Interpretation of renal biopsy

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  • Hi Hanisha, thanx.. i mostly referred to Heptinstall for d materials n pics were collected from some journals and different books, but if want a thorough knowledge about basics of renal biopsy u can refer to sternberg or heptinstall
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  • Hi ,
    you made a very gud presentation , helped me a lot .
    can u pls tell me from where u collected the material.

    Dr Hanisha Jain
    P.G at People's college, Bhopal
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Interpretation of renal biopsy

  1. 1.  The kidney is a mysterious organ that makes urine  Has role in-  Excreting wastes  Regulating body fluids  Balancing soluble ions
  2. 2.  Kidneys-bean shape organs within peritoneum  Each organ weights 125 to 170 gm in males and 115 to 150 gr in females  The renal artery divides into anterior and posterior arteries which in turn give off segmental arteries  The main renal artery gives off-  Interlobar  Arcuate  Interlobular arteries  On the cut surface-cortex and medulla  medulla is divided to 18 pyramids  Each pyramid base is located at the corticomedullary junction
  3. 3.  Nephrons- • Functional and basic unit • Composed of glomeruli,bowman’s capsule, PCT, DCT & henle’s loop. • Glomeruli-cortex • Henle’s loop-medulla • Nephrons-1 million  Glomeruli- • Malphigi first described glomerulus • Glomerulus-glomerular tuft + bowman’s capsule • Glomerulus-vascular tuft lined by endothelium,supported by mesangium • 200 μm.  Proximal tubule- • 14mm long. • Cells are cuboid/short columnar,eosinophilic cytoplasm,granular,round nucleus in centre.with brush border • Reabsorption of majority glomerular ultrafiltrate.
  4. 4.  Henle’s loop- • Between proximal and distal tubules • U-shaped unit • Cells are flat, attenuated cytoplasm, no brush border  Distal tubule- • Connects to ascending henle’s loop • No brush border  Collecting duct- • Begins near end of DCT in cortex • Potassium secretion
  5. 5.  GLOMERULUS
  6. 6.  Iverson and Brun (1951)- first renal biopsy description
  7. 7.  Nephrotic syndrome: › Adult NS › Children with atypical features  Acute renal failure: › Undiagnosed › Non resolving clinical ATN >3-4 weeks  Systemic diseases with renal dysfunction  Sub-nephrotic proteinuria › >2g/d in DM, early MGN, FSGS, IgAN › <2g/d needs clinicians discretion  Hematuria › Isolated › Associated with proteinuria and abnormal urine sediment  Post transplant  CKD-  generally contraindicated  In moderate dysfunction-potential reversibility and basic disease  Diabetes Mellitus  Microscopic hematuria  Absence of retinopathy and neuropathy  Onset of proteinuria <5years from diagnosis  Acute worsening of renal function  Systemic features
  8. 8.  Renal biopsies taken by True-cut or biopsy gun under local anesthesia  performed in prone position for native kidneys and in supine position for transplanted kidneys  It is better to use 16 or 14 guage needle  optimum location for biopsy is juxtamedullary  Other renal biopsy techniques include transjugular retrograde approach by catheter, laparascopic techniques, and open laparatomic biopsy.
