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43 renal pathology

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  • 1. TUBULOINTERSTITIAL DISEASES Terminology
    • Tubulointerstitial nephritis:
      • Primary - Inflammation limited to tubules & with uninvolved or minimally involved glomeruli/vessels .
        • Acute - Sudden onset & rapid decline in renal function associated with interstitial edema
        • Chronic - Protracted onset and slow decline in renal function associated with interstitial fibrosis
      • Secondary - Tubulointerstitial inflammation associated with primary glomerular/vascular diseases
      • Infectious – Tubulointerstitial inflammation associated with presence of live microorganism
      • Idiopathic – Tubulointerstitial nephritis where etiological agents or causes are not known
      • Reactive – Tubulointerstitial inflammation from the effects of systemic inflammation. Kidney is sterile.
  • 2. TUBULOINTERSTITIAL DISEASE Terminology ( cont.)
    • Urinary tract infection
      • colonization of excretory system by live microorganism
      • Pyelonephritis: tubulointerstitial nephritis with pelvis and calyceal involvement
        • Acute - usually suppurative inflammation involving pelvi-calyceal system and parenchyma
        • Chronic - involvement of pelvi-calyceal system and parenchyma with prominent scarring
  • 3. Tubulointerstitial nephritis Causes
    • Infections: (1) Reactive (2) Infectious
    • Drug reaction
    • Obstruction: (1) with infection: pyelonephritis / pyonephrosis (2) without infection : hydronephrosis
    • Non-obstructive : vesicoureteral reflux
    • Immune mediated : (1) with anti TBM antibodies, can be 1 0 or 2 0 (2) with IC deposition which can be 1 0 or 2 0
  • 4. Tubulointerstitial nephritis Pathogenetic mechanisms
    • Antibody mediated
      • Anti-TBM-antibody disease
      • Immune-complex disease
    • T-cell mediated
    • Associated with infections
      • Reactive
      • Infectious
  • 5. Tubuluinterstitial nephritis
    • Primary anti-TBM-antibody nephritis
      • IgG antibodies directed against tubular basement membrane
      • Linear staining on immunofluorescence microscopy
      • Edema and mononuclear cells in interstitium
      • Glomeruli and blood vessels are unremarkable
    • Secondary anti-TBM-antibody disease
      • 2 0 to 1 0 glomerulonephritidies, allograft nephropathy
  • 6. Tubulointerstitial nephritis with immune complexes
    • Primary immune complex disease
      • granular staining on IF microscopy on tubular basement membrane
      • Primary – Rare
      • Secondary – Usually associated with primary glomerulonephritidies involving TBM and interstitium
        • e.g SLE, MPGN, Membranous GN etc.
  • 7. Cell-mediated mechanism
    • Delayed-type hypersensitivity reaction
      • Activated CD4+ T and monocyte / macrophage cells releases cytokines which modulates inflammatory reactions and fibrogenesis
      • Cytotoxic T-cell injury in which CD4+ T and CD8+ T play important role
  • 8. Pathology of primary IN
    • bilaterally symmetrical enlargement of kidney
    • edema
    • inflammatory cells in interstitium
    • tubular change including tubulitis, breaks in TBM, necrosis of tubular epithelial cells etc.
  • 9. Pathology of renal failure acute chronic
  • 10. Acute renal failure (ARF)
    • Rapid deterioration of renal function in a relatively short period of time
    • Sudden inability to maintain normal fluid and electrolyte homeostasis
    • Marked decrease in renal output
    • May be of glomerular, tubular, interstitial or vascular origin
  • 11. Causes of ARF
    • acute tubular necrosis
    • infarction & cortical necrosis
    • organic diseases of renal vessels
    • severe forms of glomerulonephritis
    • severe infection
    • acute tubulointerstitial nephritis
    • outflow obstruction (post-renal)
    • impairment of blood flow (pre-renal)
  • 12. Acute tubular necrosis (ATN)
    • commonest cause of acute renal failure
    • develops due to :
      • direct poisoning of tubules (nephrotoxic lesions)
      • renal ischemia (tubulorrhexic lesions)
  • 13. Acute tubular necrosis Etiology & Pathogenesis
    • Ischemic in origin (Tubulorrhexic lesion)
    • Prolonged ischemia due to:
    • Shock: postoperative, intra-operative, post-traumatic, septic, hypotensive
    • Hemorrhage: postpartum hemorrhage, abruptio placentae
    • Other: severe burns, transfusion accidents, dehydration, heat stroke, crushing injuries, non-traumatic rhabdomyolysis, paroxysmal hemoglobinuria etc.
