Lab diag nephrotic synd 2003

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nephrotic syndrome is characterized by hypoalbuminemia, proteinuria, edema & hyperlipidemia. It is frequently found in children but also not uncommon in adults

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  • The ability to recognize the BM as being rather uniform in thickness and density is so critically important
  • Lab diag nephrotic synd 2003

    1. 1. LAB DIAGNOSIS OF NEPHROTIC SYNDROME MODERATOR : DR SANJEEV NARANG SPEAKER : DR RAVI JAIN
    2. 2. NEPHROTIC SYNDROME <ul><li>DEFINITION : the nephrotic syndrome is a clinical complex characterized by a no of renal & extra renal features, the most prominent of which are </li></ul><ul><li>Proteinuria of > 3.5 g/1.73 m 2 /24 hr </li></ul><ul><li>Hypoalbuminemia </li></ul><ul><li>Edema </li></ul><ul><li>Hyperlipidemia </li></ul><ul><li>Lipiduria </li></ul><ul><li>Hypercoaguability </li></ul>
    3. 5. Table 2 CAUSES OF THE NEPHROTIC SYNDROME
    4. 7. NEPHROTIC SYNDROME <ul><li>PATHOGENESIS: </li></ul><ul><li>Derangement in glomerular capillary walls </li></ul><ul><li>Increased permeability to plasma proteins </li></ul><ul><li>Massive proteinuria + increased renal catabolism of albumin </li></ul><ul><li>Depletion of serum albumin & reversal of A:G ratio </li></ul><ul><li>Generalized edema abnormal transport of lipids + decreased catabolism </li></ul><ul><li>Hyperlipidemia </li></ul>
    5. 8. HEAVY PROTEINURIA Figure 3.
    6. 9. Figure 4.
    7. 10. NEPHROTIC SYNDROME <ul><li>CLINICAL FEATURES: </li></ul><ul><li>Massive proteinuria </li></ul><ul><li>Hypoalbuminemia </li></ul><ul><li>Generalized edema </li></ul><ul><li>Hyperlipidemia & lipiduria </li></ul>
    8. 11. Figure 1. Nephrotic edema.
    9. 12. Figure 2. Nephrotic edema.
    10. 13. LAB DIAGNOSIS OF NEPHROTIC SYNDROME <ul><li>Specimen </li></ul><ul><li>Urine </li></ul><ul><li>Serum </li></ul><ul><li>Renal biopsy </li></ul>
    11. 14. LAB DIAGNOSIS OF NEPHROTIC SYNDROME <ul><li>Urine : </li></ul><ul><li>Protein estimation </li></ul><ul><li>Semi quantitative </li></ul><ul><li>Quantitative – 24 hr protein estimation </li></ul>
    12. 15. Protein determination in urine <ul><li>-    Normal kidney only small amount of low molecular weight </li></ul><ul><li>protein filtered most of which reabsorbed by tubule. </li></ul><ul><li>-    Normal protein excretion <150 mg/day in adult. </li></ul><ul><li>-    Daily physiological protein contain :- </li></ul><ul><li>(i) Mucoprotein (Tamm Horsfall glycoprotein 70 mg) </li></ul><ul><li>(ii) Blood group related antigen 35 mg </li></ul><ul><li>(iii) Albumin 15 mg </li></ul><ul><li>(iv) Mucopolysaccharide 15 mg </li></ul><ul><li>(v) Immunoglobulin 5 mg </li></ul><ul><li>-     Abnormal amount of protein in urine – Proteinuria </li></ul>
    13. 16. PATHOPHYSIOLOGICAL CLASSIFICATION OF PROTEINURIA <ul><li>Physiological Proteinuria        </li></ul><ul><li>  Glomerular proteinuria </li></ul><ul><li>Tubular proteniuria </li></ul><ul><li>  Overflow Proteinuria </li></ul><ul><li>  Other types </li></ul><ul><li>(i) Benign orthostatic proteinuria </li></ul><ul><li>(ii) Transient proteinuria </li></ul><ul><li>(iii) Microalbuminuria </li></ul><ul><li>(iv) Bence jones Proteinuria </li></ul>
