Renal small group

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  1. 13 year old
    Sx: periorbital "puffiness"; pedal edema
    UA: 3+ protein, occasional RBCs/hpf, no casts
    24hr urine: 4.3g protein
    Serum: protein was 4gm/dL (low), albumin 1.1 (nl >3.5), complement nl, BUN 12 (nl), Cr 0.7 (nl)
    Serology: negative for ASO, anti-hyaluronidase, anti-DNAse, ANA, HBsAg
    • Nephrotic syndrome:
    • -protein loss in urine (proteinuria)
    • -low albumin in blood
    • -edema

    Serum cholesterol elevated
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    • Normal glomerulus
    • minimal change disease (normal light microscopy)
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    • Normal glomerulus tuft
    • EM
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    • EM of minimal change disease
    • effacement of basement membrane (GBM)
    • "minimal change" = only albumin leaks out
  5. Case 1, continued
    Minimal change disease: bx findings
    Minimal change disease:-EM will show effacement of podocytes-normal light microscopy findings
  6. Case 1, continued
    Nephrotic syndrome at risk for
    • Pulmonary thromboembolism
    • loss of antithrombin III, protein C and S in urine
  7. Minimal changes disease
    • Unlikely to progress to ESRD
    • most (80%) respond well to steroids
    • many recover spontaneously without recurrence
  8. Case 2:
    21 yo
    severe episodes of intermittent, gros hematuria (usually occurring after URI)
    PE: nl
    UA: 4+ blood, RBCs TNTC, 1+ proteinuria
    24hr urine: 300mg protein (nl <100mg), nl Cr clearance
    Labs: C3, ASO and ANA all normal
    • Benign recurrent hematuria
    • transient, preceded by URI, often in children and young adults
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    • IgA nephropathy
    • prominent mesangiumm
    • IgA accumulates in the mesangium between the basement membrane and the mesangial cells
    • Focal and segmental

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  10. Case 2, continued
    bx, risk factors for progression to ESRD
    • -IgA nephropathy
    • -Mesangial granular deposits of IgA

    • Risk factors:
    • -Male sex, high blood pressure, high serum creatinine
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    • Henoch-Schoenlein Purpura
    • -Also presents with IgA nephropathy:
    • -Focal and segmental

    • Purpuric lesions (2-10mm) on lower extremities
    • Bx: leukoclastic vasculitis of small vessels with linear IgA deposits

    abdominal pain and arthritis
  12. Case 2
    IgA + Purpura on the buttocks and lower extremities
    • Henoch-Schonlein Purpura
    • -IgA nephropathy
    • -Purpura
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    • Alport's syndrome:
    • -Nephrotic syndrome
    • -Deafness
    • -Basement membrane disease involving collagen type IV

    Thinning and splitting, irregular width
  14. Case 3
    23 yo
    Sx: increasing fatigue, leg edema, weight gain (30lbs) over past 4 months; 6mo history of foamy urine
    PMH: IV drug abuse (current)
    Vitals: pulse 100, BP 140/80
    PE: decreased breath sounds, CV normal, 3+ pitting pedal edema
    UA: 4+ protein, no glucose, no casts, 3rbc/hpf, 0-2 WBC/hpf
    Serum: Cr 1.7 (nl <1.6), BUN 8, albumin 2.6, XOL 350 (high), glucose 90
    24hr urine: Cr clearance 77 (nl>100), protein 13.7gm
    Serology: normal
    • Three histopathological diagnosis consistent with presentation:
    • FSGS, antiglomerular basement membrane Ab GN

    • Most likely: FSGS
    • -associated with IV drug abuse

    • Prognosis:
    • -Progress to ESRD over time
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    Focal Segmental Glomerulosclerosis

    • -Deposition of Immunoglobulins & complement
    • -Injury to visceral epithelial cells
    • -Detachment of visceral epithelial cells
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    • FSGS
    • -Prominent mesangeal matrix
    • -deposition of hyaline masses and lipid droplets
    • -obliterated glomerular capillaries
    • -Effacement of foot process

    • Primary: 20-30% of nephrotic syndrome
    • -Associated with HIV infection, heroin abuse
    • -Worse than that of minimal change disease
  17. Case 4
    24 yo woman presents with malaise, joint pain for 3 months (systemic symptoms)
    PE: BP 140/100, no skin, swelling of proximal interphalangeal joints, no peripheral edema
    Labs: BUN 20, Cr 1.8, albumin 3
    UA: heme 2+, glucose neg, 10-20 rbc/hpf, 15-30 WBC/hpf, numerous granular and RBC casts
    Serology: positive ANA, positive dsDNA
    24hr urine: 3.4gm
    • Important findings:
    • -RBC casts
    • -Reduced renal function
    • -Nephrotic range proteinuria

    Etiology: Lupus glomerulonephritis
  18. Case 4, continued
    Complement levels in Lupus GN
    Low complement levels in blood due to immune complex formation and deposition in the kidney
  19. Case 4, continued
    SLE overview
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    Malar erythema

