Review Note

Last Update: 12/01/2024 12:06 AM

Current Deck: State Exam::Nephrology

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Acute abacterial interstitial nephritis – etiology, pathogenesis, clinical picture, diagnosis, and treatment. 
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    • Acute Tubulointerstitial Nephritis (ATIN)

      Definition:
      • Kidney lesion involving interstitial inflammatory infiltrate and edema, resulting in decreased renal function.
      • Typically develops over days to months.
      • A frequent cause of acute kidney injury (AKI) that may lead to chronic kidney disease (CKD).
      Causes:
      1. Drugs (~70–75%):
        • NSAIDs, certain antibiotics (e.g., beta-lactams, sulfonamides, fluoroquinolones), PPIs, diuretics, allopurinol, quinolones.
      2. Infections (~4–10%):
        • Examples: Streptococci, MTB, Legionella, CMV, EBV, adenovirus.
      3. Autoimmune/Systemic Diseases (~10–20%):
        • Examples: SLE, sarcoidosis, Sjögren’s syndrome.
      4. Tubulointerstitial Nephritis and Uveitis (TINU) Syndrome (<5%).
      Clinical Features:
      1. Many patients are asymptomatic.
      2. Some present with non-specific symptoms of AKI:
        • Nausea, vomiting, malaise.
      3. Other findings:
        • Polyuria and nocturia (due to impaired urinary concentration and sodium reabsorption).
        • Constitutional symptoms: Malaise, anorexia, arthralgias.
        • Hypersensitivity manifestations: Low-grade fever, rash, eosinophilia.
        • Urinary findings: Leukocyturia, microhematuria, non-nephrotic proteinuria.
      4. Suspect ATIN in patients with:
        • Elevated serum creatinine.
        • Presence of leukocyturia and systemic or hypersensitivity symptoms.
      Diagnosis:
      1. Lab Findings:
        • Blood:
          • Increased serum creatinine.
          • Decreased GFR.
          • Eosinophilia (possible in drug-induced cases).
        • Urinalysis:
          • Microhematuria, non-nephrotic proteinuria.
          • Characteristic urine sediment:
            • RBC, WBC, and WBC casts.
            • Eosinophiluria may be seen in drug-induced cases.
          • Sterile pyuria (absence of bacteria on culture).
      2. Imaging:
        • No diagnostic imaging findings; used to exclude other causes.
      3. Renal Biopsy:
        • Not always necessary (e.g., if AKI occurs after drug initiation).
        • Findings:
          • Interstitial edema with inflammatory infiltrate (mainly T-cells).
      4. Additional Tests:
        • Assess CBC, BUN, creatinine, and liver function tests (for drug-induced liver injury).
        • Serologic tests for associated diseases:
          • Anti-SSA/SSB for Sjögren’s syndrome.
          • Antinuclear antibody for SLE.
          • Serum IgG4 for IgG4-related disease.


    • Therapy:
      1. Drug-Induced:
        • Stop the offending agent immediately.
        • Severe cases of AKI requiring dialysis:
          • Perform kidney biopsy.
          • Initiate glucocorticoid (GC) therapy and dialysis:
            • IV Methylprednisolone: 500–1000 mg daily for 3 days.
            • Follow with oral Prednisolone: 1 mg/kg daily for 2–3 weeks.
        • Mild cases without the need for dialysis:
          • Observe the patient for 3–7 days after stopping the offending agent.
          • If kidney function has not stabilized:
            • Perform kidney biopsy.
            • Start GC therapy:
              • Oral Prednisolone: 1 mg/kg daily for 2–3 weeks.
        • NSAID-induced AIN generally responds poorly to GC therapy.

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