Interstitial nephritis associated with
PostInfectious GN
PRAET MARLEEN , MD, PhD
UNIVERSITY HOSPITAL GHENT
Clinical History: Background





Man
53 year
Ethyl ++ , smoking 10-12 cigars/day
1994: T3N0M0 Spinocellular Carcinoma of the glottis
2007-2010: recurrent hemoptoe presenting a cystic
lesion at the Right Upper Lobe of the Lung.
Clinical History: Recent



04/10/2011: lobectomie
Histology:
Pachypleuritis met underlying scar of the pulmonary
parenchyma. Bronchiectasy and chronic inflammation.
No malignancy.
Follow up: hydropneumothorax with infection: crp 15
mg/dL, WBC 19000 10^3/µL, fever 39°C, sputum:
H.Influenza
Admission in Emergency 3 weeks after
lobectomy



Acute renal failure:
- Creatinin 4,21 mg/dl
- Proteinuria 4.3g/L
- Macroscopic hematuria
- Oliguria
- WBC: 21700 10^3/µL
- CRP 10.6 mg/dl
Normal temperature, normal BP
Renal biopsy.
AgMethanamine x 4
Kidney biopsy containing 30 glomeruli: 4 glomeruli are completely sclerosed.
7 glomeruli undergo proliferative changes with crescent formation surrounding
the glomeruli segmentally or globally. Glomeruli, tubuli and interstitium are
infiltrated by neutrophils. No vasculitis
AG Methanamine x10
CONGORED x25
CONGORED X 10
PAS x40
Differential Diagnosis


(Focal) crescentic glomerulonephritis post infection
(PIGN).
Microangiopathic vasculitis with crescentic
glomerulonephritis: ANCA-associated systemic vasculitides
(Wegener, microscopic polyangitis, Churg- Strauss)

Sepsis with combined interstitial and glomerular
changes.
Immunofluorescence Findings



Ig G, Ig A, Ig M, C1Q: negative IF findings
Kappa, Lambda: negative IF findings
C3: strong granular staining at capillary wall 3+
SUGGESTED DIAGNOSIS: Post infectious
glomerulonephritis with crescent formation in <
50% of the glomeruli. IF findings consistent with
previous infection.
C3 Deposition at capillary wall
ORIGIN OF INFECTION

2 possibilities:
- Hydropneumothorax with infectious
agent: H. Influenzae was found in the
sputum.
- Bronchiectasy with ulcerative
inflammation and presence of germs:
however no infectious agent was
cultivated
Treatment of the patient
Original clinical diagnosis: vasculitis: plasmapheresis,
cyclophosphamide, high dosed steroids. Creat levels up tot
6. 65 mg/dl. However: ANCA: negative, anti GBM: negative
Switch of treatment after IF findings: stop plasmapheresis, stop
cyclophosphamide:
Instead: intravenous AB, steroids, dialysis.
Creat level is decreasing with recovery of the patient.
Discussion
Glomerulonephritis and infection
 - is primarily a childhood disease occuring after upper
respiratory infection(5-10 %) or impetigo (25%)
(Streptococcus A, beta – hemolytic, serotypes 12, 49)
 - in older patients: less well known



Male/female ratio 2.8:1
Immunocompromised background is present in 61 %, most often
diabetes or malignancy
Infectious agent most often found: staphylococcus (46%),
streptococcus (16%) and unusual gram- negative organisms.
Discussion

Glomerulonephritis and infection:
 IF
findings in PIGN: IgG and C3, or C3 only
 IgA dominant PIGN: strong association with
staphylococcal infections of the skin with diabetes as a
major risk. This variant of APIGN should be
distinguished from the classic IgA nephropathy (Haas M
Human Pathology 2008, 39, 1309-1316, Nasr S, D’Agati Nephron Clin

Pract 2011, 119, 18-26)
EM findings: classical PIGN: large subepithelial deposits (humps). APIGN:
often no subepithelial deposits with varied findings (subendothelial,
mesangial). Our patient: NO glomeruli in EM material.
DISCUSSION



Glomerulonephritis and infection in our patient:
no definite infectious agent revealed
But “immunocompromised”: alcoholism
NASR. ET AL.: Acute Postinfectious Glomerulonephritis in the Modern Era. Medicine, 87:21-32,
2008
NASR. ET AL.: Acute Postinfectious Glomerulonephritis in the
Modern Era. Medicine, 87:21-32, 2008





‘In Western Europe, alcoholism had become the most
important risk factor for Acute Postinfectious
Glomerulonephritis’
Upper respiratory tract > skin > lung > endocarditis >
teeth
56% complete remission
4-17% requiring renal replacement therapy
‘Evidence supporting the use of steroid therapy for
postinfectious crescentic GN is largely anecdotal’