Literature
Clinical Pearls & Morning Reports
Published October 31, 2018
What factors may help to distinguish IgA-dominant infection-associated glomerulonephritis from IgA nephropathy?
The pathophysiology of IgA-dominant infection-associated glomerulonephritis is incompletely understood. In situ immune-complex formation and the direct activation of plasmin by bacterial antigens are now thought to represent the principal mechanisms that lead to complement activation and inflammation within the glomerulus in IgA-dominant infection-associated glomerulonephritis. Read the latest NEJM Clinical Problem-Solving here.
Clinical Pearls
Q: What pathogen is most often associated with IgA-dominant infection-associated glomerulonephritis?
A: In case series, a causative pathogen was identified in at least 75% of patients with IgA-dominant infection-associated glomerulonephritis. Staphylococcus aureus was, by far, the most common pathogen, and it accounted for at least half the identified infections; streptococcus was the second most common.
Q: What are some of the clinical features of IgA-dominant infection-associated glomerulonephritis?
A: In case series, skin and the respiratory tract were the most frequent sites of infection, although a diverse range of sites was reported. IgA-dominant infection-associated glomerulonephritis appeared to be more common in male patients and in patients with diabetes; although there was a large range in the age of the patients, the median appeared to be in the late 50s, and children were infrequently affected, which represents a key contrast to poststreptococcal glomerulonephritis.
Morning Report Questions
Q: What factors may help to distinguish IgA-dominant infection-associated glomerulonephritis from IgA nephropathy?
A: In addition to IgA deposits being present in IgA-dominant infection-associated glomerulonephritis, they can also be seen in glomerulonephritis caused by IgA nephropathy or IgA vasculitis (formerly Henoch–Schönlein purpura). The degree of C3 deposition can help distinguish IgA-dominant infection-associated glomerulonephritis from IgA nephropathy or IgA vasculitis because intense C3 deposition is a hallmark of IgA-dominant infection-associated glomerulonephritis. In addition, low serum C3 levels and subepithelial electron-dense deposits are suggestive of a diagnosis of IgA-dominant infection-associated glomerulonephritis rather than primary IgA nephropathy. Acute glomerulonephritis in patients with IgA nephropathy typically occurs soon after the onset of a viral upper respiratory tract infection that itself is usually short-lived. Poststreptococcal glomerulonephritis characteristically occurs days to weeks after the precipitating infection has resolved. In contrast, IgA-dominant infection-associated glomerulonephritis often develops over weeks in the context of persistent infection.
Q: How is IgA-dominant infection-associated glomerulonephritis managed?
A: The primary treatment for IgA-dominant infection-associated glomerulonephritis consists of effective control of the source of the precipitating infection. On the basis of experience with poststreptococcal glomerulonephritis, glucocorticoids and other immunosuppressive agents have been used in the treatment of IgA-dominant infection-associated glomerulonephritis; however, outcomes have been poor, perhaps because active infection is often present as IgA-dominant infection-associated glomerulonephritis develops. Data are limited regarding the clinical outcomes of IgA-dominant infection-associated glomerulonephritis; in one case series, approximately half the patients regained their initial renal function, whereas end-stage renal disease developed in approximately 20%.