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Renal physiology, GFR & diuretics flashcards

10 high-yield MRCP Part 1 cards from the Intellect Medicos Nephrology course. Try to answer each question before you open it — then study them properly with spaced repetition, which brings each card back just before you would forget it.

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1. Which cells secrete renin?

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   Juxtaglomerular (granular) cells in the wall of the afferent arteriole.

   Why? They release renin when renal perfusion falls, when the macula densa senses low tubular NaCl, or with sympathetic (beta-1) stimulation.

2. Angiotensin II preferentially constricts which glomerular arteriole, and what does this do to GFR when renal perfusion is low?

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   The efferent arteriole; this raises intraglomerular pressure and maintains GFR.

   Why? This is why GFR depends on angiotensin II in low-perfusion states such as renal artery stenosis, dehydration or heart failure.

3. After starting an ACE inhibitor or ARB, what change in renal function is acceptable without changing the dose (NICE)?

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   A fall in eGFR of less than 25% or a rise in creatinine of less than 30% from baseline.

   Why? Some fall is expected from efferent dilatation. Repeat the test in 1–2 weeks. If eGFR falls by 25% or more (or creatinine rises by 30% or more), look for other causes (e.g. volume depletion, NSAIDs, renal artery stenosis) before stopping.

4. Which equation should UK laboratories use to estimate GFR in adults (NICE NG203)?

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   The CKD-EPI creatinine equation, without an ethnicity adjustment.

   Why? CKD-EPI is more accurate than MDRD, especially at higher GFRs. In 2021 NICE removed the old adjustment for black African or African-Caribbean family origin, because it may not be valid or accurate.

5. Which marker of GFR is largely independent of muscle mass and diet?

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   Cystatin C.

   Why? Creatinine comes from muscle, so it misleads in cachexia, amputees, the elderly or bodybuilders. Cystatin C is made by all nucleated cells at a steady rate.

6. On which transporter, and in which nephron segment, do loop diuretics act?

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   The Na+/K+/2Cl− cotransporter (NKCC2) in the thick ascending limb of the loop of Henle.

   Why? Blocking NKCC2 abolishes the medullary concentration gradient, which makes loop diuretics the most potent diuretics. They also increase urinary calcium loss.

7. On which transporter, and in which nephron segment, do thiazide diuretics act?

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   The Na+/Cl− cotransporter (NCC) in the distal convoluted tubule.

   Why? Thiazides cause hypokalaemia, hyponatraemia and hypomagnesaemia but REDUCE urinary calcium, which is why they are used to prevent calcium stones.

8. What is the mechanism of action of amiloride and triamterene?

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   They directly block the epithelial sodium channel (ENaC) in the collecting duct.

   Why? Less sodium is reabsorbed, so less potassium and H+ are secreted — they are potassium-sparing. Spironolactone and eplerenone instead block the aldosterone receptor.

9. Acetazolamide inhibits which enzyme, and which type of renal tubular acidosis can it cause?

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   Carbonic anhydrase in the proximal tubule; it causes a proximal (type 2) RTA.

   Why? Without carbonic anhydrase the proximal tubule cannot reclaim filtered bicarbonate, giving a normal anion gap metabolic acidosis.

10. Desmopressin acts on which receptor, and what is its effect in the collecting duct?

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    Vasopressin V2 receptors; it inserts aquaporin-2 water channels, increasing water reabsorption.

    Why? This concentrates the urine. It is used in cranial diabetes insipidus; tolvaptan does the opposite (V2 antagonist).