Pulmonary-Renal Syndrome Alanna Beckman MSIV
Pulmonary-Renal Syndrome <ul><li>Potentially life-threatening disorder,  </li></ul><ul><ul><li>Diffuse alveolar hemorrhage...
Diffuse Alveolar Hemorrhage <ul><li>Presentation of patients with DAH can range from cough with or without hemoptysis to s...
Rapidly Progressive Glomerulonephritis <ul><li>Acute onset (days to weeks) </li></ul><ul><li>Acute renal failure and oligu...
Pulmonary-Renal Syndromes <ul><li>ANCA-associated vasculitides account for approximately 60%  </li></ul><ul><li>Goodpastur...
 
Work-up for GN <ul><li>ANCA </li></ul><ul><li>Anti-GBM </li></ul><ul><li>Complement levels (C3,C4) </li></ul><ul><li>Depen...
Goodpastures <ul><li>Autoimmune </li></ul><ul><ul><li>Autoantibodies directed against type IV collagen    RPGN and crecen...
Goodpasture’s Syndrome <ul><ul><li>Common presentation: </li></ul></ul><ul><ul><ul><li>Hematuria </li></ul></ul></ul><ul><...
GP Diagnosis <ul><li>Diagnostic serologic marker is anti-GBM antibodies with a specificity for NCI domain of the alpha3 ch...
Normal Glomerulus RPGN/Crescentic GN <ul><ul><li>Immunofluoresence Microscopy:  </li></ul></ul><ul><ul><li>“ Linear ribbon...
GP Treatment <ul><li>Emergency plasmapheresis is done daily or on alternate days until anti-GBM antibodies are not detecte...
GP Prognosis <ul><li>Without treatment, 80% get ESRD within 1 year </li></ul><ul><li>Early Treatment </li></ul><ul><ul><li...
ANCA Vasculitis (pauci-immune) <ul><ul><ul><li>Wegener’s Granulomatosis </li></ul></ul></ul><ul><ul><ul><li>Microscopic Po...
ANCA + Vasculitis (pauci-immune) PR3 = Proteinase 3 MPO = Myeloperoxidase  (found in granules of neutrophils/monocytes) 50...
ANCA-associated small vessel vasculitis <ul><li>More common in Caucasian and elderly (mean age is 57 years) </li></ul><ul>...
ANCA-associated small vessel vasculitis <ul><li>Nonspecific lab abnormalities </li></ul><ul><ul><li>Rapid sedimentation ra...
C-ANCA    PR3
Wegener’s <ul><li>Granulomatous vasculitis of the upper and lower respiratory tracts together with glomerulonephritis.  </...
Wegener’s  <ul><li>Pathogenesis: </li></ul><ul><ul><li>Necrotizing vasculitis of small arteries and veins with granuloma f...
Wegener’s  <ul><li>Presentation </li></ul><ul><ul><li>95% have upper airway involvement </li></ul></ul><ul><ul><ul><li>Par...
Wegener’s <ul><li>Presentation </li></ul><ul><ul><li>Pulmonary involvement in 85-90% </li></ul></ul><ul><ul><ul><li>Cough,...
Wegener’s <ul><li>Diagnosis </li></ul><ul><ul><li>Demonstration of necrotizing granulomatous vasculitis on tissue biopsy i...
Wegener’s <ul><li>Treatment </li></ul><ul><ul><li>Glucocorticoids (predisone 1mg/kg/day) should be started for symptomatic...
Wegener’s  <ul><li>Treatment </li></ul><ul><ul><li>Relapse occurs in about 25% of patients.  </li></ul></ul><ul><ul><ul><l...
P-ANCA    MPO
Churg-Strauss <ul><li>AKA allergic angiitis and granulomatosis .  </li></ul><ul><li>Asthma </li></ul><ul><li>Peripheral an...
Churg-Strauss <ul><li>Incidence is estimated at 1 in 3 million. </li></ul><ul><li>Can occur at any age (not documented in ...