  9. 9. Procedure-  Informed consent  Patient in prone position with wedge or pillow below the abdomen  Light sedation  Local anesthesia with 1-2% lignocaine from the skin down to the capsule  Stab incision can be given to ease biopsy gun entry  Advance the biopsy gun, when the capsule is reached, instruct patient to take a deep breath and fire the gun  2-3 cores can be taken from the lower pole of the left kidney  Press on wound for 2-5 minutes
  10. 10. Post procedure-  Bed rest is instructed for 18-24 hours  BP and pulse are monitored in the following way-  Every 15 mins for 1 hour  Every 30 mins for 1 hour  Every hour for 4 hours  4 hourly for next remaining 24 hours  Save aliquots of each voided urine sample in clear specimen jars  Hct monitored 6-8 hours and 18-24 hours after biopsy Complications-  Hematoma  Hematuria  AV fistula
  11. 11. Fixatives-  For light microscopy, neutral buffered formaldehyde is used  suitable for immunohistochemical study and also molecular procedures  For electron microscopy, 2-3% glutaraldehyde fluid is suitable.  Immunofluorescence samples do not need any fixative and should be delivered and frozen in Michel`s media for frozen sections Specimen division-  >8mm - LM/IF/EM  4-8mm - EM/IF  <4mm - EM
  12. 12.  Adequacy of the sample: › two biopsy cylinders with a minimal length of 1 cm and a diameter of at least 1.2 mm. › 10–15 glomeruli are optimal; very often 6–10 glomeruli are sufficient › some cases even one glomerulus is enough Sectioning and staining- › After histologic processing and paraffin embedding, the tissues are sectioned by microtome › sections are prepared as thin as 3 μm or less for light microscopy. Thicker sections is needed in congo red and Immunohistochemistry staining. › Most helpful stains are-HE, PAS, Massons trichrome, JMS and congo red.
  13. 13. PAS TRICHROME SILVER Basement membrane red deep blue black Mesangial matrix red deep blue black Interstitial collagen ------ pale blue ------- Cell cytoplasm ------- rust/orange granular ------ Immune complex deposit -/+ bright red orange,homogenous ----- Fibrin weakly + Bright red orange,fibrillar ---- amyloid -------- Light blue orange ----
  14. 14. Light microscopy(LM) IHC-IF Electron Microscopy(EM)
  15. 15.  Glomeruli  Tubules  Interstitium  Vessels
  16. 16. A. Injury Localization: Glomerular/Vascular/Tubulointerstitial B. Category of Injury: Active Versus Fibrosing 1. Active lesions  a. Proliferation  b. Necrosis  c. Crescents  d. Edema  e. Active inflammation (eg, glomerulitis, tubulitis, vasculitis) 2. Fibrosing  a. Glomerulosclerosis  b. Fibrous crescents  c. Tubular atrophy  d. Interstitial fibrosis  e. Vascular sclerosis C. Types of Lesions  1. Determination of the nature and pathogenesis of lesions: examination by IF, EM and LM
  17. 17. GLOMERULI Focal/diffuse Global/segmental Number & size Cellularity Deposits Mesangium Fibrinoid necrosis & crescents TUBULOINTERSTITIUM Tubular atrophy/dilatation Necrosis Interstitial inflammation Interstiial fibrosis EM Additional features VESSELS Wall thickening Hyalinosis Fibrinoid necrosis Endothelitis
  18. 18.  Focal-Involving <50% of glomeruli  Diffuse-Involving 50% or more of glomeruli  Segmental-Involving part of a glomerular tuft  Global-Involving all of a glomerular tuft  Mesangial hypercellularity-4 or more nuclei in a peripheral mesangial segment  Endocapillary hypercellularity-Increased cellularity internal to the GBM composed of leukocytes, endothelial cells and/or mesangial cells  Extracapillary hypercellularity-Increased cellularity in Bowman’s space, i.e. > one layer of parietal or visceral epithelial cells, or monocytes/macrophages  Crescent-Extracapillary hypercellularity other than the epithelial hyperplasia of collapsing variant of FSGS  Fibrinoid necrosis-Lytic destruction of cells and matrix with deposition of acidophilic fibrin- rich material  Sclerosis-Increased collagenous extracellular matrix that is expanding the mesangium, obliterating capillary lumens or forming adhesions to Bowman’s capsule  Hyaline-Glassy acidophilic extracellular material  Membranoproliferative-Combined capillary wall thickening and endocapillary hypercellularity  Lobular -Consolidated expansion of segments that are demarcated by intervening urinary space  Mesangiolysis-lysis of mesangial matrix
  19. 19.  No abnormality by light microscopy: 1. No glomerular disease 2. Glomerular disease with no light microscopic changes (e.g. minimal change glomerulopathy, thin basement membrane nephropathy) 3. Mild or early glomerular disease (e.g. Class I lupus nephritis, IgA nephropathy, C1q nephropathy, Alport syndrome, etc.)
