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Proteinuria
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Proteinuria

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  • it would be great to start the lecture with:
    http://www.hulu.com/watch/17417/juno-pregnancy-test

    Probably the best U/A ever in a movie.

    Point is (and I do have one) a normal value defined by detection limits is a bad way to define normal





























































































































  • Transcript

    • 1. Proteinuria SIMON E. PRINCE, D.O., F.A.C.P., F.A.S.N. Clinical Assistant Professor of Medicine NYU School of Medicine Thursday, March 12, 2009
    • 2. Huge range in clinically significant proteinuria the upper limit of urinary protein is 250-300 mg of protein a day proteinuria a log unit lower (25-30 mg) is clinically significant proteinuria a log unit higher (2,500 to 3,000 mg) are commonly encountered Thursday, March 12, 2009
    • 3. The normal amount of protein was defined by the detection limits of a dip-stick U/A. Trace proteinuria on a dip, usually corresponds to 300 mg of protein on a 24-hour collection. Thursday, March 12, 2009
    • 4. this lecture will trace proteinuria from the tiniest microscopic albuminuria through normal up to tens of grams found in nephrotic syndrome. Thursday, March 12, 2009
    • 5. cells and large proteins play the peas Plasma is filtered freely Peas in the urine (e.g. proteinuria, hematuria) indicate a tear in the colander (damaged glomerulus) Thursday, March 12, 2009
    • 6. urinary space epithelial cell (podocyte) foot process basement membrain endothelial cell capillary lumen Thursday, March 12, 2009
    • 7. the glomerulus is remarkably efficient at preventing the loss of protein in the urine normal 24-hour urine albumin is less than 300 mg/day normal albumin level 4.0 g/dL normal renal plasma flow is 600 mg/min Thursday, March 12, 2009
    • 8. Thursday, March 12, 2009
    • 9. 4g 600 mL plasma 1 dL 1440 min dL plasma min 100 mL 24 hrs Thursday, March 12, 2009
    • 10. 4g 600 mL plasma 1 dL 1440 min dL plasma min 100 mL 24 hrs Thursday, March 12, 2009
    • 11. 4g 600 mL plasma 1 dL 1440 min dL plasma min 100 mL 24 hrs Thursday, March 12, 2009
    • 12. 4g 600 mL plasma 1 dL 1440 min dL plasma min 100 mL 24 hrs Thursday, March 12, 2009
    • 13. 4g 600 mL plasma 1 dL 1440 min dL plasma min 100 mL 24 hrs Thursday, March 12, 2009
    • 14. 4g 600 mL plasma 1 dL 1440 min dL plasma min 100 mL 24 hrs 34,560 g of Albumin flow through the kidney each day Thursday, March 12, 2009
    • 15. less than 0.3 g of albumin ends up in the urine, or 0.3 x 100 = 0.0008% 34,560 Thursday, March 12, 2009
    • 16. More than 0.0008% of the albumin actually passes the glomerular barrier BUT it is absorbed by the proximal tubule cells and metabolized Thursday, March 12, 2009
    • 17. Urine Dipstick Most common method of testing for proteinuria It is a plastic strip impregnated with a pH indicator which changes color in presence of proteins, due to a pH change Intensity of the color correlates with the concentration of protein Mainly albumin detected Thursday, March 12, 2009
    • 18. False Positive Dipstick Very alkaline urine (some UTIs) Pigmented urine (hematuria) Very concentrated urine (Usg >1.030) Drug interference (chlorhexidine) Contamination Thursday, March 12, 2009
    • 19. False Negative Dipstick The protein is not albumin (i.e. Multiple Myeloma) Urine is too dilute (Usg <1.005) Thursday, March 12, 2009