Churg-Strauss <ul><li>Granulomatous  reaction and  eosinophil  infiltration can occur in any organ in the body, but the  l...
Churg-Strauss <ul><li>Presentation </li></ul><ul><ul><li>Pulmonary findings clearly dominate clinical picture </li></ul></...
Churg-Strauss <ul><li>Presentation </li></ul><ul><ul><li>Skin involvement 51% </li></ul></ul><ul><ul><ul><li>Include purpu...
Churg-Strauss <ul><li>Biopsy of affected tissue (lung).  </li></ul><ul><ul><li>Microgranulomas , fibrinoid necrosis and th...
Churg-Strauss <ul><li>Treatment </li></ul><ul><ul><li>Glucocorticoids; high dose. </li></ul></ul><ul><ul><ul><li>Attempt t...
P-ANCA    MPO
Microscopic Polyangiitis. <ul><li>Necrotizing vasculitis with few or no immune complexes affecting small vessels (capillar...
Microscopic Polyangiitis <ul><li>Incidence not really established because it use to be included in PAN. </li></ul><ul><li>...
Microscopic Polyangiitis <ul><li>Presentation </li></ul><ul><ul><li>Vascular lesion is a necrotizing inflammation of capil...
Microscopic Polyangiitis <ul><li>Renal involvement 90% </li></ul><ul><ul><li>Glomerulonephritis, often rapidly progressive...
Microscopic Polyangiitis <ul><li>Diagnosis </li></ul><ul><ul><li>Biopsy of affected tissue. </li></ul></ul><ul><ul><ul><li...
Microscopic Polyangiitis <ul><li>Treatment </li></ul><ul><ul><li>Similar approach to that of Wegener’s.  </li></ul></ul><u...
 
Differential Diagnosis for Pulmonary-Renal Syndrome <ul><li>Goodpasture’s Disease </li></ul><ul><li>Systemic Vasculitis </...
 
references <ul><li>Harrison et. al, (2005), Principles of Internal Medicine, 16 th  Edition, McGraw-Hill, NY </li></ul><ul...
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  1. 1. Pulmonary-Renal Syndrome Alanna Beckman MSIV
  2. 2. Pulmonary-Renal Syndrome <ul><li>Potentially life-threatening disorder, </li></ul><ul><ul><li>Diffuse alveolar hemorrhage </li></ul></ul><ul><ul><ul><li>pulmonary capillaritis </li></ul></ul></ul><ul><ul><li>In conjunction with </li></ul></ul><ul><ul><li>Rapidly progressive glomerulonephritis </li></ul></ul><ul><li>AGN/RPGN +/- lung hemorrhage is and emergency  requires early diagnosis and treatment. </li></ul>
  3. 3. Diffuse Alveolar Hemorrhage <ul><li>Presentation of patients with DAH can range from cough with or without hemoptysis to severe respiratory distress. </li></ul><ul><li>Onset is usually abrupt. </li></ul><ul><li>Suspect DAH: </li></ul><ul><ul><li>Hemoptysis (Absent in 1/3 of patients) </li></ul></ul><ul><ul><li>Radiographic Abnormalities (Alveolar opacities, Interstitial opacities, Fibrosis) </li></ul></ul><ul><ul><li>Unexplained drop in Hematocrit </li></ul></ul>Capillaritis: neutrophile infiltrates and hemorrhage
  4. 4. Rapidly Progressive Glomerulonephritis <ul><li>Acute onset (days to weeks) </li></ul><ul><li>Acute renal failure and oliguria (400mL/day) </li></ul><ul><li>Renal Blood flow and GFR  fall </li></ul><ul><ul><li>Obstruction of the glomerular capillary lumen </li></ul></ul><ul><ul><ul><li>By infiltrating inflammatory cells </li></ul></ul></ul><ul><ul><ul><li>Proliferating resident glomerular cells. </li></ul></ul></ul><ul><ul><li>Intrarenal vasoconstricion and mesangial cell contraction </li></ul></ul><ul><ul><ul><li>Local imbalances of vasoconstrictors (leukotrienes, endothelins, thromboxanes, platelet-activating factor) and vasodilators ( NO, prostacyclin ) in the microcirculation of the kidney. </li></ul></ul></ul>
