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15 Cards in this Set
- Front
- Back
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1. What is primary TIN?
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a. Disease where dominant pathogenic process begins in the interstitial compartment
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2. What is secondary TIN?
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a. Primary process begins in the vascular, glomerular, or collecting ystem
b. Followed by damage to the interstitium |
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3. What is the pathological hallmark of TIN?
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a. Inflammatory cell infiltrate→ T-lymphocytes
b. Diffuse/patchy lesions |
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4. What usually induces TIN?
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a. Chronic abx/analgesic abuse
b. Dose and exposure duration dependent c. NSAIDs!!! |
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5. What are the common clinical findings in TIN?
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a. Sterile pyuria and WBC casts
b. No proteinuria/hypoalbuminemia c. Polyuria and nocturia d. **Fever, rash eosinophilia** |
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6. What is the term of onset of TIN?
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a. Abrupt onset of renal dysfunction
b. Progressive rise in creatinine |
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7. How can drugs affect the onset of TIN?
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a. Classic TIN occurs 10-20 days after onset of drug tx
b. May be abrupt c. May be de novo in response to previously tolerate drug |
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8. How will TIN induced by NSAIDs present?
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a. >3/5g/d proteinuria
b. Concomitant glomerular injury |
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9. What is the gold standard for dx of TIN?
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a. Renal biopsy
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10. What are the dx tools for dx of TIN?
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a. Renal biopsy
b. Slow rise in Cr compared to ARF c. UA d. Eosinophilia/eosinophiluria e. US |
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11. What will a UA show in TIN?
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a. Sterile
b. Leukocyte c. WBC casts |
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12. What will a US show in TIN?
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a. Enlarged with increased cortical echogenicity
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13. How do you tx TIN?
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a. Corticosteroid tx-- prednisone or slumedrol should be started within 7-14 days of azotemia
b. Cyclophosphamide if steroids fail |
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14. What is the prognosis of TIN?
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a. Severity of interstitial fibrosis is most important prognostic factor
b. If detected early, drug is removed and prognosis is favorable c. ARF>3 weeks=poor prognosis d. **Final GFR correlates with degree of early improvement-- inverse to age of onset** |
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15. What are the phases of recovery in TIN?
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a. Initial rapid improvement
b. Slow improvement over next year c. The faster you improve, the better the prognosis |