    • 20. Classification of Proteinuria Tubular Proteinuria Overflow Proteinuria Glomerular Proteinuria Microalbuminuria Selective Proteinuria Non-selective proteinuria Thursday, March 12, 2009
    • 21. Tubular Proteinuria Tubular dysfunction leads to small MW proteins (beta2 MG, lysozyme, light chains, AAs) freely filtered but not able to be reabsorbed. NOT detected on dipstick Thursday, March 12, 2009
    • 22. Overflow Proteinuria Occurs when the concentration of one of the small MW proteins is so high that the filtered load exceeds the tubular reabsorptive capacity Thursday, March 12, 2009
    • 23. Causes of Overflow Proteinuria Multiple Myeloma Amyoidosis Light Chain Disease Hemoglobinuria Myoglobinuria Thursday, March 12, 2009
    • 24. Glomerular Proteinuria Glomerular dysfunction at the level of the GBM Most common and clinically significant form of proteinuria Thursday, March 12, 2009
    • 25. Microalbuminuria persistent trace proteinuria which is invisible on conventional urinalysis (dipstick detects urine albumin >300 mg/day) Microalbuminuria is defined as urinary albumin excretion: 30-300 mg/day 20-200 mcg/min Thursday, March 12, 2009
    • 26. Why is Microalbuminuria important? Predicts the development of nephropathy in Diabetes Correlates with mortality in diabetics and hypertensives Thursday, March 12, 2009
    • 27. How to treat Microalbuminuria Strict blood pressure control goal at least <130/80 mmHg with ACE-inhibitors and/or Angiotensin Receptor Blockers (or Renin Inhibitors) Strict Glycemic control in Diabetics Thursday, March 12, 2009
    • 28. Types of Glomerular Proteinuria SELECTIVE NON-SELECTIVE PROTEINURIA PROTEINURIA Only intermediate- Range of different sized (<100kDa) protein sized proteins (albumin, proteins leak transferrin) leaks through including through the larger proteins glomerulus (Immunoglobulins) Thursday, March 12, 2009
    • 29. Edema The palpable swelling produced by an expansion of the interstitial fluid volume Thursday, March 12, 2009
    • 30. Pathophysiology Alteration in the capillary hemodynamics that favors the movement of fluid from the vascular space into the interstitium Retention of dietary or intravenous Na+ and H2O by the kidneys Thursday, March 12, 2009
    • 31. Edema requires change in Starling’s Forces Elevated capillary hydraulic pressure Increased capillary permeability Increased interstitial oncotic pressure Reduction in plasma oncotic pressure Thursday, March 12, 2009
    • 32. Thursday, March 12, 2009
    • 33. Thursday, March 12, 2009
    • 34. Increased capillary blood pressure blood ↑capillary pressure Causes: •Elevated plasma volume driving fluid into ↑force •Increased venous pressure interstitium - Increased general venous pressure - Increased local venous ↑formation of pressure interstitial fluid •Arteriolar dilation When greater than lymphatic compensatory return edema Thursday, March 12, 2009
    • 35. Decreased plasma colloid osmotic pressure ↓ plasma colloid Causes of Hypoproteinemia: osmotic pressure ―Decrease of protein production ↓force drawing water back into capillary from interstitium ―Excessive loss of protein ↑formation of ―Elevated catabolism of protein interstitial fluid edema Thursday, March 12, 2009
    • 36. Increased capillary permeability permeability ↑capillary Causes: Filtration of more protein from •Inflammation capillary to interstitium •Infection •Burn ↓Plasma colloid osmotic pressure •Allergic response •Trauma ↑formation of interstitial fluid •Anoxia •Acidosis edema Thursday, March 12, 2009
