43 renal pathology

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43 renal pathology

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

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