Renal and acid–base: lithium and nephrogenic diabetes insipidus: practice question

A Physiology question in the style of the NEET PG paper. Answer it first, then read why the right option is right and why each of the others is wrong.

Try it

Physiology · Renal and acid–base: lithium and nephrogenic diabetes insipidus

Sample item

A 40-year-old woman on long-term lithium therapy for bipolar disorder passes large volumes of dilute urine, and her urine osmolality barely rises after desmopressin. Which change in the nephron explains this?

Original practice item, not a recalled exam question. Nothing here is recorded.

The answer and the reasoning

A. Reduced aquaporin-2 expression in the collecting duct principal cells

Lithium enters principal cells through the epithelial sodium channel and interferes with ADH signalling, lowering aquaporin-2 expression. The collecting duct stays impermeable to water, so dilute urine continues despite ADH or desmopressin, which is nephrogenic diabetes insipidus.

Option by option

  • A. Reduced aquaporin-2 expression in the collecting duct principal cells (correct)

    Correct. Without aquaporin-2, the collecting duct cannot reabsorb water even when ADH is present.

  • B. Increased sodium chloride reabsorption in the thick ascending limb

    Greater reabsorption in the thick ascending limb would strengthen the medullary gradient, not dilute the urine.

  • C. Increased ADH secretion from the posterior pituitary

    In nephrogenic diabetes insipidus ADH is normal or raised, and the problem lies in the kidney response.

  • D. Loss of urea from the medullary interstitium by a washout

    A urea washout would impair the gradient but would not explain failure to respond to desmopressin in this setting.

Source note: Original NextPrep sample item — pending expert review. This item is original practice material awaiting independent expert review, so confirm important facts in a standard textbook.

More Physiology questions

Questions about this Physiology question

What is the answer to this Physiology question?

The best answer is A, Reduced aquaporin-2 expression in the collecting duct principal cells. Lithium enters principal cells through the epithelial sodium channel and interferes with ADH signalling, lowering aquaporin-2 expression.

Why is "Increased sodium chloride reabsorption in the thick ascending limb" not the answer?

Greater reabsorption in the thick ascending limb would strengthen the medullary gradient, not dilute the urine.

Why is "Increased ADH secretion from the posterior pituitary" not the answer?

In nephrogenic diabetes insipidus ADH is normal or raised, and the problem lies in the kidney response.

Why is "Loss of urea from the medullary interstitium by a washout" not the answer?

A urea washout would impair the gradient but would not explain failure to respond to desmopressin in this setting.

What concept does this question test?

It tests Renal and acid–base: lithium and nephrogenic diabetes insipidus in Physiology. The collecting duct stays impermeable to water, so dilute urine continues despite ADH or desmopressin, which is nephrogenic diabetes insipidus.

How hard is this question?

We tag it as an application question: it asks you to use a fact on a patient or a finding. The tag is our own editorial judgement, not an official difficulty rating, so read the reason for every option, not only the answer.

How should I study Renal and acid–base: lithium and nephrogenic diabetes insipidus?

For each system, sketch the key graph (pressure–volume loop, oxygen dissociation curve, nephron handling) and explain it aloud. Then use the flashcards and the other Physiology questions on this site to test what stuck.

Is this a real NEET PG question?

No. It is an original practice item (editorial status: sample, version 1). NextPrep does not publish recalled or leaked questions, and independent faculty review of this item has not been completed yet, so confirm important facts in a standard textbook.