    • 37. The three great edematous states Congestive Heart Failure Cirrhosis Nephrotic Syndrome Thursday, March 12, 2009
    • 38. Heart failure Thursday, March 12, 2009
    • 39. Congestive Heart Failure SYSTOLIC DIASTOLIC Thursday, March 12, 2009
    • 40. Systolic Dysfunction Decreased myocardial contractility Thursday, March 12, 2009
    • 41. Systolic Failure Cardiac Output (Q) = SV x HR Decreased stroke volume leads to decreased cardiac output and increased LVEDP Increasing the capillary hydraulic pressure Decreased CO triggers renal Na+ and H2O retention further increasing end- diastolic pressure and volume Thursday, March 12, 2009
    • 42. Diastolic Dysfunction Stroke Volume is preserved Increased LV diastolic pressure at any volume caused by a decrease in LV compliance Thursday, March 12, 2009
    • 43. Thursday, March 12, 2009
    • 44. question Thursday, March 12, 2009
    • 45. question • Why can congestive heart failure make edema? Thursday, March 12, 2009
    • 46. question • Why can congestive heart failure make edema? – ↑General venous pressure – ↓Plasma colloid osmotic pressure because of dilution of blood – Dysfunction of lymphatic return because of increased venous pressure – ↓GFR – ↑Activation of the Renin-Angiotensin-Aldosterone axis – ↑ADH Thursday, March 12, 2009
    • 47. Systolic vs Diastolic Thursday, March 12, 2009
    • 48. Cirrhosis Thursday, March 12, 2009
    • 49. Cirrhosis Increased capillary permeability (vasodilitation) leading to RAS activation and renal Na+ and H2O retention Increased plasma volume and hydraulic pressure Decreased oncotic pressure (hypoalbuminemia) Thursday, March 12, 2009
    • 50. Nephrotic Syndrome Thursday, March 12, 2009
    • 51. NEPHROTIC SYNDROME Proteinuria >3.5 g/day Generalized edema Hypoalbuminemia Hyperlipidemia Thursday, March 12, 2009
    • 52. Nephrotic Syndrome Heavy urinary loss of albumin, leads to hypoalbuminemia Reduced intravascular albumin results in decreased oncotic pressure Loss of fluid from intravascular compartment activates the RAS (under- filling hypothesis) Thursday, March 12, 2009
    • 53. Thursday, March 12, 2009
    • 54. Thursday, March 12, 2009
    • 55. Why the Hyperlipidemia? Increased hepatic synthesis cannot fully compensate for the severe urinary loss of most proteins... Except for lipoproteins which are retained. Thursday, March 12, 2009
    • 56. Hypercoagulable state Loss of proteins which are anti-coagulants such as anti-thrombin III, Protein C and S... can lead to a hypercoaguable state. Classically renal vein thrombosis (most often associated with Membranous Nephropathy) Thursday, March 12, 2009
    • 57. Causes of Nephrotic Syndrome PRIMARY (Idiopathic) Thursday, March 12, 2009
    • 58. Secondary Causes of NS Systemic Diseases- Diabetes, Amyloidosis, Multiple Myeloma Infectious Diseases- Hepatitis, HIV Immunologic Diseases- SLE Drugs- NSAIDs, gold, lithium, Captopril Neoplastic- solid tumors, leukemia Thursday, March 12, 2009
    • 59. How to Differentiate types of Nephrotic Syndrome History PMHx, Family Hx, Medications Physical Labs Renal Biopsy Thursday, March 12, 2009
    • 60. What tests to order? Comprehensive Metabolic Lipid Panel CBC HbA1c Serology based on clues ANA, dsDNA, anti-Sm ANCAs, anti-GBM Ab Complements HIV testing Hepatitis Serologies Serum protein and urine electrophoresis Thursday, March 12, 2009
    • 61. Renal Sonogram Helps with structure not function Thursday, March 12, 2009
    • 62. Renal Biopsy Thursday, March 12, 2009
