1. "View a negative experience in your life like you'd look at a photo negative. A single negative can create an unlimited number of positive prints." Gerhard Gschwandtner Founder of "Selling Power" magazine

2. Pathology of Kidney Disorders Dr. Venkatesh M. Shashidhar Associate Professor of Pathology Fiji School of Medicine

3. Anatomy-Kidney

5. Anatomy of Kidney

9. JGA GFR  Renin  Angiotensin Blood Pressure

10. Filtration Membrane:

11. Normal Kidney:

13. Congenital Anomalies: Agenesis – Potter syndrome Ectopia Fusion Dysplasia Simple cysts Polycystic kidney disease

14. Horse Shoe Kidney

15. Double Ureter:

18. ADPKD:

19. ADPKD:

21. Kidney Disorders – clinical. A Asymptomatic hematuria/proteinuria N Nephrotic syndrome N Nephritic syndrome U Urolithiasis R Rapidly progressive glomerulonephritis I Interstitial and tubular diseases C Chronic renal disease

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23. Glomerular Disorders:

25. Acute Post Strepto. GN: Synonyms : Incidence : Etiology : Clinical : Lab: Path: Clinical Course: Acute proliferative glomerulonephritis, acute post-infectious GN. Glomerular trapping of circulating anti-streptococcal immune complexes. Group A, B-hemolytic streptococci, type 12. Acute nephritic syndrome post-strept pharyngitis or pyoderma. Other infections. Nephritic urine with RBC casts. Evidence of streptococcal infection or serologic evidence of recent infection. Decreased serum complement. Children - Excellent prognosis. Adults - Worse prognosis, some develop progressive disease. Enlarged, hypercellular glomeruli with endothelial and mesangial cell proliferation. Acute inflammation. IgG and C3 in very coarsely granular pattern along GBMs. Discrete, subepithelial “hump-like” deposits. Peak incidence in children (3-14). Sporatic, mostly winter and spring.

26. Minimal Change GN: Synonyms : Incidence : Etiology : Clinical Features: Lab Features: Pathology : Clinical Course: Nil disease, lipoid nephrosis, foot process disease Idiopathic. Loss of net negative charge on capillary basement membrane. Nephrotic syndrome. History of recent URI in 30%. Association with Hodgkin’s lymphoma. Overlap with FSGS patients. Selective proteinuria. No specific laboratory findings. Spontaneous remission in 25-40%. Complete remission in 65-70% of patients. Steroid resistant patients may progress to FSGS. LM - Normal. IF - Negative. EM - Focal fusion/loss of foot processes. 80% of nephrotic syndrome in children (1-8 yrs.), mostly male. Adults in 2nd-3rd decade.

27. Membranous GN: Synonyms: Incidence : Etiology: Clinical: Lab: Path: Clinical Course: Epimembranous, extramembranous GN Immune complex disease. Idiopathic in most patients, associated with infections, drugs, carcinomas, and heavy metals. Nephrotic syndrome in 80%, asymptomatic proteinuria in 20%. Microscopic hematuria. Non-selective proteinuria ± hematuria. Excellent prognosis in children. Some adults develop ESRD. Exclusion of other diseases is required. Diffuse, uniform BM thickening with subepithelial projections (“spikes”). Diffuse, coarsely granular IgG and C3 deposits along basement membranes. Electron-dense subepithelial deposits. 40-60 Years, 50% of adult nephrotic syndrome.

28. Membranoproliferative GN Etiology : Chronic immune complex GN. Associated with chronic infections, SLE, cancer, cirrhosis, heroin abuse, etc. Clinical : Nephrotic syndrome in 50%, acute nephritic syndrome in 20%. Recent history of URI in 50%. Hypertension and/or renal insufficiency. Lab : Hypocomplementemia of classic and alternate pathways. C3 nephritic factor (C3NEF). Circulating immune complexes. Clinical Course: Progressive deterioration of renal function ± short remissions. ESRD within 10 years in 50% of children and 80% of adults. Path: Diffuse proliferative GN with thickening of the glomerular capillary walls,, and GBM splitting (“tram-tracking”). Diffuse, coarsely granular C3 and IgG deposits along GBMs. Electron-dense subendothelial deposits. Incidence : Children and young adults (5-25 years).

