1. Basic presentations
    1. Heavy proteinuria (>3.5gm/day)
    2. Hypoalbuminemia
    3. Edema
    4. Hyperlipidemia/Lipiduria
    5. Normal Complement levels
  2. Diabetic Nerophaty
    1. Info
      1. Leading cause of ESRD (1/3 of all patients)
      2. Seen in 25-40% of type 1/2 diabetics
    2. Pathogensis
      1. Systemic hyperglycemia
        1. Reccurance after transplant
        2. Glomerulosclerosis
          1. Earliest lesions
          2. Hyperfiltartion injury
          3. Mesangium epxansion
          4. Thickening of GBM
          5. Later Lesions
          6. Diffuse global glomerulosclerosis
          7. More of Early lesions
          8. Kimmeslstiel-Wilson nodules
          9. Lipids/Fibrin
          10. Fibrin Cap/Capsular drop
          11. Plasma proteins
          12. Ischemia
          13. Tubular atrophy/interstitial fibrosis
          14. Hyaline arteriolosclerosis
        3. Timeline
          1. Initially
          2. Increased GFR/ Glomerular hydrostatic pressure
          3. 7-13 yrs
          4. Microalbuminuria
          5. .3- 3g/24 hr
          6. 10-20 yrs
          7. Macroalbuminuria
          8. Nephrotic syndrome
          9. 20+ yrs
          10. Persistent heavy proteinuria
          11. HTN
          12. Decline in GFR 1-24
          13. Median 12
  3. Minimal Change
    1. Info
      1. Children/ 15% in adults
      2. Idiopathic
        1. Can also be seen
          1. Lymphoma
          2. Renal cell carcinoma
      3. Labs
        1. Serum
          1. Low albumin
          2. Selective protienuria
          3. Normal creatinine
        2. Urine
          1. Bland Urine sediment
        3. Physical Exam
          1. No HTN
          2. Edema
          3. Periorbital
          4. Pedal
      4. Progression
        1. Remission with Steroids within 8 weeks
        2. 1/3 Rule
          1. No Relaspe
          2. Few Relaspes
          3. Many Relaspes
        3. Not likely to progress to CRF/ESRD
        4. Adults have worse prognosis
    2. Pathogensis
      1. Podocyte
        1. diffuse effacement and detachement
      2. No immune complex/inflammatory injury
      3. May involve circulating glomerular permeability factors
    3. Pathology
      1. LM
        1. N
      2. IF
        1. N
      3. EM
        1. Fusion of foot processes
  4. FSGS
    1. Info
      1. 10-15% of idiopathetic nephrotic syndromes seen in children
      2. Higher incidence seen in adult AA
      3. Secondary to
        1. HIV
        2. Morbid obesity
        3. Chronic reflux nephropathy
        4. Heroin
        5. Malignancies(lymphoma)
      4. Progression
        1. Present asymptomatic proteinuria
        2. Progresses to Massive Proteinura/Microscopic hematuria
        3. HTN
        4. Persistent proteinuria/progressive decline in renal function
        5. ESRD by 5-20 yrs
        6. 50% recurrence post transplant
    2. Secondary FSGS
      1. Anything that causes a reduction in renal mass
        1. Hyperfiltration Injury
    3. Pathology
      1. LM
        1. FSGS
      2. IF
        1. Negative or Non Specific granular IgM/C3 deposits
      3. EM
        1. Patchy fusion of foot processes/effacement
  5. Membranous Nephropathy
    1. Info
      1. Presentation
        1. Nephrotic syndrome
        2. Microscopic hematuria (50%)
        3. HTN
        4. Late Renal Insufficiency
          1. 20 year follow up
          2. 25% spontaneous remission
          3. 50% persistent proteinuria/ stable or gradual loss of renal function
          4. 25% develop ESRD
        5. Renal Vein Thrombosis
    2. Progression
      1. Bad Progonsis
        1. Males
        2. >50
        3. >10gm proteinuria
    3. Pathogenesis
      1. IC deposition
        1. Sub Epithelium
        2. In situ/ cirulating
          1. Heymann Nephritis
          2. Supports in situ
      2. Complement Activation
        1. MAC activated damage of GFM
    4. Associated Causes
      1. DNA SLE
      2. Tumors
      3. Hep B
      4. Syphilis
      5. Malaria
      6. Captorpril
      7. Mercury
      8. Gold
      9. Penicillamine
    5. Pathology
      1. LM
        1. Diffuse thickening of GBM w/ minor increase in cellularity
      2. IF
        1. Subepithelial fine granular deposits of IgG/C3 in BM
      3. EM
        1. Subepithelial IC deposits with GBM spike formation
  6. Amyloidosis
    1. Pathology
      1. LM
        1. Nodular, amorphous hyaline matierial in mesangium/capillary lopps
      2. Congo Red Stain
        1. (+) w/ apple green birefringence
      3. EM
        1. Subendothelial/Mesangial fibrils
    2. Presentation
      1. Either caused by AL or AA amyloids
      2. Nephrotic syndrome
        1. Renal insufficiency in 50% by diagnosis
      3. Electrolyte abnormalities
        1. Fanconi's syndrome (loss of renal tubal reabsorptive function)
      4. Other Systemic Presentations
        1. Heart
          1. CHF
          2. Arrhythmias
          3. Heart Block
        2. GI
          1. Hepatomegaly
          2. Malabsorption
          3. Hemarrahge
        3. Neuro
          1. Ischemic stroke
          2. Neuropahty
          3. Orthostatic hypotension
        4. Skin
          1. Easy bruising
          2. Purpura
    3. Diagnosis
      1. Biopsy needed
      2. Very poor prognosis
        1. Survival drops severely as yrs pass 50% yr 1 to 5% 10 years
      3. Death due to end-organ failure of affected organ
    4. Secondary Amyloid (AA caused)
      1. RA
      2. Behcet syndrome (systemic inflammation of blood vessels)
      3. Chrons
      4. Osteomyelitis
      5. Renal cell carcionma
      6. Hodgkins lymp