADH patients


Bendz, H., & Aurell, M. (1999). Drug-induced diabetes insipidus: Incidence, prevention and management. Drug Safety, 21(6), 449–456.

Brennan, D. (n.d.-a). What Is Hypernatremia? WebMD.

Brennan, D. (n.d.-b). What to Know About Antidiuretic Hormone (ADH). WebMD.

Capriotti, Theresa, and Joan Parker Frizzell. Pathophysiology: Introductory Concepts and Clinical Perspectives. F.A. Davis Company, 2016.

Harding, M., Kwong, J., Roberts, D., Hagler, D., & Reinisch, C. (2019). Lewis’s medical-surgical nursing: Assessment and management of clinical problems. Elsevier health sciences.

Healthwise. (n.d.). Diabetes Insipidus: Care Instructions.

Holman, Honey C., et al. RN Adult Medical Surgical Nursing: Review Module. 2019.

Khositseth, S., Charngkaew, K., Boonkrai, C., Somparn, P., Uawithya, P., Chomanee, N., Payne, D. M., Fenton, R., & Pisitkun, T. (n.d.). Hypercalcemia induces targeted autophagic degradation of aquaporin-2 at the onset of nephrogenic diabetes insipidus—PubMed. 10.1016/j.kint.2016.12.005

Levy, M., Prentice, M., & Wass, J. (2019). Diabetes insipidus. BMJ, l321.

MedlinePlus. (n.d.). Syndrome of inappropriate antidiuretic hormone secretion.

NHS. (2017, October 23). Diabetes insipidus—Complications. Nhs.Uk.

Rebar, C. R., Heimgartner, N. M., & Gersch, C. J. (2019). Pathophysiology made incredibly easy! (6th ed.). Wolters Kluwer.

Society for Endocrinology. (n.d.). Anti-diuretic hormone.

TeachMe. (n.d.). Antidiuretic Hormone (ADH)—Synthesis—Release. TeachMePhysiology.

Yasir, Muhammad, and Oren J. Mechanic. “Syndrome of Inappropriate Antidiuretic Hormone Secretion.” StatPearls, StatPearls Publishing, 2021. PubMed,