29. Causes of nephrotic syndrome Disease Children (%) Adults (%) Minimal change GN 75 20 Membanous GN 5 40 MPGN I 5 5 Other GN 5 20

31. Chronic Renal Failure: ESKD

32. CRF- ESKD with transplant:

35. Diabetic Glomerulosclerosis Hyaline nodules

36. Diabetic Glomerulosclerosis KW lesion…

37. Benign Nephrosclerosis: Leathery Granularity due to minute scarring

38. Renal Artery stenosis - Atrophy Leathery Granularity Benign Nephrosclerosis

43. Renal Infarcts:

44. Renal Infarct:

45. Renal Infarct:

48. Septicemia-Microabscess

49. Septicemia-Microabscess

50. Acute Pyelonephritis with papillary necrosis (diabetes)

51. Septicemia-abscess

52. Pyelonephritis – Predisposing Cond. U Urolithiasis R Reflux (vesico-ureteric) I Infections of lower UT N Neoplasms (ureteric, vesical, prostatic) E External compression (e.g.) pregnancy retroperitoneal fibrosis

55. Urolithiasis – Stones:

57. Urolithiasis – stones: Infection 6% Other 1% Cystine 6% Uric acid 12% Magnesium ammonium phosphate (struvite, or "triple phosphate") 75% Calcium oxalate (or phosphate)

59. Urolithiasis:

60. Staghorn Calculus:

61. Urolithiasis with hydronephrosis:

62. Hydronephrosis:

63. Hydronephrosis:

64. Urolithiasis – sites of impaction

65. Hydronephrosis - Urolithiasis

66. Causes of Obstructive Uropathy

67. Urolithiasis: Incidence : Etiology : Clinical Features : Lab : Path : Clinical Course : Environmental, metabolic, infectious. Develop silently until episode of renal colic. Cause obstruction, pain, infection, hydronephrosis, and hydroureter. Gross or mcroscopic hematuria. Chemical analysis to identify type of stone. Characteristic radiographic findings. May recur. Complications are the problem. Calcium phosphate or oxalate - Hard, sharp. Uric acid - Smooth. Staghorn - Cast of calyceal system. Common, male predominance. Treatment : Surgery, lithotomy, or ultrasonic lithotripsy to remove stone. Treatment of metabolic process, if indicated. Adequate hydration.

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70. Angiomyolipoma (Benign)

72. Oncocytoma (DCT epithelia, benign)

73. Wilm’s Tumor Incidence : Etiology : Clinical Features: Lab : Path: Clinical Course: Embryonic renal tissue (metanephric blastema). Genetic abnormalities. Palpable abdominal mass. Abdominal pain, fever, anorexia, nausea/vomiting. Hematuria. No specific clinical laboratory findings. Diagnosis by radiographic techniques. 5-yr. Survival 80%. Metastases to lung, liver, bone, brain. Gross: Solitary/multiple cystic mass, sharply delineated. Soft, bulging, gray-white with focal hemorrhage and necrosis. Micro: Triphasic mesenchymal stroma, tubules, and solid areas (blastema). Primitive glomeruli, skeletal muscle, cartilage, bone, etc. (embryonic tissues) Most common renal tumor of childhood. Peak age - 2.5 - 3.5 years. Treatment: Prompt resection with chemotherapy ± radiotherapy. Synonyms : Nephroblastoma.

76. Renal Cell Carcinoma:

77. Renal Cell Carcinoma:

78. Renal Cell Carcinoma:

79. Renal Cell Carcinoma:

81. Renal Cell Carcinoma: Incidence : Etiology : Clinical Features : Lab : Path : Clinical Course: Cells of proximal convoluted tubule. Risk factors are smoking, obesity, analgesic abuse, APCKD. Hematuria*, flank pain, palpable mass. Frequently metastasize (lungs, bone, skin, liver, brain). Gross or microscopic hematuria. Specific Dx by radiographic techniques. 5-yr. survival 40%. Poor prognosis with metastases. Gross: Large yellow mass with hemorrhage and necrosis. Invade renal vein. Micro: Usually clear or granular cells with little anaplasia. Other histologic variants (“great mimicker”). 5 th and 6 th decades, most common primary renal malignancy. Treatment : Chemotherapy, surgery, immunotherapy. Synonyms : Hypernephroma, clear cell carcinoma.

83. Wilms Tumor:

85. Transitional cell Carcinoma:

86. Transitional cell Carcinoma:

87. Transitional cell Carcinoma:

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