CKD: staging, management & complications flashcards
32 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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What findings, and for how long, are needed to diagnose chronic kidney disease (NICE)?
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eGFR <60 mL/min/1.73 m² and/or ACR ≥3 mg/mmol (or other markers of kidney damage) persisting for more than 3 months.
Why? Repeat abnormal tests after 3 months before labelling CKD. A first eGFR <60 should be repeated within 2 weeks to exclude AKI.
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A 40-year-old man has an eGFR of 72 mL/min/1.73 m² on two occasions 4 months apart. ACR is 1 mg/mmol, urinalysis is normal and renal ultrasound is normal. Does he have CKD?
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No — G1–G2 eGFR counts as CKD only if there are markers of kidney damage.
Why? Markers include albuminuria, haematuria of renal origin, structural abnormality on imaging, or histological change.
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CKD G3a is an eGFR of ______ mL/min/1.73 m², and G3b is 30–44 mL/min/1.73 m².
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45–59
Why? G1 ≥90, G2 60–89, G4 15–29, G5 <15. G3b and below carry clearly higher cardiovascular and progression risk.
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CKD G3a is an eGFR of 45–59 mL/min/1.73 m², and G3b is ______ mL/min/1.73 m².
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30–44
Why? G1 ≥90, G2 60–89, G4 15–29, G5 <15. G3b and below carry clearly higher cardiovascular and progression risk.
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Albuminuria categories: A2 is an ACR of ______ mg/mmol; A3 is an ACR above 30 mg/mmol.
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3–30
Why? A1 is <3 mg/mmol. ACR (ideally on an early-morning sample) is the preferred test for proteinuria in CKD.
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Albuminuria categories: A2 is an ACR of 3–30 mg/mmol; A3 is an ACR ______ mg/mmol.
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above 30
Why? A1 is <3 mg/mmol. ACR (ideally on an early-morning sample) is the preferred test for proteinuria in CKD.
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What is the first-line test to detect and quantify proteinuria in suspected CKD?
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Urine albumin:creatinine ratio (ACR), ideally on an early-morning sample.
Why? ACR is more sensitive than protein:creatinine ratio or dipstick for low levels of proteinuria. Confirm an ACR of 3–70 mg/mmol on a repeat early-morning sample.
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Under NICE NG203, above what 5-year Kidney Failure Risk Equation (KFRE) score should an adult with CKD be referred to nephrology?
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A 5-year risk of needing renal replacement therapy greater than 5%.
Why? The 4-variable KFRE uses age, sex, eGFR and ACR. It replaced a simple eGFR cut-off as the main referral trigger in 2021.
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Above what ACR should an adult with CKD be referred to nephrology (unless the cause is diabetes and it is already appropriately treated)?
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ACR of 70 mg/mmol or more.
Why? ACR ≥70 approximates nephrotic-range proteinuria and suggests significant glomerular disease. ACR >30 with haematuria is also a referral trigger.
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In an adult with CKD and diabetes, from what ACR should an ACE inhibitor or ARB be offered (NICE)?
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An ACR of 3 mg/mmol or more (A2 or A3), titrated to the highest tolerated licensed dose.
Why? In non-diabetic CKD the threshold is higher: offer it if ACR is over 30 with hypertension, or if ACR is 70 or more (and refer to nephrology) regardless of blood pressure.
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NICE clinic BP targets in CKD: if ACR is under 70 mg/mmol aim for ______ mmHg; if ACR is 70 mg/mmol or more aim for below 130/80 mmHg.
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below 140/90
Why? Tighter control helps more when proteinuria is heavy. The systolic target ranges are 120–139 and 120–129 mmHg respectively.
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NICE clinic BP targets in CKD: if ACR is under 70 mg/mmol aim for below 140/90 mmHg; if ACR is 70 mg/mmol or more aim for ______ mmHg.
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below 130/80
Why? Tighter control helps more when proteinuria is heavy. The systolic target ranges are 120–139 and 120–129 mmHg respectively.
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Above what serum potassium should an ACE inhibitor or ARB not routinely be started in CKD, and at what level should it be stopped?
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Do not start if K+ is above 5.0 mmol/L; stop if K+ reaches 6.0 mmol/L or more (once other potassium-raising drugs are stopped).
Why? RAAS blockade reduces aldosterone, which reduces potassium excretion, especially when GFR is low.
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Which class of drug should be added to an optimised ACE inhibitor/ARB in CKD with type 2 diabetes to slow progression?
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An SGLT2 inhibitor (e.g. dapagliflozin).
Why? SGLT2 inhibitors reduce albuminuria, eGFR decline, kidney failure and heart failure admissions, largely independent of their glucose effect.
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Under NICE TA1075 (2025), an adult with CKD but no diabetes and an eGFR of 45–90 can have dapagliflozin only if the ACR is at least what?
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22.6 mg/mmol (as an add-on to an optimised ACE inhibitor or ARB unless contraindicated).
Why? At eGFR 20 to below 45 no ACR threshold is needed, and at eGFR 45–90 type 2 diabetes also qualifies. The cut-off reflects the DAPA-CKD population (about 200 mg/g). NG203 applies the same criteria to empagliflozin (TA942).
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How do SGLT2 inhibitors protect the kidney?
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They block sodium-glucose reabsorption in the proximal tubule; more sodium reaches the macula densa, causing afferent vasoconstriction and lowering intraglomerular pressure.
Why? This restores tubuloglomerular feedback and reduces hyperfiltration. An early, small fall in eGFR is expected and is not a reason to stop.
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Which statin and dose does NICE recommend for primary prevention of CVD in adults with CKD?
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Atorvastatin 20 mg daily.