    14. 17. Difference between glomerular and Tubular proteinuria Glomerular Tubular Due to injury of Renal glomerulus Due to Injury Involving Tubulointerstitial region Comprises predominantly albumin Comprises low molecular wt protein (  2 microglobilin Protein excretion >3 – 3.5 gm/dl < 2 gm/dl. Urinary protein electrophoresis More albumin than globulin More globulin Albumin  micro globulin ratio > 1000 : 1 100:1 (N – 50-200:1) Cause -   G lomerulonephritis -          - Hypertension - Lipoid Nephrosis -    -   Pyelonephritis -    -   Interstitial Nephritis - Rejection of kidney allograft
    15. 18. Qualitative tests for protein <ul><li>Reagent strip method </li></ul><ul><li>Precipitation method </li></ul><ul><li>(a) Heat and acetic acid test </li></ul><ul><li>(b) Sulphosalicylic acid test </li></ul><ul><li>(c) Heller’s nitric acid test </li></ul>
    16. 19. Precipitation method Urine Protein: SSA
    17. 20. Chemical Tests on Urine: (Reagent Strip/Dipstick Analysis): Procedure
    18. 21. Reagent strip method <ul><li>Dipstick more sensitive to albumin than globulin, mucoproteins, Bence-Jones protein </li></ul><ul><li>Protein 1+ (30 mg/dl) significant in any urine </li></ul><ul><li>- Trace may be important if sp.gr. <1.010 </li></ul><ul><li>False Positives: </li></ul><ul><li>- Chlorhexidine, quartenary ammonium antispetic or detergent residual left in container </li></ul><ul><li>- Vaginal secretions </li></ul><ul><li>- Highly buffered urine with pH >6.5 </li></ul>
    19. 22. Chemical Examination – Dipstick Analysis Colour Chart
    20. 23. PROTEIN - URINE <ul><li>Semi quantitaive norms </li></ul><ul><li>Normal : < 20 mg % </li></ul><ul><li>Reagent strip/ stick </li></ul><ul><li>Negative : 0 – 5 mg/dl </li></ul><ul><li>Trace : 5 – 20 mg/dl </li></ul><ul><li>1+ : 30 mg/dl </li></ul><ul><li>2+ : 100 mg/dl </li></ul><ul><li>3+ : 300 mg/dl </li></ul><ul><li>4+ : 1000 mg/dl </li></ul>
    21. 24. PROTEIN - URINE <ul><li>False +ve in semiquantitative test </li></ul><ul><li>Incorrect matching of reagent strip to the color chart </li></ul><ul><li>Prolonged exposure of the strip or stick to the urine </li></ul><ul><li>Hematuria </li></ul><ul><li>Drugs </li></ul><ul><li>Acetazolamide </li></ul><ul><li>Amino salicylic acid </li></ul><ul><li>Chlorpromazine </li></ul><ul><li>Penicillin </li></ul>
    22. 25. PROTEIN - URINE <ul><li>False -ve in semiquantitative test </li></ul><ul><li>Very dilute urine </li></ul><ul><li>Highly buffered alkaline urine </li></ul><ul><li>Urine high in sodium </li></ul><ul><li>Urea splitting organisms </li></ul>
    23. 26. 24 hour protein estimation <ul><li>This test is indicated when a random urine sample is positive for more than a trace of protein. </li></ul><ul><li>Protein substances are excreted at different rates & at varying times in a 24 hr period </li></ul><ul><li>24 hr protein estimation provides the most accurate reflection of kidney function </li></ul>