  5. 5. Pulmonary-Renal Syndromes <ul><li>ANCA-associated vasculitides account for approximately 60% </li></ul><ul><li>Goodpasture's Syndrome for approximately 20% of the cases. </li></ul><ul><li>Other causes 20% </li></ul>
  6. 7. Work-up for GN <ul><li>ANCA </li></ul><ul><li>Anti-GBM </li></ul><ul><li>Complement levels (C3,C4) </li></ul><ul><li>Depending on history/clinical suspicion: </li></ul><ul><ul><li>ANA </li></ul></ul><ul><ul><li>ASLO </li></ul></ul><ul><ul><li>BCx </li></ul></ul><ul><ul><li>Cryocrit </li></ul></ul><ul><ul><li>Hepatitis serologies </li></ul></ul><ul><li>Renal Biopsy </li></ul><ul><ul><li>Immunofluorescence </li></ul></ul><ul><ul><li>Electron microscopy </li></ul></ul><ul><ul><li>(Light microscopy) </li></ul></ul><ul><li>Consider GN mimics: thrombotic microantiopathy, cholesterol emboli, AIN, myeloma </li></ul><ul><li>For Pulmonary-Renal Syndrome you will also want to bx other tissues. </li></ul>
  7. 8. Goodpastures <ul><li>Autoimmune </li></ul><ul><ul><li>Autoantibodies directed against type IV collagen  RPGN and crecentic glomerulonephritis. </li></ul></ul><ul><ul><li>50-80% have lung hemorrhage. </li></ul></ul><ul><ul><li>Bimodal distribution: </li></ul></ul><ul><ul><ul><li>Typically young males (5-40years) Male:Female ratio = 6:1 </li></ul></ul></ul><ul><ul><ul><li>Presentation in second peak, 6 th decade, generally do not have lung hemorrhage and have almost equal sex distribution. </li></ul></ul></ul>
  8. 9. Goodpasture’s Syndrome <ul><ul><li>Common presentation: </li></ul></ul><ul><ul><ul><li>Hematuria </li></ul></ul></ul><ul><ul><ul><li>Nephritic urinary sediment (dysmorphic RBC &/or RBC casts) </li></ul></ul></ul><ul><ul><ul><li>Subnephrotic proteinuria (<3.5 g/24 hours) </li></ul></ul></ul><ul><ul><ul><li>Rapidly progressive renal failure over weeks </li></ul></ul></ul><ul><ul><ul><li>With or without pulmonary hemorrhage </li></ul></ul></ul><ul><ul><ul><ul><li>Pulmonary hemorrhage, when it does occur, usually predates nephritis by weeks or months. </li></ul></ul></ul></ul><ul><ul><ul><ul><li>Lung involvement can vary from fluffy pulmonary infiltrates on CXR with mild dyspnea on exertion to potentially fatal pulmonary hemorrhage </li></ul></ul></ul></ul><ul><ul><ul><li>Usually not hypertensive. </li></ul></ul></ul>
  9. 10. GP Diagnosis <ul><li>Diagnostic serologic marker is anti-GBM antibodies with a specificity for NCI domain of the alpha3 chain of type IV collagen. </li></ul><ul><li>These antibodies are detected in >90% of patients with anti-GBM nephritis. </li></ul><ul><li>RENAL BIOPSY is the GOLD STANDARD for diagnosis of anti-GBM nephritis. </li></ul><ul><ul><li>Light microscopy : diffuse proliferative GN with focal necrotizing lesions and crescents in >50% of glomeruli. </li></ul></ul><ul><ul><li>Immunofluorescence : linear ribbon-like deposits of IgG </li></ul></ul><ul><ul><li>Electron Microscopy : inflammatory change without immune deposits </li></ul></ul>
