Post Infectious Glomerulonephritis in the Adult Patient
Minh-Chi Tran, MD; Rebecca Sonu, MD; Rajendra Ramsamooj, MD; Calvin Hirsch, MD
Department of Medicine, University of California, Davis, Sacramento, California
Department of Pathology, University of California, Davis, Sacramento, California
Introduction
Radiology
Pathology
•  Acute kidney injury associated with bacterial
infections is not uncommon and determining
the etiology of kidney injury is imperative to
determine further patient management
Pathophysiology
Antigens thought to induce PIGN have been noted
to:
1.  Activate the alternative pathway of the
complement system
2.  Localizes with complement deposits and
within subepithelial electron-dense deposits
(humps)
3.  Staphylococcus associated PIGN are
characterized by glomerular IgA deposits
and biopsy findings can mimic idopathic
IgA nephropathy
•  Acute post-infectious glomerulonephritis (PIGN)
was once common worldwide but has seen a
decline in incidence in developed countries
over the last three decades
•  While classically associated with streptococcal
infections, it is also known to occur with
staphylococcal infections particularly in the
setting of bacteremia
Treatment
• Prevention with early antibiotics helps prevents
the spread of nephritis-associated infection
Hospital Course
• The use of corticosteroids is controversial as
there is a theoretical increased risk of relapse
and case reports have demonstrated resolution
of PIGN with and without steroid doses
HPI
53-year-old female presented to the emergency
department with painful sore throat and initially
discharged with pain control. On return visit she
was noted to have a retropharyngeal phlegmon and
a small retropharyngeal abscess.
Prognosis
• Children who develop PIGN have an excellent
prognosis with a mortality of 0.5% and < 2%
progressing to end-stage renal failure while
Management
The abscess was not drainable and she was
treated with a dexamethasone burst, fluids, and IV
antibiotics. She was also noted to have methicillin
sensitive Staphlococcus aureus (MSSA)
bacteremia and remained hospitalized for multiple
issues including pain control, delayed clearance of
her bacteremia, and hyponatremia.
Complication
• On hospital day 8 she developed acute kidney
injury (AKI) with creatinine increase from 0.7 mg/dL
to 2.04 mg/dL, peaking at 6.98 mg/dL. She became
anuric requiring temporary hemodialysis.
• Initial urine microscopy and urine electrolytes
implied pre-renal etiology but further testing noted
low complement levels and renal biopsy confirmed
suspicions for PIGN and rapidly progressive
glomerulonephritis (RPGN).
Outcome
She was treated supportively and at one-month
follow-up, she completed her IV antibiotic course
with repeat imaging showing improvement of her
retropharyngeal infection. She sustained moderate
chronic kidney disease with a creatinine of 1.28 mg/
dL.
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Discussion
Figure 3, 4. Periodic acid-Schiff and silver stain
showing proliferative glomerulonephritis
characterized by a segmental endothelial
hypercellularity due to influx of inflammatory cells
(arrow).
References
1. Marshall CS, et al. Acute post-streptococcal glomerulonephritis
in the Northern Territory of Australia: a review of 16 years data
and comparison with the literature. Am J Trop Med Hyg 2011; 85
(4): 703-10.
2. Rodriguez-Iturbe B, Musser JM. The current state of
poststreptococcal glomerulonephritis. J Am Soc Nephrol 2008; 19
(10): 1855-64.
3. Zeledon JI, et al. Glomerulonephritis causing acute renal failure
during the course of bacterial infections. Histological varieties,
potential pathogenetic pathways and treatment. Int Urol Nephrol
2008; 40(2): 461-70.
4. Satoskar AA, et al. Staphylococcus infection-associated
glomerulonephritis mimicking IgA nephropathy. Clin J Am Soc
Nephrol 2006; 1(6): 1179-86.
Figure 1 and 2. Initial magnetic resonance imaging
and computerized tomography scan with contrast
demonstrating small abscess of the left longus
muscle and oral and hypopharyngeal pharyngitis
with retropharyngeal phlegmon and early abscess
formation C2-C4/5
Labs
UA: protein >500, WBC 25, RBC >100
FeUrea: 25%
Urine Microscopy: granular, muddy brown casts
C3/C4: 66/16 mg/dL
Complement Activity: 29 units
Renal U/S and Doppler: within normal limits
• Adults and the elderly have a higher likelihood of
up to 41% in developing azotemia and chronic
kidney disease.
Acknowledgments
Figure 5. Immunofluorescence showing mesangial
and subendothelial immune complex deposits.
We thank the Department of Pathology from the
University of California, Los Angeles for providing the
renal biopsy images