    24. 27. 24 HOUR PROTEIN ESTIMATION <ul><li>Early morning is the preferred time for 24 hr urine collection </li></ul><ul><li>Discard the first morning urine specimen </li></ul><ul><li>Save all the urine voided for 24 hr in a clean refrigerated container </li></ul><ul><li>Include the urine voided at the end of the 24 hour period </li></ul>
    25. 28. 24 HOUR PROTEIN ESTIMATION <ul><li>Quantitative norms : </li></ul><ul><li>Adults : 30 – 150 mg/ 24 hrs </li></ul><ul><li>Children < 10 years : < 100 mg/ 24 hrs </li></ul><ul><li>New born : increased protein in urine for 3 days after delivery </li></ul>
    26. 29. 24 HOUR PROTEIN ESTIMATION <ul><li>False +ve quantitative test : </li></ul><ul><li>Drugs </li></ul><ul><li>Acetazolamide </li></ul><ul><li>Amino salicylic acid </li></ul><ul><li>Aspirin </li></ul><ul><li>Barbiturates </li></ul><ul><li>Cephalosporins </li></ul><ul><li>Penicillin </li></ul>
    27. 30. 24 HOUR PROTEIN ESTIMATION <ul><li>False -ve quantitative test : </li></ul><ul><li>Urine accidently discarded during 24 hr collection </li></ul><ul><li>Urine lost during defecation </li></ul>
    28. 31. PROTEIN ELECTROPHORESIS - URINE <ul><li>Principle -The term electrophoresis describes the migration of a charged particle under the influence of an electric field. Many important biologic molecules, such as amino acids, peptides, proteins, nucleotides and nucleic acids, possess ionizable groups and, therefore, at any given pH, in solution as electrically charged species either as cations(+) or anions(-) </li></ul><ul><li>Under the influence of an electric field these charged particles will migrate either to the cathode or to the anode, depending on the nature of their net charge. </li></ul>
    29. 32. PROTEIN ELECTROPHORESIS - URINE <ul><li>Normal urine electrophoretograms show individual variance & show a globulin pattern that is generally diffuse . </li></ul><ul><li>The dominant protein is albumin. </li></ul><ul><li>Normally there is only a trace amt of ά 1 globulin & ά 2 globulin . </li></ul><ul><li>β & γ globulins are negligible to absent. </li></ul><ul><li>Albumin : 37.9 % </li></ul><ul><li>ά 1 globulin : 27.3 % </li></ul><ul><li>ά 2 globulin : 19.5 % </li></ul><ul><li>β globulin : 8.8 % </li></ul><ul><li>γ globulin : 3.3 % </li></ul>
    30. 33. PROTEIN ELECTROPHORESIS - URINE <ul><li>INTERPRETATION: </li></ul><ul><li>Proteinuria associated with increased glomerular permeability exhibits an electrophoretic pattern that is dominated by albumin, with moderate β globulin , some ά globulin & trace γ globulin </li></ul>
    31. 34. PROTEIN ELECTROPHORESIS - URINE <ul><li>Factors that affect result: </li></ul><ul><li>Contamination of the specimen with the stool invalidates the test. </li></ul><ul><li>Drugs </li></ul><ul><li>Amikacin </li></ul><ul><li>Amphotericin B </li></ul><ul><li>Penicillin </li></ul><ul><li>Phenylbutazone </li></ul>