  10. 11. Normal Glomerulus RPGN/Crescentic GN <ul><ul><li>Immunofluoresence Microscopy: </li></ul></ul><ul><ul><li>“ Linear ribbon like” deposition of IgG along GBM </li></ul></ul>
  11. 12. GP Treatment <ul><li>Emergency plasmapheresis is done daily or on alternate days until anti-GBM antibodies are not detected in circulation </li></ul><ul><li>Prednisone (1mg/kg per day) is started simultaneously along with cyclophosphamide (2 to 3 mg/kg per day) or azathioprine (1 to 2 mg/kg per day) to suppress new synthesis of anti-GBM antibodies. </li></ul>
  12. 13. GP Prognosis <ul><li>Without treatment, 80% get ESRD within 1 year </li></ul><ul><li>Early Treatment </li></ul><ul><ul><li>If treatment is started early, before creatinine is over 5mg/dL, then 1 year survival is over 90%. It is 80% if renal failure is more advanced. </li></ul></ul><ul><li>If patients require dialysis at time of presentation, they rarely recover renal function. </li></ul><ul><li>If crescents exist in >50% of glomeruli, then usually survival <2 yrs </li></ul><ul><li>Better response to treatment if ANCA + </li></ul>
  13. 14. ANCA Vasculitis (pauci-immune) <ul><ul><ul><li>Wegener’s Granulomatosis </li></ul></ul></ul><ul><ul><ul><li>Microscopic Polyangiitis </li></ul></ul></ul><ul><ul><ul><li>Churg-Strauss Arteritis </li></ul></ul></ul>
  14. 15. ANCA + Vasculitis (pauci-immune) PR3 = Proteinase 3 MPO = Myeloperoxidase (found in granules of neutrophils/monocytes) 50% P-ANCA (anti-MPO) + 70% 45% + Churg-Strauss Syndrome 70% P-ANCA (anti-MPO) - 50% 90% - Microscopic polyantiitis 90% C-ANCA (anti-PR3) - 90% 80% + Wegener’s granulo-matosis ANCA positive ANCA type Asthma Pulmonary Renal Granulomas Disease
  15. 16. ANCA-associated small vessel vasculitis <ul><li>More common in Caucasian and elderly (mean age is 57 years) </li></ul><ul><li>Usual presentation: nonspecific constitutional symptoms and signs </li></ul><ul><ul><li>Lethargy </li></ul></ul><ul><ul><li>Mailaise </li></ul></ul><ul><ul><li>Anorexia </li></ul></ul><ul><ul><li>Weight loss </li></ul></ul><ul><ul><li>Fever </li></ul></ul><ul><ul><li>Arthralgia </li></ul></ul><ul><ul><li>Myalgias </li></ul></ul>
  16. 17. ANCA-associated small vessel vasculitis <ul><li>Nonspecific lab abnormalities </li></ul><ul><ul><li>Rapid sedimentation rate </li></ul></ul><ul><ul><li>Elevated C-reactive protein </li></ul></ul><ul><ul><li>Leukocytosis </li></ul></ul><ul><ul><li>Thrombocytosis </li></ul></ul><ul><ul><li>Normochromic/normocytic anemia </li></ul></ul><ul><ul><li>Normal complement levels (usually) </li></ul></ul>
  17. 18. C-ANCA  PR3
  18. 19. Wegener’s <ul><li>Granulomatous vasculitis of the upper and lower respiratory tracts together with glomerulonephritis. </li></ul><ul><li>Prevalence is 3/100,000, very rare in blacks. M:F=1:1 </li></ul><ul><li>Mean age of onset = 40 (but age of onset can vary widely) </li></ul>