  • 14. Acute tubular necrosis Etiology and Pathogenesis
    • Direct effects of toxins (Nephrotoxic lesion)
    • Therapeutic agents :
      • Antibiotics : Aminoglycosides, NSAIDs,
    • chemotherapeutic agents, etc.
      • Heavy metals: mercury, lead, gold etc.
      • Radiocontrast agents
      • Multiple bee stings, scorpion bites etc.
  • 15. Gross pathology
    • bilaterally enlarged & swollen kidney due to edema
    • Cut surface bulges and has a flabby consistency
    • widened & pale cortex
    • dark & congested medulla
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  • 18. Light microscopy
    • dilated lumen with flattened epithelial cells
    • Greatest change in proximal tubules, varies in two forms
    • loss of brush borders- proximal tubules
    • evidence of regeneration of epithelial cells
    • hyaline, granular and pigmented casts
    • interstitial edema & inflammation
    • Intra-vascular collection of nucleated red blood cells
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  • 20. ATN- Prognosis
    • depends upon underlying cause, over all mortality rate  50%
    • post-traumatic (62%), post-operative (56%), medical (46 %), obstetric (17 %)
    • Higher in older debilitated pts. & in pts.with multiple organ disease
    • good for uncomplicated and younger patients
  • 21. Chronic renal failure
    • Occurs in all cases of end-stage renal disease of whatever etiology
    • GFR falls below 20% of normal
    • End result of all chronic renal disease which can be glomerular, tubulointerstitial or vascular in origin
    • Characterized by prolonged signs and symptoms of uremia
    • Is a major cause of death in renal disease
  • 22. Chronic renal failure
    • Systemic (visceral) manifestations
      • Enlarged heart & pericarditis
      • Uremic pneumonitis & pleuritis
      • Uremic colitis
      • Uremic encephalopathy
      • Hypoplastic anemia
  • 23. TUBULO-INTERSTITIAL DISEASE
    • Urinary tract infection
      • colonization of excretory system by live microorganism
      • Most caused by gram negative enteric organism
      • Most common form of renal involvement is:
        • Pyelonephritis: bacterial infection of the kidney that affects parenchyma, calyces and pelvis
          • Acute - usually suppurative inflammation involving
            • pelvi-calyceal system and parenchyma
          • Chronic - involvement pelvi-calyceal system and parenchyma with prominent scarring
  • 24. Pyelonephritis
      • Acute : usually suppurative, often associated
      • (1) with / without obstruction
      • (2) ascending infection through vesicoureteral reflux (3) from hematogenous dissemination.
      • Chronic : inflammation with prominent scarring; may be
      • (1) obstructive with recurrent infection
      • (2) non-obstructive with vesicoureteral reflux -> reflux nephropathy
  • 25. Acute Pyelonephritis Predisposing factors
    • Urinary obstruction: congenital or acquired
    • Instrumentation of urinary tract
    • Vesicoureteral reflux
    • Pregnancy: 4-6% develops bacteriuria
    • Gender and age
    • Preexisting renal lesions
    • Diabetes mellitus, immunosuppression & immunodeficiency
  • 26. Acute pyelonephritis
    • route of invasion :
      • via blood stream
      • ascending route
    • obstructive
    • non-obstructive
    • role of vesicoureteral reflux and infected urine
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  • 32. Chronic pyelonephritis
      • It is a chronic tubulointerstitial inflammation involving renal parenchyma, pelvis and calyces associated with scarring
      • non-obstructive
        • reflux nephropathy
      • obstructive
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