    • Lupus nephritis
    • -Focal GN with focal necrotising lesion
    • -Subendothelial

    • WHO classification:
    • I. Minimal
    • II. Mesangeal
    • III. Focal proliferative
    • IV. Diffuse proliferative including crescentic and membranoproliferative
    • V. Membranous
  20. Case 5
    48yo man
    Hx: 5 mo edema, HTN
    PE: 160/90, 4+ pedal edema and scrotal edema
    UA: 4+ protein, 3-5 RBC/hpf, granular casts and hyaline casts
    Serum: Cr 1, BUN 10, albumin 2.0, XOL 320
    24hr urine: Cr clearance 150ml/min; urine protein 18.9gm
    Nephrotic syndrome... bland sediment

    *Hyaline casts: the kidney isn't being perfused well

    Histology: thickening of the basement membrane (Membranous GN)
  21. Case 5, continued
    potential pathogenetic mechanism
    Antibodies directed against antigens present on the epithelial cell

    • Membranous GN, diffuse thickening of GBM
    • Deposition of IgG
    • 70% of cases: receptor for phospholipase A2 is the antigen on the podocyte

    • Progression:
    • Image Upload
  22. Case 5, continued
    Renal disorders present with nephrotic syndrome and bland urinary sediment
    • Malignancy of the GI tract == Membranous nephropathy
    • Chronic Osteomyelitis == Amyloidosis
    • IV drug abuse == FSGS
  23. Case 6
    35 yo woman
    Hx: 3 weeks of generalized aches/pains with respiratory flu-like syndrome; decreased urine output x3days
    PE: 180/110, mild pedal edema
    UA: 2+ protein, 2+ heme, 3-5 WBC/hpf, 5-10rbc/hpf, 3-5 granular casts/hpf and 3-5 RBC casts/hpf
    Serum: Cr 6.9, BUN 96
    US: normal-sized kidney
    Syndrome: Rapidly progressive glomerulonephritis
  24. RPGN

    • Type I: GBM antibody crescentic GN
    • -Goodpastures
    • -Idiopathic

    • Type II: Immune complex
    • -Post-infectious GN
    • -Systemic lupus erythematosus
    • -Henoch-Schoenlein
    • -Idiopathic

    • Type III: Pauci-Immune ANCA associated
    • -Wegener's granulomatosis
    • -Idiopathic
  25. Case 6, continued
    lab tests and results for RPGN
    • ASO titer == post-streptococcal GN
    • c-ANCA == Wegener granulomatosis
    • Hepatitis C antigen == Membranoproliferative GN
    • Anti-glomerular basement membrane antibody == Goodpasture's GN
  26. Case 6, continued
    Characteristic histology
    • Linear immunoglobulin deposits
    • Goodpasture's GN
  27. Case 7
    Hx: DM, new finding of swelling of ankles
    PE: 145/105, 2+ pedal edema
    Serum: Cr 2, albumin 2.8
    24hr urine: Protein 4gm
    • Diabetes glomerulonephritis
    • -Same series of events in type I and II DM

    Histology: glomerular hyalinosis/sclerosis and thickening of the GBM
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    • Diabetic glomerulosclerosis
    • -Diffuse
    • -Nodular


    • Effacement of podocyte foot processes
    • No immune deposits
  29. Case 7, continued
    First line antihypertensive med
    • ACE-Inhibitor
    • (or ARB, if ACE-In not tolerated)

    Never use NSAIDs (or only occasionally) 

    Caution with beta blockers and thiazides (both cause hyperglycemia
  30. Case 7, continued
    Factors that delay, slow down progression
    Tight glucose control, tight BP control

    Only 20-30% of diabetic nephropathy progress to ESRD

    • Recommendations:
    • -130/80
    • -120/80 if there is protein in urine
  31. Case 8
    65yo woman
    Presentation: generalized edema, SOB; progressed over last 2+ years
    PE: CHF, proteinuria (14gm/24hrs), BP normal,
    Serum: Cr 1
    PMH: pulmonary TB
    US: bilaterally enlarged kidneys
    Urine electrophoresis and X-ray
    Nephrotic syndrome and heart failure, insidious onset


    • enlarged kidney: ddx
    • -amyloidosis
    • -sarcoidosis
    • -TB
    • -tumor
    • -DM
    • -PCKD
  32. Case 8, continued
    why electrophoresis
    To investigate presence of Bence-Jones proteins

    majority of amyloid is not this... ?
  33. Case 8, continued
    why order the xrays
    To investigate the presence of bone lytic lesions
  34. Case 8, continued
    pathognomonic, histopathology
    Image Upload
    • Congo red stain
    • confirm with polarized light
    • "birefringes apple green"
Card Set:
Renal small group
2013-03-08 02:08:30
Renal II

renal small group slides
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