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Nephrotic syndrome, amyloid & diabetic kidney flashcards

18 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. What three features define nephrotic syndrome?

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   Proteinuria above 3.5 g/24 h (heavy proteinuria), serum albumin below 30 g/L and oedema.

   Why? Hyperlipidaemia is usually present too. The cause is podocyte injury, so protein leaks through the filtration barrier.

2. Why are patients with nephrotic syndrome at high risk of venous thrombosis, including renal vein thrombosis?

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   Urinary loss of antithrombin III (and other anticoagulant proteins) with increased hepatic production of clotting factors.

   Why? Renal vein thrombosis presents with flank pain, haematuria and a sudden fall in renal function. Prophylactic anticoagulation is considered when albumin is very low, especially in membranous nephropathy.

3. What is the characteristic electron microscopy finding in minimal change disease?

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   Diffuse effacement (fusion) of podocyte foot processes.

   Why? Light microscopy is normal and immunofluorescence is negative — hence 'minimal change'.

4. What is the first-line treatment of minimal change disease?

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   Oral corticosteroids (prednisolone).

   Why? Most children (and many adults) respond well. For frequent relapses or steroid dependence, use a calcineurin inhibitor, cyclophosphamide, mycophenolate or rituximab.

5. Name a drug class and a malignancy associated with secondary minimal change disease.

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   NSAIDs; Hodgkin lymphoma.

   Why? In an adult with new minimal change disease, review the drug history and consider lymphoma.

6. Name three secondary causes of focal segmental glomerulosclerosis (FSGS).

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   Any three of: HIV, heroin use, obesity, hypertension, bisphosphonates (pamidronate), interferon, CMV.

   Why? Secondary FSGS is managed by treating the cause plus ACEi/ARB; immunosuppression is mainly for primary FSGS.

7. Which gene variant, common in people of African ancestry, increases the risk of FSGS and HIV-associated nephropathy?

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   APOL1 (apolipoprotein L1).

   Why? APOL1-associated FSGS tends to be steroid-resistant and progresses faster.

8. What is the first-line immunosuppression for primary FSGS, and the next step if it fails?

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   High-dose corticosteroids; if steroid-resistant, a calcineurin inhibitor (tacrolimus or ciclosporin).

   Why? All patients also get supportive care: ACEi/ARB, statin, diuretics for oedema and weight loss if obese.

9. Which autoantibody is found in about 70–80% of primary membranous nephropathy?

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   Anti-phospholipase A2 receptor (anti-PLA2R) antibody.

   Why? Anti-PLA2R titres help with diagnosis and monitoring response. Anti-THSD7A is a rarer target antigen.

10. In an adult with newly diagnosed membranous nephropathy, what must you always screen for?

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    Secondary causes — especially an underlying solid-organ malignancy (also hepatitis B/C, SLE and drugs such as NSAIDs, gold and penicillamine).

    Why? Membranous nephropathy can be paraneoplastic (e.g. lung, colon, breast, prostate cancer). Class V lupus nephritis is membranous.

11. What is the electron microscopy finding in membranous nephropathy, and its appearance on silver stain?

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    Subepithelial immune deposits on EM; silver stain shows GBM 'spikes' between the deposits (the 'spike and dome' pattern).

    Why? Immunofluorescence shows granular IgG and C3 along capillary loops; light microscopy shows a thickened GBM.

12. What immunosuppression is used for membranous nephropathy at high risk of progression?

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    Rituximab, or cyclophosphamide plus corticosteroids (modified Ponticelli regimen).

    Why? All patients get ACEi/ARB and statin, plus anticoagulation if thrombotic risk is high. About one-third remit spontaneously, so low-risk patients are observed.

13. What is the diagnostic staining result for amyloid on tissue biopsy?

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    Congo red staining showing apple-green birefringence under polarised light.

    Why? Amyloid is misfolded protein in a β-pleated sheet. An abdominal fat pad aspirate is a simple first biopsy site; rectal or salivary gland biopsy can also be used.

14. From which protein is AA (secondary) amyloid derived, and name two conditions that cause it.

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    Serum amyloid A (an acute-phase protein made in the liver); e.g. rheumatoid arthritis, IBD, TB, bronchiectasis, familial Mediterranean fever.

    Why? Chronically high acute-phase reactants drive AA amyloid. It mainly affects the kidney (nephrotic syndrome).

15. Name two clinical features seen in AL (light-chain) amyloidosis but not typically in AA amyloidosis.

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    Macroglossia, carpal tunnel syndrome, periorbital purpura or peripheral neuropathy (any two).

    Why? AL amyloid comes from monoclonal light chains (usually lambda) from a plasma cell dyscrasia, and often involves the heart (restrictive cardiomyopathy, low-voltage ECG).

16. What is the classic light microscopy lesion of diabetic nephropathy?

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    Kimmelstiel–Wilson nodules (nodular glomerulosclerosis — PAS-positive mesangial nodules).

    Why? Earlier changes are GBM thickening and mesangial expansion.

17. What is the earliest clinically detectable stage of diabetic nephropathy?

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    Microalbuminuria (A2, ACR 3–30 mg/mmol).

    Why? It also marks endothelial dysfunction and higher cardiovascular risk. Screen people with diabetes with an annual ACR.

18. What is the classic histology of HIV-associated nephropathy, and what do the kidneys look like on ultrasound?

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    Collapsing FSGS; enlarged, echogenic kidneys.

    Why? Most CKD causes small kidneys. HIVAN presents with nephrotic-range proteinuria and rapidly falling GFR; treat with antiretroviral therapy plus ACEi/ARB.