  20. 20.  Thick capillary walls without hypercellularity or mesangial expansion: 1. Membranous glomerulopathy (primary or secondary) (>Stage I) 2. Thrombotic microangiopathy with expanded subendothelial zone 3. Preeclampsia/eclampsia with endothelial swelling 3. Fibrillary glomerulonephritis with predominance of capillary wall deposits
  21. 21.  Thick walls with mesangial expansion but little or no hypercellularity: 1. Diabetic glomerulosclerosis with diffuse rather than nodular sclerosis 2. Secondary membranous glomerulopathy with mesangial immune deposits 3. Amyloidosis 4. Monoclonal immunoglobulin deposition disease 5. Fibrillary glomerulonephritis 6. Dense deposit disease (type II membranoproliferative glomerulonephritis)
  22. 22. Focal segmental glomerular sclerosis without hypercellularity: 1. Focal segmental glomerulosclerosis (primary or secondary) 2. Chronic sclerotic phase of a focal glomerulonephritis 3. Hereditary nephritis (Alport syndrome)
  23. 23. Mesangial or endocapillary hypercellularity: 1. Focal or diffuse mesangioproliferative glomerulonephritis* 2. Focal or diffuse (endocapillary) proliferative glomerulonephritis* 3. Acute (“exudative”) diffuse proliferative postinfectious glomerulonephritis 4. Membranoproliferative glomerulonephritis (type I, II or III)
  24. 24. Extracapillary hypercellularity: 1. ANCA crescentic glomerulonephritis (paucity of immunoglobulin by IFM) 2. Immune complex crescentic glomerulonephritis ((granular immunoglobulin by IFM) 3. Anti-GBM crescentic glomerulonephritis (linear immunoglobulin by IFM) 4. Collapsing variant of focal segmental glomerulosclerosis (including HIV nephropathy)
  25. 25. Membranoproliferative, lobular or nodular pattern: 1. Membranoproliferative glomerulonephritis (type I, II/DDD, or IIIB/IIIS) 2. Diabetic glomerulosclerosis with nodular mesangial expansion (KW nodules) 3. Monoclonal immunoglobulin deposition disease with nodular sclerosis 4. Idiopathic (smoking associated) nodular glomerulosclerosis 5. Thrombotic microangiopathy 6. Fibrillary glomerulonephritis 7. Immunotactoid glomerulopathy
  26. 26. Advanced diffuse global glomerular sclerosis 1. End stage glomerular disease 2. End stage vascular disease 3. End stage tubulointerstitial disease
  27. 27.  Directed at identification of pathogenic Ig and complement.  Abs used routinely-IgG, IgA, IgM, Kappa & lambda light chains, C3, C4, C1q, fibrinogen  Glomerular/extraglomerular location,intensity & pattern of staining  Glomerular staining catagorized as-mesangial, capilary wall or both  Capillary staining –granular,linear,band like Capillary granularmesangial both
  28. 28. Coarse granular granular Fine granular Band like coarsely granular
  29. 29. Linear cap wall Granular mesangial Granular cap wall Diffuse smudgy mes & cap wall •Anti GBM disease(IgG, C3) •Monoclonal Ig deposition disease(mostly kappa chain) •Diabetic nephropathy(IgG,albumin) •Dense deposit disease( ribbonlike,thick C3) •Rarely fibrillary GN (IgG) •IgA nephropathy •WHO Class II lupus( full house) •C1q nephropathy •IgM is idiopathic nephrotic syndrome •Other mesangioproliferative GN •Finely granular (membranous GN with/without SLE) •Coarsely granular (MPGN, WHO Class III, or IV lupus) •Scattered ,coarse granules (poststreptococcal GN) •Primary amyloidosis(usually λ) •Fibrillary GN(IgG) •Monoclonal Ig deposition disease
  30. 30.  Detailed evaluation of cellular & extracellular contents  Assesment of thickness,contour, & integrity of GBM & mesangial matrix  Fibrillary GN & immunotactoid GP can be diagnosed only on EM
  31. 31. Mesangial dense deposit(IgA) Mesangial & subendothelial dense deposit(lupus IV) SUBEPITHELIAL HUMP Subendothelial dense deposit