  19. 20. Wegener’s <ul><li>Pathogenesis: </li></ul><ul><ul><li>Necrotizing vasculitis of small arteries and veins with granuloma formation (either intra- or extravascular). </li></ul></ul><ul><ul><li>Lung involvement typically appears as multiple bilateral, nodular cavitary infiltrates. On biopsy they reveal typical necrotizing granulomatous vasculitis. </li></ul></ul><ul><ul><li>Upper airway lesions (especially sinuses and nasopharynx) reveal inflammation, necrosis and granuloma formation. </li></ul></ul><ul><ul><li>Renal involvement can be focal and segmental glomerulitis early in the disease but typically progresses to RPGN. RARELY are granulomas seen on renal biopsy. </li></ul></ul>
  20. 21. Wegener’s <ul><li>Presentation </li></ul><ul><ul><li>95% have upper airway involvement </li></ul></ul><ul><ul><ul><li>Paranasal sinus pain </li></ul></ul></ul><ul><ul><ul><li>Purulent or bloody nasal discharge with or without nasal mucosal ulceration. </li></ul></ul></ul><ul><ul><ul><li>Nasal septal perforation can occur leading to saddle nose deformity. </li></ul></ul></ul><ul><ul><ul><li>Serous otitis media can occur as a result of blockage of eustachian tube. </li></ul></ul></ul><ul><ul><ul><li>16% will have subglottic tracheal stenosis (from active disease or scarring) which can cause airway obstruction. </li></ul></ul></ul>
  21. 22. Wegener’s <ul><li>Presentation </li></ul><ul><ul><li>Pulmonary involvement in 85-90% </li></ul></ul><ul><ul><ul><li>Cough, hemoptysis, dyspnea, chest discomfort. </li></ul></ul></ul><ul><ul><ul><li>Endo-bronchial disease (from active disease or scarring) can leads to obstruction with atelectasis </li></ul></ul></ul><ul><ul><li>Renal involvement dominates the clinical picture </li></ul></ul><ul><ul><ul><li>If left untreated, it accounts directly or indirectly for most mortality of the disease. </li></ul></ul></ul>
  22. 23. Wegener’s <ul><li>Diagnosis </li></ul><ul><ul><li>Demonstration of necrotizing granulomatous vasculitis on tissue biopsy in a patient with compatible clinical features. </li></ul></ul><ul><ul><ul><li>Pulmonary tissue biopsy offers the highest diagnostic yield. </li></ul></ul></ul><ul><ul><ul><li>Renal biopsy can confirm pauci-immune glomerulonephritis. </li></ul></ul></ul><ul><ul><ul><li>Upper airway tissue biopsy usually shows granulomatous inflammation with necrosis but may or may not show vasculitis. </li></ul></ul></ul>
  23. 24. Wegener’s <ul><li>Treatment </li></ul><ul><ul><li>Glucocorticoids (predisone 1mg/kg/day) should be started for symptomatic improvement and then tapered over 6 months. </li></ul></ul><ul><ul><li>Cyclophosphamide (2mg/kg/day) </li></ul></ul><ul><ul><ul><li>Monitor leukocyte count to adjust dose to maintain count above 3000/microL (neutrophile count of 1500). Gives you clinical remission without severe leukopenia and associated infectious risk. </li></ul></ul></ul>
  24. 25. Wegener’s <ul><li>Treatment </li></ul><ul><ul><li>Relapse occurs in about 25% of patients. </li></ul></ul><ul><ul><ul><li>Treatment for relapse is the same (goal is to achieve remission again). </li></ul></ul></ul><ul><ul><ul><li>Methotrexate or azathioprine can be given after remission is achieved and cyclophosphamide is stopped to maintain remission in patients that do relapse. </li></ul></ul></ul>
  25. 26. P-ANCA  MPO
  26. 27. Churg-Strauss <ul><li>AKA allergic angiitis and granulomatosis . </li></ul><ul><li>Asthma </li></ul><ul><li>Peripheral and tissue eosinophilia </li></ul><ul><li>Extravascular granuloma formation </li></ul><ul><li>Vasculitis of multiple organ systems. </li></ul>