    • 63. Glomerular Diseases NEPHROTIC NEPHRITIC Thursday, March 12, 2009
    • 64. NEPHROTIC Urinary Sediment: “bland” Heavy proteinuria Possible lipuria Rare-few cells/ casts HTN less frequent Relatively preserved renal function Thursday, March 12, 2009
    • 65. Common causes of Primary Nephrotic Syndrome Minimal Change Disease Focal Segmental Glomerulosclerosis Membranous Nephropathy Thursday, March 12, 2009
    • 66. Minimal Change Disease Thursday, March 12, 2009
    • 67. Minimal Change Disease Named because no changes seen on Light Microscopy (AKA Nil disease or lipoid nephropathy) Thursday, March 12, 2009
    • 68. Minimal Change Disease Most common cause of NS in children 90% in children <10 years old >50% cases in older children 10-15% adult cases Thursday, March 12, 2009
    • 69. Causes of MCD Primary or Idiopathic (most common) Secondary Drugs: NSAIDs, rifampin, PCN, Lithium Heme Malignancy: Hodgkins (most common), NHL, Leukemia Toxins: Mercury, lead, bee stings Infectious: Mononucleosis, HIV Obesity Thursday, March 12, 2009
    • 70. Signs and Symptoms of MCD Massive edema Ascites Pleural and Pericardial effusions HTN uncommon Hematuria uncommon Renal function impairment uncommon Thursday, March 12, 2009
    • 71. Urinary Findings in Minimal Change Disease Thursday, March 12, 2009
    • 72. Total FP effacement Characteristic EM Thursday, March 12, 2009
    • 73. Treatment of MCD Steroids are mainstay of therapy Complete Remission ~90% Children remit more rapidly- 50% within 2 wks; nearly all by 8 weeks Adults can take 12-16 wks DOSE: 1 mg/kg/d Prednisone or 2mg/kg/qod DURATION: 8-16 weeks (continue 1-2 wks after remission) then taper Thursday, March 12, 2009
    • 74. COMPLETE REMISSION: <300 mg/d proteinuria PARTIAL REMISSION: decrease >50% proteinuria RELAPSE: return to >3.5 g/d in pt who was in complete or partial remission STEROID DEPENDENCE: need to cont. Tx to maintain remission STEROID RESISTANCE: little or no reduction after 12-16 wks of steroid therapy Thursday, March 12, 2009
    • 75. Alternative Therapies for MCD Alkylating agents (Cyclophosphamide, Chlorambucil) CellCept (MMF) Azathioprine (Imuran) Cyclosporin (Neoral) FK506 (Prograf) Levamisole Thursday, March 12, 2009
    • 76. Focal Segmental Glomerulosclerosis Thursday, March 12, 2009
    • 77. FSGS Most common cause of nephrotic syndrome in adults especially in AA FOCAL: <50 % glomeruli effected SEGMENTAL: sclerosis with hyalinosis involving portions of the glomerulus Primary- Idiopathic most common Thursday, March 12, 2009
    • 78. Secondary FSGS Obesity OSA Sickle Cell HIV/AIDS Hematologic malignancies Decreased nephron number Chronic vesicoureteral reflux DRUGS: Lithium, Heroin, alpha-IF Thursday, March 12, 2009
    • 79. Clinical Features of FSGS Proteinuria- often nephrotic Can range from 1 gram to 20-30 g/d HTN common: ~45-65% Microscopic Hematuria 30-50% Decreased GFR at presentation 35-50% Normocomplementemia Thursday, March 12, 2009
    • 80. Light Microscopy in FSGS Thursday, March 12, 2009
    • 81. Renal Biopsy in FSGS LM: Sclerosis in segments (focal) of the glomeruli (especially juxtaglomerular) Tubulointerstitial fibrosis IF: non-specific “trapping” EM: diffuse loss of podocyte foot processes Thursday, March 12, 2009
    • 82. Treatment of FSGS Immunosuppressive Tx for Primary FSGS CORTICOSTEROIDS Similar to MCD but longer duration required with longer tapering Second line: Cyclosporin or Cyclophosphamide Third line: CellCept or Prograf Thursday, March 12, 2009
    • 83. Membranous Nephropathy Thursday, March 12, 2009
