Self-assessment questions: Evaluation and management of IgA nephropathy
Regarding clinical presentation in IgA nephropathy (IgAN):
Recurrent episodes of macroscopic haematuria classically occur 1–2 weeks following an upper respiratory tract infection
Development of IgAN is related to high levels of circulating levels of IgA
Although sporadic instances of IgAN occur, IgAN is typically familial
Acute kidney injury is a rare manifestation which may be related to the toxic effects of haematuria on the renal tubules
IgAN may occur secondary to chronic liver disease or coeliac disease
A renal biopsy:
Is always required for diagnosis of IgAN
May not be necessary in cases of non-visible haematuria with preserved renal function and no proteinuria
Shows predominant mesangial deposition of IgA on immunofluorescent staining
During episodes of macroscopic haematuria may show the presence of crescents
Will always show abnormalities on light microscopy if there are IgA deposits
Regarding treatment of IgAN:
Proteinuria >1 g/day is associated with a worse renal prognosis and should be treated by renin-angiotensin system (RAS) blockade
A trial of corticosteroids may be considered in those with proteinuria who have failed to respond to maximal RAS blockade and blood pressure control
Mycophenolate mofetil has been shown to be of benefit in Caucasian patients
All patients with nephrotic syndrome and IgAN should be treated with corticosteroids
Results from randomised controlled trials suggest that crescentic IgAN should be treated with corticosteroids and cyclophosphamide
Prognosis in IgAN:
May be predicted by scoring using the Oxford Classification of pathological findings.
Is related to the extent of IgA glycosylation
Is improved by reducing proteinuria to <1 g/day
Is worse in those with recurrent episodes of visible haematuria
Recurrence of IgAN in transplant kidneys commonly causes transplant failure
Answers to these self-assessment questions can be found on page s92.
- © 2012 Royal College of Physicians
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