  27. 28. Churg-Strauss <ul><li>Incidence is estimated at 1 in 3 million. </li></ul><ul><li>Can occur at any age (not documented in infants). </li></ul><ul><li>Mean age is 48yrs. </li></ul><ul><li>M:F ratio= 1:1.2 </li></ul>
  28. 29. Churg-Strauss <ul><li>Granulomatous reaction and eosinophil infiltration can occur in any organ in the body, but the lungs predominate. Other areas involved include: </li></ul><ul><ul><li>Skin </li></ul></ul><ul><ul><li>Cardiovascular system </li></ul></ul><ul><ul><li>Kidney </li></ul></ul><ul><ul><li>Peripheral nervous system </li></ul></ul><ul><ul><li>Gastrointestinal tract </li></ul></ul>
  29. 30. Churg-Strauss <ul><li>Presentation </li></ul><ul><ul><li>Pulmonary findings clearly dominate clinical picture </li></ul></ul><ul><ul><ul><li>Severe asthma attacks and presence of pulmonary infiltrates. </li></ul></ul></ul><ul><ul><ul><li>Mononeuritis multiplex </li></ul></ul></ul><ul><ul><ul><li>Allergic rhinitis and sinusitis </li></ul></ul></ul><ul><ul><li>Heart disease (14%) = Most frequent cause of death. </li></ul></ul>
  30. 31. Churg-Strauss <ul><li>Presentation </li></ul><ul><ul><li>Skin involvement 51% </li></ul></ul><ul><ul><ul><li>Include purpura in addition to cutaneous and subcutaneous nodules. </li></ul></ul></ul><ul><ul><li>Renal involvement 45% </li></ul></ul><ul><ul><ul><li>Less common than seen in Wegener’s and MPA </li></ul></ul></ul><ul><ul><ul><li>Severe glomerulonephritis </li></ul></ul></ul>
  31. 32. Churg-Strauss <ul><li>Biopsy of affected tissue (lung). </li></ul><ul><ul><li>Microgranulomas , fibrinoid necrosis and throbosis of small arteries and veins ( necrotizing vasculitis ) with eosinophilic infiltrates. </li></ul></ul><ul><li>Classification criteria (4 of 6 criteria is 85% Sensitive and 99.7% specific) </li></ul><ul><ul><li>Asthma </li></ul></ul><ul><ul><li>Eosinophilia >10% </li></ul></ul><ul><ul><li>Mono- or polyneuropathy </li></ul></ul><ul><ul><li>Migratory or transitory pulm infiltrates </li></ul></ul><ul><ul><li>Paranasal sinus abnormality </li></ul></ul><ul><ul><li>Extravascular eosinophils on biopsy </li></ul></ul>
  32. 33. Churg-Strauss <ul><li>Treatment </li></ul><ul><ul><li>Glucocorticoids; high dose. </li></ul></ul><ul><ul><ul><li>Attempt to taper. Asthma makes tapering difficult, patients may need to be maintained on low-dose prednisone for years after clinical recovery from vasculitis to control asthma. </li></ul></ul></ul><ul><ul><li>Patients who do not respond to glucocorticoids alone, can be treated with cyclophosphamide and prednisone (similar to Wegener’s treatment). </li></ul></ul>
  33. 34. P-ANCA  MPO
  34. 35. Microscopic Polyangiitis. <ul><li>Necrotizing vasculitis with few or no immune complexes affecting small vessels (capillaries, venules, or arterioles). </li></ul><ul><li>Glomerulonephritis and pulmonary capillaritis are common in Microscopic Polyangiitis. ( NO pulmonary capillaritis in PAN). </li></ul><ul><li>Not associated with HBV like PAN </li></ul><ul><li>ABSENCE of granulomatous inflammation differentiates this disease from Wegener’s granulomatosis. </li></ul>