    • 84. Characteristics of MN Among most common causes of NS especially white males >40 yo Nephrotic Syndrome: 60-70% others subnephrotic Majority normal CrCl 10-20% decreased CrCl HTN uncommon at presentation Urine sediment often bland 30-40% microscopic hematuria Renal Vein Thrombosis seen in up to 20% cases Thursday, March 12, 2009
    • 85. Causes of MN Primary- Idiopathic Secondary NEOPLASM: solid organ, Lymphoma, Leukemia INFECTIOUS: Malaria, Hepatitis B/C, Syphilis, Leprosy DRUGS: Penicillamine, gold IMMUNOLOGIC: SLE, MCTD Sickle Cell Disease Thursday, March 12, 2009
    • 86. Light Microscopy in MN Early MN appears normal Later increased size and # of immune complexes in subEPIthelial space produces thickened GBMs Thursday, March 12, 2009
    • 87. Special Stain Classic “spikes” can be seen as complexes accumulate and disrupt the GBM Thursday, March 12, 2009
    • 88. IF MN Stains positive for IgG and C3 in a typical “beaded appearance” Thursday, March 12, 2009
    • 89. EM MN SUBEPITHELIAL DEPOSITS Stage I deposits subepi GBM Stage II deposits partially surrouned by new BM Stage III deposits fully surrounded Stage IV deposits lucent Thursday, March 12, 2009
    • 90. Therapy in MN Non-specific vs. Immunosuppression Thursday, March 12, 2009
    • 91. Non-Immunosuppressive Therapy for Proteinuria BlOOD PRESSURE BLOOD PRESSURE BLOOD PRESSURE oh yeah... don’t forget.. BLOOD PRESSURE Thursday, March 12, 2009
    • 92. Blood Pressure and Proteinuria Goal BP: < 130/80 mmHg or <125/75 mmHg if >1 gram/d proteinuria Preferred medications: ACE inhibitors Angiotensin Receptor Blockers Renin Inhibitors Aldosterone Antagonists Non-Dihydropyridine CCBs Thursday, March 12, 2009
    • 93. Other non-specific therapy for proteinuria Tight glycemic control in DM Goal HbA1c < 7 Dietary protein restriction 0.6 g / kg/ day Statin based lipid therapy Goal LDL at least <100 Thursday, March 12, 2009
    • 94. Immunosupression in MN More intensive than in MCD or FSGS Who should we treat? Thursday, March 12, 2009
    • 95. Rule of Thirds 1/3 Spontaneously Remit 1/3 Partially Remit 1/3 Progress towards ESRD Thursday, March 12, 2009
    • 96. Who’s at Risk for Progression? LOW RISK Normal Serum Creatinine Proteinuria <4grams/d over 6 month observation MEDIUM RISK Near normal Creatinine / CrCl Proteinuria 4-8 grams/d HIGH RISK Elevated Serum creatinine Persitently high grade proteinuria >8 grams/d Poor prognositic signs on renal biopsy Thursday, March 12, 2009
    • 97. LOW AND HIGH RISK No immunosuppression Non-specific anti-proteinuric strategy is most prudent Both groups: Risk > Benefit MEDIUM RISK Receive immunosuppression to attempt to achieve remission Thursday, March 12, 2009
    • 98. Immunosuppression in MN Steroids alone are NOT recommended FIRST LINE: Corticosteroids + Cytotoxic agent (Cyclophosphamide or chlorambucil) SECOND LINE: Cyclosporin ALTERNATIVES: CellCept, Prograf, Azathioprine, Rituxan, IvIg Thursday, March 12, 2009
    • 99. Diabetic Nephropathy Thursday, March 12, 2009
    • 100. Diabetic Nephropathy Most common type of Secondary NS Can occur in both Type I and II DM Prognosis can be improved with aggressive monitoring and therapy Thursday, March 12, 2009
    • 101. Which diabetics are at risk for DN? Poor glycemic control (inc HbA1c) Suboptimal BP control Genetic factors (Family h/o ESRD) Race (African Americans higher risk) Age Smoking ?OCP Thursday, March 12, 2009
    • 102. Stages of DN STAGE 1 Hyperfiltration Elevated CrCl Glomerular Hypertrophy Thursday, March 12, 2009
