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Diagnosis: Crescentic glomerulonephritis.
Proliferative endo and extracapillary GN, Postinfectious

In the biopsy there are diffuse endocapillary proliferation and extense cellular crescent formation (in 9 of 12 glomeruli); there is also capillary wall rupture, as seen in methenamine-silver staining. Diffuse granular capillary wall IgG and C3 deposits were evidenced and there is history of upper respiratory tract infection, in addition ASLO were increased, although this fact is not specific.

There are three disease types that lead to crescentic GN: immune-complex deposition disease, anti-GBM disease, and pauci-immune GN (usually ANCA-associated). Our case showed immune non linear deposits and this feature indicates immune-mediated GN. All these facts permit us the diagnosis of postinfectious GN.

Glomerular crescent formation is a feature of most severe forms of postinfectious GN. This is a form of immune complex GN which seem to have a better prognosis that other crescentic GN, but a relatively poorer prognosis that non-crescentic postinfectious GN. The development of crescentic GN in cases of postinfectious GN does seem to be more common in adults. Many cases of crescentic postinfectious glomerulonephritis resolve with successful.

Iinfection-associated GN should be considered a serious disease in adults, particularly when there is a previous disease and/or when it is associated with severe interstitial infiltration at renal biopsy. Even in favorable cases recovery may require several months. Patients with incomplete recovery should be regularly monitored as many of them may progress to chronic renal insufficiency. The treatment with steroids did not improve the outcome. A careful management of underlying diseases, abstinence from alcohol and strict control of arterial hypertension may be of use in slowing the renal progression in these patients (Moroni G, et al. Nephrol Dial Transplant. 2002;17:1204-11. [PubMed link] [Full text link]).

In developed countries, the incidence of the typical post-streptococcal glomerulonephritis is progressively decreasing probably due to the improved standard of living, better public health services and the early treatment of pharyngeal infections. In the meantime, however, the number of cases of glomerulonephritis either caused by atypical infective agents, or developed in patients with an underlying disease, and showing atypical clinical and/or histological features at presentation is increasing. Morono G. et al found that the atypical sites of infection, the number of older patients, and the number of renal biopsies with interstitial infiltration did significantly increase. Of much importance, the number of patients with an immunocompromized background also significantly increased (Moroni G, et al. Nephrol Dial Transplant. 2002;17:1204-11. [PubMed link] [Full text link]).

See the chapter Proliferative endocapillary glomerulonephritis (English version).

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Bibliography

• El-Husseini AA, Sheashaa HA, Sabry AA, Moustafa FE, Sobh MA. Acute postinfectious crescentic glomerulonephritis: clinicopathologic presentation and risk factors. Int Urol Nephrol. 2005;37(3):603-9. [PubMed link]
• Sotsiou F, Dimitriadis G, Liapis H. Diagnostic dilemmas in atypical postinfectious glomerulonephritis. Semin Diagn Pathol. 2002 Aug;19(3):146-59. [PubMed link]
• Moroni G, Pozzi C, Quaglini S, Segagni S, Banfi G, Baroli A, Picardi L, Colzani S, Simonini P, Mihatsch MJ, Ponticelli C. Long-term prognosis of diffuse proliferative glomerulonephritis associated with infection in adults. Nephrol Dial Transplant. 2002;17:1204-11. [PubMed link] [Full text link]
• Sotsiou F. Postinfectious glomerulonephritis. Nephrol Dial Transplant. 2001;16 Suppl 6:68-70. [PubMed link] [Free full text]
  

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