    32. 35. PROTEIN - SERUM <ul><li>NAME OF METHOD – BIURET METHOD </li></ul><ul><li>PRINCIPLE – Protein reacts with cupric ions in alkaline medium to form violet colored complex .The intensity of color produced is directly proportional to protein present in specimen which can be measured on a photometer at 530 nm. </li></ul>
    33. 36. PROTEIN - SERUM <ul><li>Normal values : </li></ul><ul><li>Adults : 6.0 – 8.0 g/dl </li></ul><ul><li>Children : 4.3 – 7.6 g/dl </li></ul><ul><li>Premature : 4.6 – 7.4 g/dl </li></ul><ul><li>Newborn : 6.0 – 6.7 g/dl </li></ul><ul><li>Infant : 6.2 – 8.0 g/dl </li></ul>
    34. 37. PROTEIN - SERUM <ul><li>Factors that affect result: </li></ul><ul><li>Hemolysed or lipemic specimen </li></ul><ul><li>Falsely elevated value occur upto 48 hr after use of sulfo- bromopthalein contrast dye </li></ul><ul><li>Recent dialysis </li></ul><ul><li>Hyperglycemia </li></ul><ul><li>Bed ridden patients – lower values </li></ul>
    35. 38. PROTEIN ELECTROPHORESIS - SERUM <ul><li>Norms : </li></ul><ul><li>Total protein : 100 % </li></ul><ul><li>Albumin : 58 – 74 % </li></ul><ul><li>ά 1 globulin : 2.0 – 3.5 % </li></ul><ul><li>ά 2 globulin : 5.4 – 10.6 % </li></ul><ul><li>β globulin : 7.0 – 14.0 % </li></ul><ul><li>γ globulin : 8.0 – 18.0 % </li></ul>
    36. 39. PROTEIN ELECTROPHORESIS - SERUM in NEPHROTIC SYNDROME <ul><li>Increased ά globulin zone intensity ( ά 2 globulin ) </li></ul><ul><li>Increased ά 2 - β 1 globulin interzone intensity </li></ul><ul><li>Increased β globulin zone intensity </li></ul><ul><li>Decreased albumin zone intensity </li></ul><ul><li>Decreased γ globulin zone intensity </li></ul>
    37. 40. LIPID PROFILE TESTS for HYPERLIPIDEMIA <ul><li>TOTAL LIPIDS </li></ul><ul><li>SERUM TOTAL CHOLESTEROL </li></ul><ul><li>SERUM H.D.L – C </li></ul><ul><li>TC / H.D.L – C </li></ul><ul><li>SERUM TRIGLYCERIDES </li></ul><ul><li>SERUM PHOSPHOLIPIDS </li></ul>
    38. 41. CHOLESTEROL – ENZYMATIC METHOD <ul><li>PRINCIPLE : These measure total cholesterol directly in plasma/serum through a series of reaction in which cholesterol esters are hydrolyzed , the 3- OH group of cholesterol is oxidized & H2O2 is liberated which is measured . </li></ul>
    39. 42. CHOLESTEROL – ENZYMATIC METHOD <ul><li>Cholesteryl esters + h2o ---------- cholesterol + free fatty acids </li></ul><ul><li>Cholesterol + o2 --------------------------------------- </li></ul><ul><li>---cholesten-4 en-3one + h2o2 </li></ul><ul><li>H2o2 + phenol + 4-aminoantipyrine -------- quinoenimine +2h2o </li></ul><ul><li>The absorbance of quinoenimine produced is measured at 500 nm. </li></ul>
    40. 43. TRIGLYCERIDE-ENZYMATIC METHOD <ul><li>PRINCIPLE : </li></ul><ul><li>Serum TG are hydrolysed to glycerol & free fatty acids by lipase. </li></ul><ul><li>In presence of ATP & glycerokinase , glycerol is converted to Gly – PO4 which is then oxidised to yield h2o2. </li></ul><ul><li>H2o2 reacts with ESPAS to form colored complex, the intensity of which is measured at 546 nm </li></ul><ul><li>( 530-570 nm ) </li></ul>
