Basic Sciences in Nephrology

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Question 1 of 20

1. Question

In a patient with a normal anion gap metabolic acidosis, what does a positive urine anion gap (urine sodium + potassium − chloride) indicate?

Impaired renal ammonium excretion indicating renal tubular acidosis.
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Appropriate renal ammonium excretion in response to gastrointestinal bicarbonate loss.
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Ingestion of an exogenous acid load.
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Presence of unmeasured urinary cations such as lithium.
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Volume depletion with enhanced proximal sodium reabsorption.
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Question 2 of 20

2. Question

What is the principal mechanism of the metabolic acidosis in type 4 renal tubular acidosis?

Aldosterone deficiency or resistance with hyperkalaemia-induced impairment of ammoniagenesis.
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Autoantibody-mediated inhibition of the basolateral chloride–bicarbonate exchanger.
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Failure of the distal H⁺-ATPase to generate a steep transtubular pH gradient.
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Reduced proximal tubular threshold for bicarbonate reabsorption.
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Retention of unmeasured organic anions from reduced nephron mass.
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Question 3 of 20

3. Question

By which mechanism do sodium–glucose cotransporter 2 inhibitors reduce intraglomerular pressure?

Increased sodium chloride delivery to the macula densa causing adenosine-mediated afferent arteriolar constriction.
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Blockade of endothelin-1 receptors on mesangial cells.
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Direct inhibition of renin release from granular cells of the afferent arteriole.
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Efferent arteriolar vasodilatation through reduced local angiotensin II generation.
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Increased prostaglandin-dependent medullary blood flow.
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Question 4 of 20

4. Question

Which antigen is the target of the autoantibody responsible for the majority of cases of primary membranous nephropathy?

Phospholipase A2 receptor on the podocyte membrane.
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Nephrin on the podocyte slit diaphragm.
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The α3 chain non-collagenous domain of type IV collagen.
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Thrombospondin type-1 domain-containing 7A on glomerular endothelium.
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Uromodulin in the thick ascending limb.
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Question 5 of 20

5. Question

A persistently low serum C3 with a normal C4 in glomerulonephritis indicates activation of which complement pathway?

Alternative pathway.
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Classical pathway.
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Classical and lectin pathways combined.
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Lectin pathway via mannose-binding lectin.
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Terminal pathway only, without upstream activation.
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Question 6 of 20

6. Question

Linear immunoglobulin G staining along the glomerular basement membrane on immunofluorescence reflects antibody binding to which antigen?

The α3 chain non-collagenous 1 domain of type IV collagen.
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Laminin beta-2 of the lamina densa.
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Myeloperoxidase released from neutrophil granules.
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Podocyte phospholipase A2 receptor.
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The α5 chain of type IV collagen expressed in Bowman's capsule.
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Question 7 of 20

7. Question

What is the primary molecular abnormality initiating IgA nephropathy?

Impaired galactosylation of O-linked glycans in the IgA1 hinge region.
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Deficiency of secretory IgA at mucosal surfaces with compensatory IgM production.
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Failure of hepatic asialoglycoprotein receptor clearance of polymeric IgA2.
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Mesangial cell overexpression of the polymeric immunoglobulin receptor.
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Somatic mutation of the IgA heavy chain constant region.
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Question 8 of 20

8. Question

Which gene defect accounts for the majority of cases of Alport syndrome?

COL4A5 variants.
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COL4A3 biallelic variants.
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COL4A4 heterozygous variants.
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MYH9 variants.
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NPHS2 variants.
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Question 9 of 20

9. Question

In autosomal dominant polycystic kidney disease, which measurement best predicts the future rate of decline in glomerular filtration rate?

Height-adjusted total kidney volume.
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Cyst fluid sodium concentration.
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Number of hepatic cysts.
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Renal resistive index on Doppler ultrasound.
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Urine albumin:creatinine ratio.
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Question 10 of 20

10. Question

What is the effect of fibroblast growth factor 23 on renal vitamin D metabolism?

Inhibits 1α-hydroxylase and induces 24-hydroxylase.
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Inhibits 24-hydroxylase and induces 1α-hydroxylase.
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Enhances 24-hydroxylase and enhances 1α-hydroxylase activity.
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Has no effect on vitamin D metabolism but inhibits parathyroid hormone secretion.
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Increases hepatic 25-hydroxylase activity.
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Question 11 of 20

11. Question

What is the mechanism of action of hypoxia-inducible factor prolyl hydroxylase inhibitors used for anaemia of chronic kidney disease?