    • 103. Stage II DN Microalbuminuria UAE 30-300 mg/d Typically begins >5 yrs after overt DM diagnosed compared with normoalbuminuric patients, those with microalbuminuria are at 300-400% increased risk of ESRD Thursday, March 12, 2009
    • 104. Stage III DM Overt proteinuria UAE >300 mg/day Starts about 10-20 yrs after DM onset BP elevated Glomerular lesion worsens Thursday, March 12, 2009
    • 105. Stage IV DM Progressive nephropathy After 15-25 yrs of DM Dipstick positive proteinuria HTN 75% Reduced GFR Hyperlipidemia Retinopathy and autonomic neuropathy Thursday, March 12, 2009
    • 106. Stage V DN ESRD Progression to ESRD 5-15 yrs after the development of overt proteinuria Thursday, March 12, 2009
    • 107. Pathogenesis of the structural injury in DN Hyperglycemia Accumulation of glycosylation products increased advanced glycation end-products (AGE) stimulate synthesis of various growth factors as well as causing cytokine mediated damage and oxidative stress Intraglomerular HTN Systemic HTN Thursday, March 12, 2009
    • 108. Thursday, March 12, 2009
    • 109. Pathology of DN Thursday, March 12, 2009
    • 110. Pathologic Findings in DN GBM thickening Kimmelstiel-Wilson lesion (nodular sclerosis) Tubulointerstitial fibrosis Thursday, March 12, 2009
    • 111. Treatment of DN Tight glycemic control Tight BP control Lipid Therapy Smoking Cessation Weight loss Thursday, March 12, 2009
    • 112. Case Presentation Thursday, March 12, 2009
    • 113. Case Presentation 70 yr old affluent white male CC: Swelling in Legs Thursday, March 12, 2009
    • 114. What do you want next? Past Medical History Family History Social History Medications Physical Exam Anything Else? Thursday, March 12, 2009
    • 115. History PMHx: HTN, GERD, Hyperlipidemia, OA Social Hx: Married, worked in finance, Denies tobacco or illicit drug use, Social EtOH Family Hx: No Kidney Disease, ESRD Medications: Amlodipine, Prilosec, Lipitor, Motrin Thursday, March 12, 2009
    • 116. Physical Exam VS: BP 134/76 mmHg P 96 R 14 HEENT: NCAT OP Clear Neck: Supple no JVD no bruits Chest: CTA B/L Cor: S1 S2 RRR no M/R/G Abd: Soft NT ND +BS, no HSM Ext: +2 pitting edema B/L mild Right > Left Anything else? Thursday, March 12, 2009
    • 117. Labs What do you want to order? Thursday, March 12, 2009
    • 118. Lab Values CBC: WBC 7.6 Hb 11.9 PLT 195 CMP: Na 138 K 4.3 Cl 108 HCO3 23 BUN 11 Creat 1.4 TBili 0.6 AST 22 ALT 25 AlkP 106 TP 6.2 Alb 3.0 Cholesterol: Chol 222 HDL 29 LDL 168 UA: +3 protein, trace blood, no casts, no LE or nitrates Want anything else? Thursday, March 12, 2009
    • 119. Other Lab Tests to consider SPEP/ IEP / UPEP Hepatitis Panel Compliments, Serology 24 Hour urine Creatinine Clearance and total proteinuria (U TP/Creat) Thursday, March 12, 2009
    • 120. 24 Hour urine collection Creatinine Clearance 69 ml/min Total proteinuria: 3,890 mg Thursday, March 12, 2009
    • 121. What next? Thursday, March 12, 2009
    • 122. Renal Biopsy! Thursday, March 12, 2009
    • 123. Biopsy Thursday, March 12, 2009
    • 124. Biopsy Findings Thursday, March 12, 2009
    • 125. Diagnosis? Thursday, March 12, 2009
    • 126. Membranous Nephropathy Thursday, March 12, 2009
    • 127. What Should We do Next? How Should we Treat? What is the prognosis? Thursday, March 12, 2009
    • 128. FIN Simon Prince, DO, FACP, FASN Assistant Professor of Medicine; NYU School of Medicine email: sprince@nsneph.com www.nsneph.blogspot.com Thursday, March 12, 2009

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