What does the nurse state as the most common intrarenal cause of acute kidney injury?

Rationale:
A. This is incorrect because tissue plasminogen activator (tPA) is most beneficial when given early, ideally within 3 hours of symptom onset (and up to 4.5 hours in selected patients). Early administration improves cerebral blood flow, limits infarct size, and enhances neurologic recovery. Therefore, onset less than 3 hours is not a reason to withhold tPA.

B. This is incorrect because transient ischemic attacks (TIAs) resolve spontaneously and do not involve persistent cerebral vessel occlusion. Since neurologic deficits are temporary and no active clot remains, tPA is not indicated and would expose the patient to unnecessary bleeding risk.

C. This is incorrect because increased intracranial pressure (ICP), often associated with cerebral edema or intracranial bleeding, is a contraindication to tPA. Administering a thrombolytic in this situation significantly increases the risk of intracranial hemorrhage and can worsen patient outcomes.

D. This is correct because tPA is not recommended if the onset of ischemic stroke symptoms occurred more than 3 hours ago (or beyond the extended window for select patients). After this time, brain tissue damage becomes irreversible, and the risk of hemorrhagic transformation outweighs the potential benefit. Establishing the exact time of onset is critical to determine eligibility and ensure safe administration of tPA.

Rationale:
A. Fatigue is incorrect because, although patients with diabetes insipidus (DI) may experience fatigue, this symptom is nonspecific. Fatigue can result from many conditions, including dehydration, electrolyte imbalances, chronic illness, or sleep disturbances. In DI, fatigue may develop secondary to fluid and electrolyte loss, but it is not a primary or diagnostic feature of the disorder.

B. Polydipsia is correct because it is the most indicative and classic symptom of DI. Diabetes insipidus results from either a deficiency of antidiuretic hormone (ADH, also called vasopressin) in central DI or the kidneys’ inability to respond to ADH in nephrogenic DI. Without adequate ADH activity, the kidneys cannot concentrate urine, leading to the excretion of large volumes of dilute urine (polyuria), sometimes up to 3–20 liters per day in severe cases. The body attempts to compensate for this fluid loss by triggering intense thirst (polydipsia), often resulting in the patient drinking large amounts of water to prevent dehydration. Polydipsia is thus a hallmark symptom and a key diagnostic clue for DI.

C. Weight gain is incorrect because the fluid loss associated with DI typically causes weight loss rather than gain. Patients may have decreased body mass due to the ongoing loss of water and potential electrolyte depletion. Weight gain is not associated with DI unless there is excessive water intake beyond renal capacity, which is uncommon.

D. Diarrhea is incorrect because DI affects renal water reabsorption, not gastrointestinal function. Diarrhea is unrelated to the pathophysiology of DI and may indicate a separate gastrointestinal issue rather than the endocrine disorder itself.