postinfectious glomerulonephritis; infection-related glomerulonephritis
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Etiology
- Staphylococcus as common as Streptococcus
- poststreptococcal glomerulonephritis
- bacterial endocarditis
- more common with acute than subacute bacterial endocarditis
- especially common with staphyloccal endocarditis
- gram negative bacteria
- infected ventriculoatrial shunt
- deep visceral bacterial abscesses
- empyema
- severe pneumonia
- osteomyelitis
- certain viral infections
Pathology
- immune complex glomerulonephritis
- antigen in immune complex is derived from infectious agent[3]
- deposition of immune complex in subepithelium
- preformed immune complexes or in-situ immune complex formation
- complement activation
- recruitment of inflammatory cells
- proliferative glomerulonephritis
- complement C3 staining by immunofluorence microscopy
- IgA deposition can be seen with Staphylococcus infections[3]
- exudative-proliferative pattern of glomerulonephritis[3]
- subepithelial humps on electron microscopy[3]
Clinical manifestations
- variable, may present as asymptomatic microscopic hematuria or
- rapidly progressive glomerulonephritis (acute nephritic syndrome)
- can develop at the time of infection or weeks later
- onset 1-6 weeks after acute pyogenic infection
- rapid onset edema, hypertension, oliguria
- can develop at the time of infection or weeks later
- symptoms generally remit after several weeks
- hematuria generally resolves over 3-6 months
- proteinuria may persist for > 6 months[3]
Laboratory
- streptozyme test[8]
- anti-streptolysin O titer
- anti-DNAse titer
- anti-hyaluronidase
- anti-streptokinase
- anti-NAD-ase
- complement C3 in serum is low
- urinalysis:
Diagnostic procedures
- renal biopsy
- progressive renal failure
- symptoms fail to remit in expected time frame
Differential diagnosis
- IgA nephropathy (normal C3 in serum, no delay in hematuria)
Management
- treatment is supportive
- control hypertension
- diuresis for volume overload
- dialysis as needed
- no evidence to support use of glucocorticoids or other immunosuppressive agents
- prevention
- early treatment of bacterial infections with appropriate antibiotics can prevent or lessen severity of postinfectious glomerulonephritis[3]
- improvement occurs with control of infection[3]
More general terms
More specific terms
References
- ↑ Manual of Medical Therapeutics, 28th ed, Ewald & McKenzie (eds), Little, Brown & Co, Boston, 1995, pg 270
- ↑ Mayo Internal Medicine Board Review, 1998-99, Prakash UBS (ed) Lippincott-Raven, Philadelphia, 1998, pg 605
- ↑ 3.0 3.1 3.2 3.3 3.4 3.5 3.6 3.7 Medical Knowledge Self Assessment Program (MKSAP) 11, 15, 16, 17, 18, 19. American College of Physicians, Philadelphia 1998, 2009, 2012, 2015, 2018, 2021.
Medical Knowledge Self Assessment Program (MKSAP) 19 Board Basics. An Enhancement to MKSAP19. American College of Physicians, Philadelphia 2022 - ↑ Nasr SH, Share DS, Vargas MT, D'Agati VD, Markowitz GS Acute poststaphylococcal glomerulonephritis superimposed on diabetic glomerulosclerosis. Kidney Int. 2007 Jun;71(12):1317-21 PMID: https://www.ncbi.nlm.nih.gov/pubmed/17311069
- ↑ Nadasdy T, Hebert LA. Infection-related glomerulonephritis: understanding mechanisms. Semin Nephrol. 2011 Jul;31(4):369-75 PMID: https://www.ncbi.nlm.nih.gov/pubmed/21839370
- ↑ Nasr SH, Radhakrishnan J, D'Agati VD. Bacterial infection-related glomerulonephritis in adults. Kidney Int. 2013 May;83(5):792-803. Review. PMID: https://www.ncbi.nlm.nih.gov/pubmed/23302723
- ↑ Glassock RJ, Alvarado A, Prosek J et al Staphylococcus-related glomerulonephritis and poststreptococcal glomerulonephritis: why defining "post" is important in understanding and treating infection-related glomerulonephritis. Am J Kidney Dis. 2015 Jun;65(6):826-32. PMID: https://www.ncbi.nlm.nih.gov/pubmed/25890425
- ↑ 8.0 8.1 NEJM Knowledge+ Nephrology/Urology