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Tubulointristitial Nephritis

Tubulointristitial Nephritis. A disorder of the interstitium and tubules. Acute Interstitial Nephritis. 70% Drug hypersensitivity 30% Antibiotics: PCNs (Methicillin), Cephalosporins, Cipro Sulfa drugs NSAIDs Allopurinol... 15% Infection Strep, Legionella, CMV, other bact/viruses

amela-velasquez
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Tubulointristitial Nephritis

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  1. Tubulointristitial Nephritis A disorder of the interstitium and tubules

  2. Acute Interstitial Nephritis 70% Drug hypersensitivity • 30% Antibiotics: PCNs (Methicillin), Cephalosporins, Cipro • Sulfa drugs • NSAIDs • Allopurinol... 15% Infection • Strep, Legionella, CMV, other bact/viruses 8% Idiopathic 6% Autoimmune Dz (Sarcoidosis, Tubulointerstitial nephritis/Uveitis)

  3. Drug Causes of AIN

  4. AIN from Drugs Renal damage is NOT dose-dependent May take weeks after initial exposure to drug • More common is seen several months to a year after use But as early as 1 week after medication is begun • Fever (27%) • Serum Eosinophilia (23%) • Maculopapular rash (15%) • Bland sediment or WBCs, RBCs, non-nephrotic proteinuria • WBC Casts are pathognomonic! • Urine eosinophils on Wright’s or Hansel’s Stain • Also see urine eos in RPGN, renal atheroemboli • Leukocytoclastic vasculitis

  5. Interstitial nephritis • Acute allergic IN- presents with fever, maculopapular rash, arthralgia, eosinophilia with use of certain drugs or systemic infection • UA_ microscopic hematuria, pyuria, non nephrotic proteinuria, eosinophiluria • Usually resolves after d/c of offending drug and steroids

  6. Clinical Presentation Drug-Induced AIN AIN of any cause • Rash 15% • Fever 27% • Eosinophilia 23% • Triad 10% Nausea Vomiting Malaise

  7. Laboratory Manifestions • Acute rise in plasma creatinine concentration • Eosinophilia and eosinophiluria • Urine sediment: wbcs, rbcs, white cell casts • Proteinuria (< 1 g/day) • Signs of tubulointerstitial damage

  8. Infectious Causes of AIN

  9. Acute bilateral pyelonephritis • Flank pain, toxic, febrile • U/A : pyoria, hematuria, proteinuria, bacteriuria • B/C & U/C help to diagnosis

  10. Infiltrative/Autoimmune Causes of AIN Sarcoidosis Sjogren’s Syndrome TINU Leukemia Lymphoma Systemic lupus erythematosus

  11. Acute Renal Failure

  12. Renal biopsy Indications Uncertainty of diagnosis Advanced renal failure Lack of spontaneous recovery following removal of offending drug

  13. Treatment Discontinuation of offending agent Corticosteroids • Prednisone 1 mg/kg to a max of 40-60 mg x 1-2 weeks • IV Methylprednisolone 0.5 – 1 g/day x 3 days

  14. AIN Management • Remove offending agent • Most patients recover full kidney function in 1 year • Poor prognostic factors • ARF > 3 weeks • Advanced age at onset

  15. Causes of chronic interstitial nephritis • Toxins( analgesic nephropathy, lead nephropathy) • Infection (chronic pyelonephritis) • Autoimmune( Sjogren syndrome, SLE, renal rejection) • Metabolic( hyperuricemia, hypercalcemia) • Radiation • Neoplastic infiltration( leukemia, lymphoma, multiple myeloma) • Hereditary renal diseases(ADPKD,MCD,MSK)

  16. Analgesic abuse nephropathy • chronic interstitial nephritis • Result from excessive consumption (Phenacetin & Aspirin) • Dose dependent (at least 1 kg) • Being responsible for 1% to 3% of ESRD cases

  17. The earliest lesion is thickening of GBM of vasa recta and capillary medulla then at later stage, focal area of necrosis in medulla and fibrosis and atrophy of tubules that leads to papillary necrosis and calcification. • Pathogenesis: phenacetin and its metabolites concentrate in the medulla where induce the generation of reactive metabolites • Aspirin potentiate the toxicity of phenacetin

  18. Bacterial infection • bacterial infection of the renal parenchyma causes interstitial nephritis • infection without anatomical abnormality seldom produces permanent damage • obstruction (stones, prostate etc) in combination with infection can cause progressive disease • tuberculosis causes extensive destruction from granulomata, fibrosis and caseation

  19. The upper and lower poles with compound papilla in ascending infection • At first, interstitial edema and PMN infiltration, then formation of irregular abscesses and eventually scars • Risk factors: diabetes mellitus obstruction delayed antimicrobial therapy severe infection with ATN reflux nephropathy papillary necrosis

  20. Consequences of urinary tract obstruction • Reduced glomerular filtration rate • Reduced renal blood flow (after initial rise) • Impaired renal concentrating ability • Impaired distal tubular function • Nephrogenic diabetes insipidus • Renal salt wasting • Renal tubular acidosis • Impaired potassium concentration • Reduced RBF leads to renal ischemia tubular atrophy

  21. baseline Hours Acute urinary tract obstruction Functional consequences

  22. myeloma • Bence-Jones protein (light chains from malignant plasma cell clone) causes interstitial nephritis, tubular obstruction(cast nephropathy) and amyloid deposition • Myeloma kidney :the classic pathologic include THP+LC casts in dilated, atrophic distal tubuls with infiltration monocyte & macrophage & plasma cells that produce giant cells • LCs are nephrotoxic through direct injury of tubular epithelial cells & intrarenal obstruction from cast formation

  23. Predisposing factors: LC concentration LC isoelectric point intraluminal PH tubular flow rate presence of Tamm-Horsfall Pr

  24. Hypercalcemic Nephropathy • Chronic hypercalcemia is seen in Hyperparathyroidism Sarcoidosis Multiple myeloma Vitamin D toxicity Metastasis bone disease

  25. Hypercalcemia decrease GFR through renal vasoconstriction • Calcium deposition in distal nephron and interstitial that leads to mononeuclear cell infiltration and tubular necrosis • Defective concentration ability, poliuria, nocturia • Nephrocalcinosis & nephrolitiasis

  26. WBC Casts Cells in the cast have nuclei (unlike RBC casts) Pathognomonic for Acute Interstitial Nephritis

  27. 1. hyaline casts 2. muddy brown casts 3. RBCs 4. RBC casts 5. Oval fat bodies 6. eosinophils A. ATN B. prerenal azotemia C. glomerulonephritis D. nephrolithiasis E. interstitial disease F. nephrotic syndrome Match:

  28. Question • 1. 65 year old with H/o HTN, ventricular arrythmias controlled on Amiodarone, OA on NSAIds presents with puffiness on face on waking up. Has bilateral pitting dema. UA 3+ prot, 3 RBC., 15-20 WBC • 24 h prot – 4 g/day • BUN/creat 80/5 • Serum albumin 2.8, TSH normal. The most likely diagnosis? • A) amiodarone induced hypothyroidism • B) RPGN • C) NSAIDs induced nephrotic sdr and interstitial nephritis

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