    41. 44. TRIGLYCERIDE Concentration of TG Condition < 150 mg/dl No disease 250-500 mg/dl Peri vascular disease > 500 mg/dl High risk of pancreatitis > 1000 mg/dl 1)Hyper lipidemia type I or IV 2)Substantial risk of pancreatitis > 5000 mg/dl <ul><li>Eruptive xanthoma </li></ul><ul><li>Lipemia retinalis </li></ul>
    42. 45. HDL-CHOLESTEROL: HOMOGENOUS ASSAY <ul><li>PRINCIPLE : The method depends on the properties of detergent which solubilizes only the HDL so that HDL-C is released to react with the cholesterol esterase & cholesterol oxidase & chromogen to give color. </li></ul><ul><li>The intensity of color is formed proportional to conc. Of HDL in sample, the absorbance of which is measured at 600 nm( 600- 670 nm ) </li></ul>
    43. 46. LDL-CHOLESTEROL <ul><li>FRIDEWALD CALCULATION : </li></ul><ul><li>LDL-C (MMOL/L) = (TC – HDL CHOLESTEROL) – PLASMA TG / 2.175 </li></ul><ul><li>LDL-C (MG/DL) = (TC – HDL CHOLESTEROL) – PLASMA TG / 5 </li></ul>
    44. 47. VLDL-C/ PLASMA TG ratio <ul><li>VLDL-C/PLASMA TG ratio may be useful in evaluation of type III hyperlipoproteinemia </li></ul><ul><li>Expressed in mol/mol or mass/mass </li></ul><ul><li>Ranges 0.230-0.575 in samples without </li></ul><ul><li>beta VLDL </li></ul><ul><li>Type III subjects have ratio > 0.689, usually in range of 0.689 – 0.0919 </li></ul>
    45. 48. NORMAL LEVELS S.No lipid level 1 TOTAL LIPIDS 400-800 MG/DL 2 TOTAL CHOLESTEROL 150-250 MG/DL 3 TRIGLYCERIDES 10-90 MG/DL 4 PHOSPHOLIPIDS 150-380 MG/DL 5 FREE FATTY ACIDS 9.0-15.0 MMOL/L 6 PHOSPHOLIPID PHOSPHORUS 8.0-11.0 MG/DL
    46. 49. LIPID PROFILE IN NEPHROTIC SYNDROME <ul><li>Increased LDL – C </li></ul><ul><li>Increased Total Cholesterol </li></ul><ul><li>Increased VLDL </li></ul><ul><li>Increased TG </li></ul>
    47. 50. SERUM CALCIUM <ul><li>NORMS : </li></ul><ul><li>Adults : </li></ul><ul><li>18 – 60 yrs : 8.2 – 10.7 mg/dl </li></ul><ul><li>60 – 90 yrs : 8.8 – 10.2 mg/dl </li></ul><ul><li>> 90 yrs : 8.2 – 9.6 mg/dl </li></ul><ul><li>Children : </li></ul><ul><li>< 10 days : 7.6 – 10.4 mg/dl </li></ul><ul><li>10 days – 2 yrs : 9.0 – 11.0 mg/dl </li></ul><ul><li>2 – 12 yrs : 8.8 – 10.8 mg/dl </li></ul><ul><li>12 – 18 yrs : 8.4 – 10.2 mg/dl </li></ul>
    48. 51. SERUM CALCIUM <ul><li>Serum calcium is decreased in nephrotic syndrome </li></ul>
    49. 52. SERUM CERULOPLASMIN <ul><li>NORMS: </li></ul><ul><li>Adult : 14 – 40 mg/dl </li></ul><ul><li>Newborn : 1 – 30 mg/dl </li></ul><ul><li>6 – 12 mths : 15 – 50 mg/dl </li></ul><ul><li>1 – 12 yrs : 30 – 65 mg/dl </li></ul>
    50. 53. SERUM CERULOPLASMIN <ul><li>Serum ceruloplasmin is decreased in nephrotic syndrome </li></ul>
    51. 54. SERUM FIBRINOGEN <ul><li>NORMS : </li></ul><ul><li>Quantitative is 200 – 400 mg/dl </li></ul><ul><li>Lower values can occur in newborn. </li></ul><ul><li>It is increased in Nephrotic syndrome resulting in increased ESR </li></ul>
    52. 55. SERUM C3 COMPLEMENT <ul><li>NORMS : </li></ul><ul><li>Adult : 88 – 201 mg/dl </li></ul><ul><li>Children : </li></ul><ul><li>Between 1 – 2 yrs : 87 – 181 mg/dl </li></ul><ul><li>Between 2 – 3 yrs : 84 – 177 mg/dl </li></ul><ul><li>Between 3 – 5 yrs : 80 – 178 mg/dl </li></ul><ul><li>Between 5 – 11 yrs : 89 – 203 mg/dl </li></ul><ul><li>Between 12 – 18 yrs : 88 – 201 mg/dl </li></ul>
