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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 Discussion

Hospital Course

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.

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.

•  Acute kidney injury associated with bacterial infections is not uncommon and determining the etiology of kidney injury is imperative to determine further patient management

•  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

References

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

Treatment • Prevention with early antibiotics helps prevents the spread of nephritis-associated infection

• 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

Prognosis • Children who develop PIGN have an excellent prognosis with a mortality of 0.5% and < 2% progressing to end-stage renal failure while

• Adults and the elderly have a higher likelihood of up to 41% in developing azotemia and chronic kidney disease.

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.

Acknowledgments

Radiology Pathology

We thank the Department of Pathology from the University of California, Los Angeles for providing the renal biopsy images

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

Figure 5. Immunofluorescence showing mesangial and subendothelial immune complex deposits.

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

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).