IgA Nephropathy — SAQ · MBBS SAQ

Question

15 marks12 min

Stem

A candidate is asked to manage a classic presentation of IgA Nephropathy in an exam setting. Use precise definitions, scores, doses, and decision thresholds. [1]

Core knowledge (model answer backbone)

IgA nephropathy (Berger disease) is the commonest primary glomerulonephritis worldwide, defined by mesangial deposition of galactose-deficient IgA1 immune complexes. Classically presents with synpharyngitic gross haematuria 1 to 2 days after a mucosal infection. Diagnosis is renal biopsy showing dominant mesangial IgA on immunofluorescence. Foundation of management is RAAS blockade plus an SGLT2 inhibitor; steroids, targeted-release budesonide and complement-directed therapy are reserved for high-risk progressive disease. [1]

Red flags

Recognise severe/complicated IgA Nephropathy early
Do not delay definitive management in unstable IgA Nephropathy

High-yield structure examiners expect

Cover: Overview & Definition, Classification, Epidemiology & Risk Factors, Pathophysiology, Clinical Presentation, Differential Diagnosis.

Key doses / thresholds (from topic teaching)

referring to nephrology when ACR is over 30 mg/mmol (approximately 0
under 1 g/day)**, normal renal function and often
typically 1 to 3 g/day) and a gradually falling eGFR
ACR over 30 mg/mmol) is the trigger for nephrology ref
under 0.5 g/day) may be monitored without biopsy**
and proteinuria under 0.5 g/day has a very low 5-year risk and does [1]

Questions

a) Define the condition and give the most important classification or severity framework used in exams. (3 marks) [1]

Clear one-line definition matching standard teaching.
Named classification / stages / types with discriminating features.
One sentence on why classification changes management. [1]

b) Outline pathophysiology in a mechanism chain that explains the main clinical features. (3 marks) [1]

Initiating insult → intermediate pathway → end-organ effect.
Link at least two symptoms/signs to mechanism.
Mention one complication pathway (e.g. shock, perforation, herniation, arrhythmia). [1]

c) List discriminating clinical features and bedside assessment. (3 marks) [1]

Classic presentation plus one atypical group (elderly, pregnancy, child, immunocompromised).
Named signs/manoeuvres if relevant.
What must never be missed on exam/bedside (pregnancy test, airway, glucose, etc.). [1]

d) Investigations with thresholds and one named score if applicable. (3 marks) [1]

First-line tests and what positive findings mean.
Gold-standard or definitive investigation when needed.
Score components reproduced exactly if a named score is standard for this topic. [1]

e) Immediate resuscitation and definitive management with doses where standard. (3 marks) [1]

ABC / time-critical steps first.
First-line drug(s) with agent + dose + route (or procedure steps).
Escalation triggers (theatre, ICU, thrombolysis window, antidote, etc.).
Disposition and safety-netting. [1]

Marking tips

Full marks require specificity (numbers, names, doses) not generic "give antibiotics/fluids." Regional practice (ICMR / NICE / AHA) may be cited as alternative where relevant. [1]

References

[1]Roberts IS. Pathology of IgA nephropathy. Nature Reviews Nephrology, 2014.PMID 24861083
[2]Cheung CK, Alexander S, Reich HN, et al. The pathogenesis of IgA nephropathy and implications for treatment. Nature Reviews Nephrology, 2025.PMID 39232245
[3]Lv J, Zhang H, Wong MG, et al. Effect of oral methylprednisolone on clinical outcomes in patients with IgA nephropathy: the TESTING randomized clinical trial. JAMA, 2017.PMID 28763548
[4]Rauen T, Eitner F, Fitzner C, et al. Intensive supportive care plus immunosuppression in IgA nephropathy. New England Journal of Medicine, 2015.PMID 26630142
[5]Lafayette RA, Canetta PA, Rovin BH, et al. Efficacy and safety of a targeted-release formulation of budesonide in patients with primary IgA nephropathy (NefIgArd): 2-year results from a randomised phase 3 trial. The Lancet, 2023.PMID 37591292
[6]Empa-Kidney Collaborative Group. Empagliflozin in patients with chronic kidney disease. New England Journal of Medicine, 2023.PMID 36331190
[7]Kidney Disease: Improving Global Outcomes (KDIGO) Glomerular Diseases Work Group. KDIGO 2021 clinical practice guideline for the management of glomerular diseases. Kidney International, 2021.PMID 34556256
[8]Cattran DC, Coppo R, Cook HT, et al. The Oxford classification of IgA nephropathy: pathology definitions, correlations, and reproducibility. Kidney International, 2009.PMID 19571790
[9]Lv J, Wong MG, Hladunewich MA, et al. Effect of Oral Methylprednisolone on Decline in Kidney Function or Kidney Failure in Patients With IgA Nephropathy: The TESTING Randomized Clinical Trial. JAMA, 2022.PMID 35579642
[10]Rovin BH, Barratt J, Heerspink HJL, et al. Efficacy and safety of sparsentan versus irbesartan in patients with IgA nephropathy (PROTECT): 2-year results from a randomised, active-controlled phase 3 trial. The Lancet, 2023.PMID 37931634