    53. 56. SERUM C3 COMPLEMENT <ul><li>Serum C3 complement is normal in idiopathic lipoid nephrosis but decreased when there is underlying glomerulonephritis </li></ul>
    54. 57. SERUM C3 COMPLEMENT <ul><li>DECREASED C3 </li></ul><ul><li>SLE </li></ul><ul><li>SABE </li></ul><ul><li>Shunt nephritis </li></ul><ul><li>Acute post streptococcal GN </li></ul><ul><li>Membrano -proliferative GN </li></ul><ul><li>NORMAL C3 </li></ul><ul><li>Polyarteritis nodosa </li></ul><ul><li>Wegener granulomatosis </li></ul><ul><li>Henoch scholein purpura </li></ul><ul><li>Good pasture syndrome </li></ul><ul><li>IgG-IgA nephropathy </li></ul><ul><li>Idiopathic RPGN </li></ul><ul><li>Anti GBM disease </li></ul><ul><li>Immune complex disease </li></ul>
    55. 58. RENAL BIOPSY <ul><li>Renal biopsy is a valuable tool in adults with nephrotic syndrome for establishing a definitive diagnosis, guiding therapy & assessing prognosis </li></ul><ul><li>Renal biopsy is not required in majority of children with nephrotic syndrome as most cases are due to MCD & respond to empirical T/t with corticosteroids </li></ul>
    56. 59. LESIONS THAT PRESENT AS NEPHROTIC SYNDROME <ul><li>Minimal Change Disease </li></ul><ul><li>Focal Segmental GS </li></ul><ul><li>Membranous GN </li></ul><ul><li>Diabetic nephropathy </li></ul><ul><li>Amyloidosis </li></ul><ul><li>Light Chain Deposition Disease </li></ul>
    57. 60. MINIMAL CHANGE GLOM. (LIPOID NEPHROSIS or NIL LESION or FOOT PROCESS DISEASE) <ul><li>MOST COMMON CAUSE of NEPHROTIC SYNDROME in CHILDREN </li></ul><ul><li>EFFACEMENT of FOOT PROCESSES </li></ul>
    58. 61. MINIMAL CHANGE DISEASE <ul><li>Most common cause of paediatric NS. </li></ul><ul><li>H & E stained normocellular glomerulus </li></ul><ul><li>Patent capillary loops </li></ul><ul><li>Basement membrane normal in thickness </li></ul><ul><li>No tubular atrophy </li></ul><ul><li>No interstitial scarring. </li></ul>
    59. 62. MINIMAL CHANGE DISEASE <ul><li>Periodic acid –methenamine silver (Jones) </li></ul><ul><li>Shows basement membrane & mesangial matrix black. </li></ul><ul><li>Epithelial cells and mesangial cells appear grey-pink. </li></ul>
    60. 63. LIPOID NEPHROSIS <ul><li>Lipid & protein droplets accumulate in cell cytoplasm of convoluted tubules. </li></ul><ul><li>LIPOID CELLS . </li></ul><ul><li>Masson’s trichrome stain. </li></ul><ul><li>Tubular BM is light blue, cells rusty. </li></ul>
    61. 64. FOCAL & SEGMENTAL GLOMERULOSCLEROSIS <ul><li>PRIMARY </li></ul><ul><li>Typical -Segmental sclerosis in one or more lobules of the glomerular tuft near axial region. </li></ul><ul><li>Collapsing GP. </li></ul><ul><li>Glomerular tip lesion. </li></ul>
    62. 65. MEMBRANOUS GN <ul><li>MC cause of adult NS. </li></ul><ul><li>Epi/extra membranous or subepithelial deposits. </li></ul><ul><li>STAGE-I : Glomeruli appear normal by light microscopy. </li></ul><ul><li>D/D MCD </li></ul>