  32. 32.  Diseases primarily affecting the tubules are considered under the following headings  Acute tubular necrosis  Tubular casts  Chronic changes/tubular atrophy  Tubulitis  Tubular basement membrane changes
  33. 33.  Charaterised morphologically by destruction/severe injury of the renal tubular epithelium  2 major causes are-toxins & ischaemia  Evidence of ATN/injury are-  Degeneration & necrosis of individual tubular epithelial cells  Swelling of tubular epithelium(ballooning)  Detachment of tubular epithelium from underlying BM  Loss of PAS positive brush border of PCT  Thinning of tubular epithelium  Dilatation of tubular Lumina  Interstitial edema  Casts ( hyaline, pigmented, eosinophilic, cellular, granular debris)  Tubular lumen contains sloughed epithelial cells, leukocytes, cellular debris  Rupture of tubular BM
  34. 34.  Hyaline droplet change-small to large eosinophilic PAS positive droplets  Vacuolar change-  Hydropic change  Foam cells  Fatty change  Hypokalemic nephropathy  Pigmented tubular epithelium  Intranuclear inclusions
  35. 35. Hydropic change Fatty change
  36. 36. Inclusions in lead intoxication CMV inclusions
  37. 37.  Lymphocytes or other inflammatory cells on epithelial side of tubular BM infiltrating the tubular epithelium  Marker of active tubulointerstitial inflammation.
  38. 38.  Hyaline casts  WBC casts  Epithelial / granular casts  RBC casts  Large hyaline fractured casts  Myoglobin/hemoglobin casts
  39. 39.  Tubules are non functioning & it is no longer capable of regenerating and resuming function.  Accompanied by thickening of tubular BM  Tubular BM are thickned & wrinkled  3 types of atrophic tubules- 1. Classic atrophic tubules-thick wrinkled ocassional lamellated tubular BM ,simplified cuboidal non descript epithelium 2. Endocrine tubules-narrow/no tubular lumen. clear epithelial cells, thin/absent BM 3. Thyroidized tubules-round tubules, simplified epithelium, uniform intratubular casts that mimic thyroid 4. Super tubules-enlarged, dilated. either hypertrophic/hyperplastic
  40. 40. Thickened BM THYROIDIZATION
  41. 41.  No abnormality on LM-  No interstitial disease  Interstitial disease with no change  Early disease  Interstitial expansion by edema  ATN  Renal vein thrombosis  Nephrotic syndrome(MCD)  AGN (acute lupus,APSGN)  Thrombotic microangiopathy(HUS)  Interstitial expansion by eosinophilic material  Collagen-fibrosis  Sickle cell disease  Radiation nephritis  amyloid
  42. 42.  Interstitial expansion by leukocytes  Polymorphs(APSGN, drug induced, sepsis)  Lymphoplasmacytic(chr nephritsi, vasculitis, rejection)  Eosinophils (vasculitis, drug induced, lupus)  Epitheloid(TB, sarcoidosis, drug induced, malakoplakia)  Expansion by foam cells  Hereditary nephritis(alports syndrome)  Abundant,prolonged proteinuria or Nephrotic syndrome(membranous GN)  Interstitial hemorrhage  Acute rejection  Severe GN with rupture of bowmans capsule  Malignant HTN  Vasculitis
  43. 43.  Interstitial expansion by neoplastic cells-  Lymphoma  Leukemia  Primary renal ca  Metastasis  Crystals & mineral deposits  Nephrocalcinosis(ca carbonate)  ARF(ca oxalate)  Uric acid(gout)  Cholesterol(glomerular disease with nephrotic syndrome)
  44. 44. edema Int nephritis polymorphs granuloma DLBCL
  45. 45.  Vasculitis  Fibrinoid necrosis  Thrombosis  Pseudoaneurysm  Infarct  Endothelitis  Deposition of material-  Amyloid  Hyaline arteriolosclerosis  Toxins  Thrombotic microangiopathy  Peripheral hyalin  Hypertension induced changes  Medial hypertrophy  Intimal thickening  Replication of elastic lamina
  46. 46. THANK YOU

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