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Intersitial nephritis (Chronic interstitial nephritis (chronic tubulo…

- - - - Aminoacyduria, glykozuria, urykozuria, phosphaturia
        
        Defect in urine concentration
        
        Markers of tubular damage - RBP (retinol binding protein), Alfa-1 microglobulin, Beta-2 microglobulin, NAG (N-acethylglucosaminidase)
        
        Increased and early anaemia symptoms
  - - - aim – preventing the renal scaring and subsequent renal failure
        
        Continuous antimicrobial therapy
        
        Surgical repair (antireflux surgery). The surgery should be performed as soon as possible since the critical time for the formation of scars in children is infancy and early childchood. IV and V grades of reflux should be treated with surgery.
- - - - the immunologically induced hypersensitivity reaction to an antigen that is classically a drug.
        
        The extrarenal antigens induce AIN by different mechanism:
        •Binding to kidney structures
        •Acting as haptens that modify the immunogenicity of native renal proteins
        •Mimicking renal antigens
        
        MECHANISM: Antibody-mediated or cell-mediated immune mechanism
    - - Antimicrobial agents: eg. penicilin G, ampicillin, ciprofloxacin, co-trimoxazole, sulfonamides
        
        NSAIDs: aspirin, fenoprofen, ibuprofen, piroxicam, naproxen, indomethacin
        
        Anticonvulsant: phenytoin, Analgetics: clometacin
        
        Diuretics: furosemide, hydrochlorothiazide
        
        Others: allopurinol, cimetidine, captopril, fenofibrate
    - - renal symptoms
        
        The beginning of symptoms typically within 3 weeks after initiation therapy
        
        Flank pain reflecting distension of the renal capsule
        
        Hematuria (no red blood cells cast usually)
        
        Pyuria (leukocyte cast often), Mild proteinuria
        
        Kidney: normal size or slightly enlarged
        
        Sudden impairment of renal function (mild to severe)
        
        Oliguria
      - extrarenal symptoms
        
        Clinical signs of hypersensitivity reaction: (presnet in ~ 40-50%)
        low-grade fever, maculopapularrash, mild arthalgias, eosinophilia and eosinophiluria
        
        Other symptoms: fatique, nausea, vomitus
      - specific drug associations
        
        NSAID: nephrotic syndrome, days or a few months after drug initiation, extrarenal symptoms rarely
        
        Allopurinol: AIN occurs often in patients with kidney dysfunction, rash, liver dysfunction
        
        Methicillin: abnormal urinalysis and extrarenal symptoms often present
        
        Rifampicin: gastrointerstitial symptoms, myalgia, hepatitis, hemolysis, thrombocytopenia
        
        Hemolitic anaemia (rifampicin, allopurinol, penicilin)
    - - The halmark of AIN is the presence of patchy inflammatory infiltrates within interstitium: (deep cortex outer medulla predominantly). They are comprised mostly of T cells (CD4 subset) and monocytes/macrophages.
        
        Interstitial edema is present, which is responsilbe for separating the tubules.
        
        Interstitial non-necrotic granulomas (sometimes)
        
        Focal tubular lessions (sometimes)
        
        Glomeruli appear normal (sometimes)
        
        Imunofluorescence and electron microscopy are negative (no immune deposits)
    - - The renal biopsy: the most acurate way to diagnose
        
        Eosinophiluria (>1% of WBC in urine) ~ 40-91% sensivity; ~72-85% specificity
        
        An increased renal uptake of gallium (67Ga) -
    - - Hematuria, leucocyturia, proteinuria usually disappear within 2 weeks
        
        Complete recovery of renal function (observed in 60-90% of patients) is delayed (average 1.5 months)
        
        Minority may be left with intersitial fibrosis and progressive chronic interstitial nephritis
      - Poor prognosis factors:
        renal failure lasting more than 2 weeks
        diffuse macrophage-rich infiltrates or granolomas in interstitium
    - - Identification and stoping the inciting agent
        
        The treatment of acute renal failure
        
        Corticosteroids (prednison 1mg/kg) – 1 month
        patients with AIN confirmed by renal biopsy
        patients whose renal function fails to improve within 1 week after stoping the inciting agent
        patients whose renal biopsy shows poor prognosis