The Multifaceted Relationship Between Infection and Glomerulonephritis

In a recent article published in AJKD, Glassock et al argue that the term post-infectious glomerulonephritis not be used indiscriminately for all cases where there is a clinical history of both an infection and glomerulonephritis. It is suggested that the term is best used for patients where the infection has resolved, and a latent period precedes the onset of glomerular injury.

The chief merit of this restricted definition is that it does not apply to cases where there is still evidence of active infection. Labeling these latter cases as post-infectious glomerulonephritis may trigger steroid or other immunosuppressive therapy, which can exacerbate an infection. They describe cases whereby patients with active Staphylococcal-associated glomerulonephritis have developed severe sepsis or died following ill-advised steroid therapy.  As a corollary, whenever subepithelial immune complex deposits are found on a kidney biopsy, nephrologists should diligently evaluate the patients for chronic bacterial, fungal, or viral infection.

Conversely, cases of ANCA-associated crescentic glomerulonephritis can be triggered by infection, and may still require immunosuppressive therapy.  Another circumstance in which steroid therapy may be required despite chronic infection is immune reconstitution syndrome. A report of an HIV-positive patient with miliary tuberculosis who developed pulmonary and renal inflammation following initiation of HAART therapy is an example.  Bronchoalveolar lavage was negative for Mycobacteria by culture, and a kidney biopsy showed non-destructive granulomas. Antituberculous therapy was supplemented by a 2 week course of prednisone at 2 mg/Kg.

What do our readers think?


Professor Parmjeet Randhawa, MD
AJKD Blog Contributor

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1 Comment on The Multifaceted Relationship Between Infection and Glomerulonephritis

  1. Tuncay Sahutoglu // June 11, 2015 at 8:44 am // Reply

    I recently had a pateint who apparently presented with cholcystitis and acute worsening renal injury. Renal functions deteriorated within a few days under effective antibiotherapy and urine tests revealed hematuria and nonnephrotic proteinuria. Renal biopsy showed crescentic glomerulonephritis without immune deposits and ANCA was negative.
    Steroid was added to antibiotics and dramatic response was seen.
    I believe that under effective antimicrobial treatment, steroids should always be considered as a salvage therapy when life/organ threatening involvement is considered. Cytopathic or tissue injurious effects of a pathogen may indeed be followed by exagerated/uncontrolled destructive response of the immune system, which is where the immunosuppressives should find a place.

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