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 functionassociated with interstitial edema
      • Chronic -Protracted onset and slow decline in renalfunction associated with interstitial fibrosis
    • Secondary-Tubulointerstitial inflammation associatedwith primary glomerular/vascular diseases
    • InfectiousTubulointerstitial inflammation associated withpresence of live microorganism
    • IdiopathicTubulointerstitial nephritis where etiological agents orcauses are not known
    • ReactiveTubulointerstitial inflammation from the effects ofsystemic inflammation. Kidney is sterile.

2. TUBULOINTERSTITIAL DISEASE Terminology ( cont.)

  • Urinary tract infection
    • colonization of excretory system by live microorganism
    • Pyelonephritis: tubulointerstitial nephritiswith pelvis and calyceal involvement
      • Acute- usually suppurative inflammation involvingpelvi-calyceal system and parenchyma
      • Chronic- involvement ofpelvi-calyceal systemand 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 0or 2 0 (2) with IC deposition which can be 1 0or 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 0to 1 0glomerulonephritidies, 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: postpartumhemorrhage, abruptio placentae
  • Other:severe burns, transfusion accidents, dehydration, heatstroke, crushing injuries,non-traumaticrhabdomyolysis, 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

16. 17. 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

19. 20. ATN- Prognosis

  • depends upon underlying cause, over all mortality rate50%
  • 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 kidneythat affects parenchyma, calyces and pelvis
        • Acute- usually suppurative inflammation involving
          • pelvi-calyceal system and parenchyma
        • Chronic- involvement pelvi-calyceal system andparenchyma 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 Predisposi

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