TOPIC 9: acute tubulo-interstitial nephritis Flashcards
1
Q
What is acute tubulo-int nephritis?
epidemiology
A
- Divided into two main entities:
1. Acute tubular necrosis (AKN)
2. Acute interstitial nephritis (AIN)
2
Q
Acute interstitial nephritis (AIN)
A
- Parenchymal cause of AKI
- peak incidence in middle age but can affect all ages, men and women equally
- 70-90% drug induced
- characterised by inflammatory infiltrate in renal interstitium
- occasionally associated with systemic delayed type hypersensitivity reaction (fever, arthiritis, rash)
3
Q
common causes of AIN
A
- Drugs (75-90%)
- NSAIDS
- Penicillin, cephalosporins, rifampin, sulfonamides
- PPI
- diuretics
- allopurinol
- antiretrovirals
2.Infections:
-TB
-Legionella
-Leptospirosis
(TLL)
3.Autoimmune disease:
-sarcoidosis
-sjogren syndrome
-TIN with uveitis
(SST)
4
Q
Clinical presentations of AIN
A
- often asymptomatic until AKI
- includes classical symptoms of AKI (hematuria, pyuria, mild proteinuria) –> “HPM”
- extrarenal symptoms: fever, arthralgia, rash–> “FAR”
- FLANK PAIN IS UNCOMMON
- systemic symp if eg sarcoidosis
–> all these may occur 3-21 days after drug or can be delayed up to 18months after
5
Q
Investigations In AIN
A
- urine-analysis (proteinuria, eosinophilia, white cell casts)
- urea and electrolytes (increased Ca+ in sarcoidosis)
- FBC (eosinophilia)
- Increased ESR
- ANA, anti-Ro and anti-La( sjogren sy)
- US shows normal kidneys
- CXR (sarcoidosis)
- RENAL BIOPSY NEEDED FOR DIAGNOSIS
6
Q
Histology of AIN
A
- Intense interstitial inflammatory infiltrate (lymphocytes, monocytes, eosinophils)
- giant cells and granuloma
- interstitial fibrosis imparts worse prognosis
- NORMAL GLOMERULI
7
Q
Management of AIN
A
- Infection–> antibiotics
- drug induced–> discontinue
- autoimmune–> corticosteroids
8
Q
Prognosis of AIN
A
- 40% pts with drug related will be left with CKD
- 10% progress to ESRD
- of those with milder disease, they will return to baseline renal function
- mortality rate <5%
