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Nephrol Dial Transplant (1999) 14: 2279-2282
© 1999 European Renal Association-European Dialysis and Transplant Association

Editorial Comments

Glomerular IgA deposition in liver disease

Shideh Pouria1 and John Feehally2

1 Renal Unit, King's College Hospital, London and 2 Department of Nephrology, Leicester General Hospital, UK

Correspondence and offprint requests to: Dr Shideh Pouria, Renal Unit, Kings College Hospital, Bessemer Road, London SE5 9RS, UK.

Introduction

IgA nephropathy associated with liver disease (hepatic IgAN) is the commonest form of secondary IgAN. It is particularly common in alcoholic liver disease, which itself is associated with disorders of the IgA immune system [1,2] but also occurs in other forms of cirrhosis and chronic hepatitis. It is characterized by microscopic haematuria, proteinuria, elevated serum IgA levels and mesangial deposits of IgA. Although usually a clinically silent condition, a small percentage of patients present with nephrotic syndrome and renal impairment that can rarely progress to end-stage renal failure.

Is hepatic IgAN a distinct clinicopathological entity?

An association between glomerular disease and cirrhosis has been known since the 1950s although early autopsy studies did not always take account of viral infection, bacterial sepsis, and other factors that might also provoke glomerular injury. Glomerular lesions are reported in more than 50% of cirrhotics [3] and this rises to 100% in studies of end-stage . . . [Full Text of this Article]

Renal histology

Clinical features of hepatic IgAN

The human IgA system

IgA synthesis
IgA clearance
Animal models of hepatic IgAN

IgA system abnormalities in hepatic IgAN

Serology
Tissue IgA deposition
What is the pathogenesis of hepatic IgAN?

Increased pIgA production
Production of abnormal IgA
Origin of the deposited IgA?
Decreased IgA clearance
Why does IgA deposit in the mesangium?
Conclusion

References


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