    63. 66. MGN STAGE-II <ul><li>H & E stain </li></ul><ul><li>Thickened capillary walls. </li></ul><ul><li>No increase in cellularity. </li></ul>
    64. 67. MGN STAGE III <ul><li>Capillary walls markedly thick </li></ul><ul><li>Deposits covered by a newly formed BM. </li></ul><ul><li>Lumen narrowed. </li></ul><ul><li>BM shows a reduplicated or MOTH EATEN appearance. </li></ul>
    65. 68. MGN STAGE IV <ul><li>Further thickening of the basement membrane. </li></ul><ul><li>Faded deposits. </li></ul><ul><li>Glomerular tufts show segmental or total sclerosis. </li></ul>
    66. 69. MEMBRANOPROLIFERATIVE GN <ul><li>Mesangiocapillary GN. </li></ul><ul><li>Type-I </li></ul><ul><li>- Diffusely enlarged glomerulus. </li></ul><ul><li>Lobular GN. </li></ul><ul><li>Subendothelial deposits. </li></ul><ul><li>Variants: </li></ul><ul><li>Exudative, crescentric, </li></ul><ul><li>Focal segmental. </li></ul>PAS STAIN
    67. 70. TYPE-II MPGN Vs NORMAL
    68. 71. TYPE-III MPGN <ul><li>Uncommon. </li></ul><ul><li>Burkholder variant– type-I MPGN + MGN. </li></ul><ul><li>Second variant—type-I + type-II MPGN </li></ul>
    69. 72. Ig A NEPHROPATHY <ul><li>BERGER’S DISEASE . </li></ul><ul><li>MC form of prim GN. </li></ul><ul><li>Mesangial widening </li></ul><ul><li>Increased matrix,hypercellularity. </li></ul><ul><li>May appear as FSGN </li></ul><ul><li>Subendo or subepith depo in severe disease. </li></ul>
    70. 73. DIABETIC NEPHROPATHY <ul><li>Microangiopathy- </li></ul><ul><li>increased vascular BM material. </li></ul><ul><li>Glomerulosclerosis is most commonly diffuse. </li></ul><ul><li>Thickened capillary walls </li></ul><ul><li>Mild increase in mesangial matrix. </li></ul>
    71. 74. DIFFUSE GS <ul><li>Advanced lesion </li></ul><ul><li>Greater increase in matrix and cellularity. </li></ul><ul><li>Thickened GBM – most consistent finding. </li></ul>
    72. 75. NODULAR GS <ul><li>KIMMELSTIEL- WILSON LESION. </li></ul><ul><li>Acellular nodules in intercapillary regions. </li></ul><ul><li>Masses of extracellular mesangial matrix. </li></ul><ul><li>Narrowed capillary lumens. </li></ul>
    73. 76. RENAL AMYLOIDOSIS <ul><li>Extracellular deposition of fibrillar proteins, β pleated sheet configuration on diffraction analysis </li></ul><ul><li>On L/M,amorphous, eosiniphilc, </li></ul><ul><li>PAS negative or scanty positive extracellular material. </li></ul>
    74. 77. NEPHROTIC SYNDROME <ul><li>COMPLICATIONS: </li></ul><ul><li>EDEMA </li></ul><ul><li>HYPERLIPIDEMIA </li></ul><ul><li>THROMBO EMBOLIC COMPLICATIONS – renal vein thrombosis </li></ul>
    75. 78. CONGENITAL NEPHROTIC SYNDROME <ul><li>Due to mutations in certain genes </li></ul><ul><li>Congenital nephrotic syndrome of finnish type – mutation in NPHS 1 which encode protein nephrin. </li></ul><ul><li>Steroid resistant nephrotic syndrome – mutation in NPHS 2 which encode protein podocin. </li></ul>
    76. 80. BY : DR RAVI JAIN <ul><li>THANK YOU….. </li></ul>

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