Why? CKD is a major cardiovascular risk factor, so adults with CKD are offered atorvastatin for primary or secondary prevention. For primary prevention aim for a >40% fall in non-HDL cholesterol; increase the dose if this is not met and eGFR is 30 or more, and agree higher doses with a renal specialist if eGFR is below 30.
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When should oral sodium bicarbonate be considered in CKD (NICE)?
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When eGFR is below 30 mL/min/1.73 m² and serum bicarbonate is below 20 mmol/L.
Why? Correcting metabolic acidosis may slow CKD progression and protect bone and muscle.
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Below what eGFR should metformin be stopped (BNF)?
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Below 30 mL/min/1.73 m² (review the dose below 45).
Why? Metformin is renally cleared; accumulation raises the risk of lactic acidosis.
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A 72-year-old smoker with hypertension and peripheral vascular disease has an eGFR fall from 48 to 25 two weeks after starting ramipril. He has had two episodes of 'flash' pulmonary oedema. An abdominal bruit is heard. What is the most likely diagnosis?
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Bilateral (atherosclerotic) renal artery stenosis.
Why? Glomerular filtration in stenosed kidneys depends on angiotensin II constricting the efferent arteriole; ACE inhibitors remove this, so GFR falls sharply.
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Which cause of renal artery stenosis typically affects young women, and what is its angiographic appearance?
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Fibromuscular dysplasia — a 'string of beads' appearance.
Why? It causes renovascular hypertension in young people and usually responds well to balloon angioplasty (without stenting).
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What is the main cause of anaemia in CKD?
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Reduced erythropoietin production by peritubular interstitial fibroblasts in the renal cortex.
Why? Fibrosis destroys the EPO-producing cells. Functional iron deficiency (raised hepcidin) adds to the anaemia.
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Which hormone, raised by chronic inflammation, causes functional iron deficiency in CKD?
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Hepcidin (made by the liver).
Why? Hepcidin blocks ferroportin, so iron stays trapped in macrophages and gut absorption falls. Ferritin is normal or high but transferrin saturation is below 20%.
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What ferritin level indicates absolute iron deficiency in non-dialysis CKD?
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Ferritin below 100 µg/L.
Why? Ferritin is an acute-phase protein, so higher thresholds are used in CKD; the course notes use <200 µg/L on dialysis. NICE prefers % hypochromic red cells >6% or reticulocyte Hb <29 pg; if these are unavailable it uses transferrin saturation <20% plus ferritin <100 µg/L.
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What is the first step in treating anaemia of CKD in an iron-deficient haemodialysis patient?
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IV iron (e.g. iron sucrose or ferric carboxymaltose) before any ESA.
Why? ESAs do not work well if iron stores are low. Oral iron is poorly absorbed in CKD because of high hepcidin. NICE recommends a high-dose IV iron regimen (e.g. iron sucrose) for iron-deficient patients on in-centre haemodialysis.
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What haemoglobin range should be targeted when treating anaemia of CKD with an erythropoiesis-stimulating agent?
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100–120 g/L.
Why? Aiming for normal Hb with ESAs increases stroke, thrombosis and hypertension without extra benefit.
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What is the most common side effect of erythropoiesis-stimulating agents (epoetin, darbepoetin)?
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Hypertension.
Why? Other risks are thrombosis (including AV fistula thrombosis), stroke, seizures and, rarely, pure red cell aplasia from anti-EPO antibodies.
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What is the typical biochemistry of secondary hyperparathyroidism in CKD?
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Low or normal calcium, high phosphate, high PTH and high ALP.
Why? Falling GFR retains phosphate and reduces 1α-hydroxylation of vitamin D, so calcium falls and PTH rises. This causes high-turnover bone disease (osteitis fibrosa cystica).
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What is the first-line phosphate binder for adults with CKD stage 4–5 and hyperphosphataemia (NICE)?
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Calcium acetate.
Why? Sevelamer (a non-calcium binder) is used if calcium acetate is unsuitable, e.g. hypercalcaemia or low PTH. First control dietary phosphate.
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Why is alfacalcidol or calcitriol used instead of plain cholecalciferol to treat hypocalcaemia in advanced CKD?
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They are already 1α-hydroxylated, so they do not need renal activation.
Why? The diseased kidney cannot perform 1α-hydroxylation. NICE first treats vitamin D deficiency with colecalciferol or ergocalciferol, then uses alfacalcidol or calcitriol if CKD–mineral and bone disorder persists with eGFR below 30. Monitor calcium and phosphate, as both can rise.
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What is the mechanism of action of cinacalcet?
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A calcimimetic — it allosterically activates the calcium-sensing receptor on the parathyroid gland, lowering PTH.
Why? NICE (TA117) restricts it to refractory secondary hyperparathyroidism in patients on maintenance dialysis. IV etelcalcetide (TA448) is an option on haemodialysis if cinacalcet is unsuitable.
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A haemodialysis patient on warfarin develops exquisitely painful necrotic skin ulcers on the thighs with surrounding livedo reticularis. Phosphate is persistently high. Which specific drug treatment is used for this condition?
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IV sodium thiosulfate (with stopping warfarin and controlling phosphate).
Why? This is calciphylaxis (calcific uraemic arteriolopathy) — calcification of small skin arterioles. Mortality is high and it needs urgent nephrology input.
More Nephrology topics
- Renal physiology, GFR & diuretics
- Acute kidney injury, contrast & TMA
- Dialysis & transplantation
- Nephrotic syndrome, amyloid & diabetic kidney
- Nephritic syndrome, GN & vasculitis
- RTA & inherited tubular disorders
- Cystic, inherited & renal tumours
- Renal stones
- UTI, prostatitis & incontinence
- Prostate, testis & haematuria
- Sodium, potassium & calcium