Question

15 marks12 min

Stem

A candidate is asked to manage a classic presentation of IgA Nephropathy in an exam setting. Use precise definitions, scores, doses, and decision thresholds. [1]

Core knowledge (model answer backbone)

Red flags

Recognise severe/complicated IgA Nephropathy early
Do not delay definitive management in unstable IgA Nephropathy

High-yield structure examiners expect

Cover: Overview & Definition, Classification, Epidemiology & Risk Factors, Pathophysiology, Clinical Presentation, Differential Diagnosis.

Key doses / thresholds (from topic teaching)

referring to nephrology when ACR is over 30 mg/mmol (approximately 0
under 1 g/day)**, normal renal function and often
typically 1 to 3 g/day) and a gradually falling eGFR
ACR over 30 mg/mmol) is the trigger for nephrology ref
under 0.5 g/day) may be monitored without biopsy**
and proteinuria under 0.5 g/day has a very low 5-year risk and does [1]

Questions

a) Define the condition and give the most important classification or severity framework used in exams. (3 marks) [1]

Clear one-line definition matching standard teaching.
Named classification / stages / types with discriminating features.
One sentence on why classification changes management. [1]

b) Outline pathophysiology in a mechanism chain that explains the main clinical features. (3 marks) [1]

Initiating insult → intermediate pathway → end-organ effect.
Link at least two symptoms/signs to mechanism.
Mention one complication pathway (e.g. shock, perforation, herniation, arrhythmia). [1]

c) List discriminating clinical features and bedside assessment. (3 marks) [1]

Classic presentation plus one atypical group (elderly, pregnancy, child, immunocompromised).
Named signs/manoeuvres if relevant.
What must never be missed on exam/bedside (pregnancy test, airway, glucose, etc.). [1]

d) Investigations with thresholds and one named score if applicable. (3 marks) [1]

First-line tests and what positive findings mean.
Gold-standard or definitive investigation when needed.
Score components reproduced exactly if a named score is standard for this topic. [1]

e) Immediate resuscitation and definitive management with doses where standard. (3 marks) [1]

ABC / time-critical steps first.
First-line drug(s) with agent + dose + route (or procedure steps).
Escalation triggers (theatre, ICU, thrombolysis window, antidote, etc.).
Disposition and safety-netting. [1]

Marking tips

Full marks require specificity (numbers, names, doses) not generic "give antibiotics/fluids." Regional practice (ICMR / NICE / AHA) may be cited as alternative where relevant. [1]

References

[1]Roberts IS. Pathology of IgA nephropathy. Nature Reviews Nephrology, 2014.PMID 24861083
[2]Cheung CK, Alexander S, Reich HN, et al. The pathogenesis of IgA nephropathy and implications for treatment. Nature Reviews Nephrology, 2025.PMID 39232245
[3]Lv J, Zhang H, Wong MG, et al. Effect of oral methylprednisolone on clinical outcomes in patients with IgA nephropathy: the TESTING randomized clinical trial. JAMA, 2017.PMID 28763548
[4]Rauen T, Eitner F, Fitzner C, et al. Intensive supportive care plus immunosuppression in IgA nephropathy. New England Journal of Medicine, 2015.PMID 26630142
[5]Lafayette RA, Canetta PA, Rovin BH, et al. Efficacy and safety of a targeted-release formulation of budesonide in patients with primary IgA nephropathy (NefIgArd): 2-year results from a randomised phase 3 trial. The Lancet, 2023.PMID 37591292
[6]Empa-Kidney Collaborative Group. Empagliflozin in patients with chronic kidney disease. New England Journal of Medicine, 2023.PMID 36331190
[7]Kidney Disease: Improving Global Outcomes (KDIGO) Glomerular Diseases Work Group. KDIGO 2021 clinical practice guideline for the management of glomerular diseases. Kidney International, 2021.PMID 34556256
[8]Cattran DC, Coppo R, Cook HT, et al. The Oxford classification of IgA nephropathy: pathology definitions, correlations, and reproducibility. Kidney International, 2009.PMID 19571790
[9]Lv J, Wong MG, Hladunewich MA, et al. Effect of Oral Methylprednisolone on Decline in Kidney Function or Kidney Failure in Patients With IgA Nephropathy: The TESTING Randomized Clinical Trial. JAMA, 2022.PMID 35579642
[10]Rovin BH, Barratt J, Heerspink HJL, et al. Efficacy and safety of sparsentan versus irbesartan in patients with IgA nephropathy (PROTECT): 2-year results from a randomised, active-controlled phase 3 trial. The Lancet, 2023.PMID 37931634