  35. 36. Microscopic Polyangiitis <ul><li>Incidence not really established because it use to be included in PAN. </li></ul><ul><li>Age of onset is about 57 years. </li></ul><ul><li>Slightly more occurrence in males than females. </li></ul>
  36. 37. Microscopic Polyangiitis <ul><li>Presentation </li></ul><ul><ul><li>Vascular lesion is a necrotizing inflammation of capillaries, venules, as well as small and medium-sized arteries. </li></ul></ul><ul><ul><li>Rare immunoglobulin deposition seen in the vascular lesions. </li></ul></ul><ul><ul><li>Renal lesion is identical to that of Wegener’s granulomatosis lesion. </li></ul></ul>
  37. 38. Microscopic Polyangiitis <ul><li>Renal involvement 90% </li></ul><ul><ul><li>Glomerulonephritis, often rapidly progressive. </li></ul></ul><ul><ul><li>Can quickly lead to renal failure </li></ul></ul><ul><li>Lung involvement 50% </li></ul><ul><ul><li>Alveolar hemorrhage (12%)= hemoptysis </li></ul></ul><ul><li>Mononeuritis multiplex </li></ul><ul><li>Gastrointestinal tract vasculitis </li></ul><ul><li>Cutaneous vasculitis. </li></ul><ul><li>(upper airway disease and pulmonary nodules are not typically found - if found: suggests Wegener’s) </li></ul>
  38. 39. Microscopic Polyangiitis <ul><li>Diagnosis </li></ul><ul><ul><li>Biopsy of affected tissue. </li></ul></ul><ul><ul><ul><li>Necrotizing pauci-immune inflammation of arterioles, capillaries and venules WITHOUT granulomas or eosinophilic infiltrates . </li></ul></ul></ul><ul><ul><li>ANCA positive </li></ul></ul>
  39. 40. Microscopic Polyangiitis <ul><li>Treatment </li></ul><ul><ul><li>Similar approach to that of Wegener’s. </li></ul></ul><ul><ul><li>Relapse occurs in up to 34% of patients. </li></ul></ul>
  40. 42. Differential Diagnosis for Pulmonary-Renal Syndrome <ul><li>Goodpasture’s Disease </li></ul><ul><li>Systemic Vasculitis </li></ul><ul><ul><li>Wegener’s Granulomatosis </li></ul></ul><ul><ul><li>Microscopic Polyangiitis </li></ul></ul><ul><ul><li>Churg-Strauss syndrome </li></ul></ul><ul><ul><li>Cryoglobulinemia </li></ul></ul><ul><ul><li>Henoch-Schonlein Purpura </li></ul></ul><ul><li>Connective Tissue Disease </li></ul><ul><ul><li>Polymyositis/Dermatomyositis </li></ul></ul><ul><ul><li>Progressive Systemic Sclerosis </li></ul></ul><ul><ul><li>SLE </li></ul></ul><ul><li>Primary Glomerular Disease </li></ul><ul><ul><li>IgA nephropathy </li></ul></ul><ul><ul><li>Post-Infectious GN </li></ul></ul><ul><ul><li>Membranoproliferative GN </li></ul></ul>Pleural effusions/Lupus Pneumonitis + SLE GN + ASO titer, can continue to have pulmonary symptoms by the time renal symptoms manifest.
  41. 44. references <ul><li>Harrison et. al, (2005), Principles of Internal Medicine, 16 th Edition, McGraw-Hill, NY </li></ul><ul><li>Jennette J. (1997), Small Vessel Vasculitis. New England Journal of Medicine; 21: 1512-1523. </li></ul><ul><li>PubMed: Renal-Pulmonary Syndrome. Retrieved on (9/1/09) from: http://www.ncbi.nlm.nih.gov/pubmed/15905974 </li></ul><ul><li>Sabatine, Marc S,(2008) Pocket Medicine, 3 rd Edition, Lippincott Williams &Wilkins, Philadelphia </li></ul><ul><li>Toy, et.al. (2007), Case Files: Internal Medicine, Second Edition, McGraw-Hill, NY </li></ul>
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