Prevention of hypoxia-inducible factor degradation, increasing endogenous erythropoietin transcription.
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Agonism of the erythropoietin receptor on erythroid progenitor cells.
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Direct neutralisation of circulating hepcidin.
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Inhibition of erythroferrone signalling in hepatocytes.
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Stimulation of transferrin receptor shedding from reticulocytes.
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Question 12 of 20

12. Question

By which mechanism does chronic lithium therapy cause nephrogenic diabetes insipidus (arginine vasopressin resistance)?

Entry into principal cells via the epithelial sodium channel with downregulation of aquaporin-2.
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Competitive antagonism of the V2 receptor by lithium ions.
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Inhibition of NKCC2 in the thick ascending limb, abolishing the medullary gradient.
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Osmotic diuresis due to impaired proximal tubular glucose reabsorption.
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Suppression of hypothalamic vasopressin release.
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Question 13 of 20

13. Question

Why is the fractional excretion of urate increased in the syndrome of inappropriate antidiuresis?

Mild volume expansion suppresses proximal tubular sodium and urate reabsorption.
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Distal tubular secretion of urate is stimulated by vasopressin acting on V1 receptors.
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Hyponatraemia directly inhibits the URAT1 transporter independently of volume status.
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Reduced glomerular filtration rate increases the filtered load of urate.
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Urate becomes more soluble at the low plasma osmolality, favouring excretion.
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Question 14 of 20

14. Question

Which histological feature is most characteristic of chronic calcineurin inhibitor nephrotoxicity?

Nodular arteriolar hyalinosis with striped interstitial fibrosis.
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Diffuse peritubular capillary C4d deposition.
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Intranuclear viral inclusions with SV40 large T antigen positivity.
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Segmental fibrinoid necrosis with cellular crescents.
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Transmural arteritis with intimal inflammatory infiltration.
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Question 15 of 20

15. Question

Why is C4d a useful marker of antibody-mediated rejection in kidney allograft biopsies?

It binds covalently to endothelium and persists as a footprint of classical complement activation.
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It is an inflammatory cytokine released by graft-infiltrating T cells.
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It is deposited only when donor-specific antibody is absent from the circulation.
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It is the terminal lytic complex that directly causes endothelial cell death.
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It reflects alternative pathway amplification independent of immunoglobulin.
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Question 16 of 20

16. Question

Cystinuria results from a defect in the transport of which group of solutes in the proximal tubule?

Cystine and the dibasic amino acids ornithine, lysine and arginine.
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Glucose, phosphate and bicarbonate.
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Glycine, proline and hydroxyproline.
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Neutral amino acids including tryptophan.
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Oxalate and glycolate.
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Question 17 of 20

17. Question

Which urinary protein is least reliably detected by standard reagent strip (dipstick) testing?

Immunoglobulin free light chains.
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Albumin.
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Alpha-1 microglobulin at nephrotic concentrations.
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Haemoglobin.
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Transferrin.
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Question 18 of 20

18. Question

Why does angiotensin-converting enzyme inhibition reduce glomerular filtration rate in the presence of critical bilateral renal artery stenosis?

Loss of angiotensin II-mediated efferent arteriolar constriction, lowering filtration fraction.
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Afferent arteriolar constriction mediated by adenosine A1 receptors.
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Bradykinin-mediated increase in glomerular capillary permeability.
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Direct toxicity of the drug to proximal tubular epithelium.
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Mesangial cell contraction reducing filtration surface area.
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Question 19 of 20

19. Question

Which finding distinguishes Gitelman syndrome from Bartter syndrome?

Hypocalciuria with marked hypomagnesaemia.
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Hypercalciuria with nephrocalcinosis.
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Hyperkalaemic metabolic acidosis.
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Low urinary chloride excretion.
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Suppressed plasma renin activity.
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Question 20 of 20

20. Question

What is the molecular defect in Liddle syndrome?

Gain-of-function of the epithelial sodium channel due to impaired ubiquitin-mediated degradation.
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Activating mutation of the mineralocorticoid receptor increasing ligand sensitivity.
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Deficiency of 11β-hydroxysteroid dehydrogenase type 2 allowing cortisol to activate the mineralocorticoid receptor.
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Gain-of-function of the WNK1/WNK4 kinase pathway increasing NCC activity.
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Overactivity of the basolateral sodium–potassium ATPase in principal cells.
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Basic Sciences in Nephrology

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