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STEP1 Renal
ANATOMY & PHYSIOLOGY Top High-Yield Topics Kidney Anatomy Body Fluid Compartments Glomerular Physiology Glomerular Filtration Barrier Renal Clearance Glomerular Filtration Rate (GFR) Filtration Nephron Physiology Nephron Schematic Free Water Clearance Reabsorption and Secretion Rate Glucose Clearance Amino Acid Clearance Relative Concentrations Along Proximal Tubule Endocrine

Nephritic Syndrome
Author: Medbullets Team

9 Topic updated on 06/18/13 9:22am

Overview Nephritic syndrome is an inflammatory process General nephritic syndrome disorder findings include symptoms periorbital puffiness due to decreased plasma oncotic pressure physical exam hypertension studies azotemia oliguria with BUN:Cr ratio >15 proteinuria (< 3.5 g/day) hematuria and RBC casts in urine RBCs are dysmophic key finding to differentiate nephritic from nephrotic syndrome Acute poststreptococcal glomerulonephritis Introduction prototype acute glomerulonephritis classically occurs in children weeks after an infection with group A hemolytic streptococci (S. pyogenes) most commonly from a skin infection (e.g. impetigo) and less commonly due to pharyngitis but can follow any viral or bacteria infection disease caused by antigen-antibody complex on the glomerular membrane
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Presentation general presentation of nephritic syndrome (above) Evaluation elevated ASO decreased serum C3 immunofluorescence shows granular subepithelial deposits composed of IgG, IgM, and C3 Immunofluorescence pattern Granular Location of IC deposition Subepithelial Compliment type activated Alternative

Light microscopy shows: enlarged and hypercellular glomeruli neutrophilic infiltrate Prognosis younger patients have better prognosis usually self- limited and treatment not required because immune complex driven, does not improve with antibiotics Rapidly progressive (crescentic) glomerulonephritis (RPGN) Progresses to renal failure within weeks or months May be part of PIGN or other systemic disease Many disease processes may result in this pattern Goodpasture syndrome type II hypersensitivity (does not involve immune complex deposition) antibodies to GBM resulting in a linear immunofluorescence pattern antibodies to the alveolar basement membrane result in hemoptysis and lung disease male-dominant disease pauci immune processes Wegener's granulomatosis c-ANCA microscopic polyarteritis p-ANCA polyarteritis nodosa Churg-Strauss
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immune complex disorders Henoch-Schonlein purpura cryoglobinemia hypersensitivity vasculitis SLE Light microscopy and immunofluorescence crescent-moon shape crescent consists of fibrin and plasma proteins with glomerular parietal cells, monocytes, and macrophages Presents with symptoms of nerphritic syndrome (above) hemoptysis present if Goodpasture's is the cause Treat with prednisone or plamapheresis Diffuse proliferative glomerulonephritis Most common type of kidney disease in SLE patients Most common cause of death in SLE Due to DNA-anti-DNA immune complexes Immunofluorescence pattern Granular Location of IC deposition Subendothelial Compliment type activated Classical

Microscopic appearance "wire looping" of capillaries hyaline thrombi in capillary lumen Can present as nephrotic syndrome Berger's disease (IgA glomerulonephropathy) Most common worldwide nephropathy not to be confused with Buerger's disease (vasculitis) Due to IgA immune complexes in mesangium serum IgA increased in 40% immunofluorescent stains show IgA
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overlapping features with Henoch Schonlein's purpura (IgA vasculitis) Immunofluorescence pattern Granular Location of IC deposition Mesangial Compliment type activated Alternative

Presents with symptoms of general nephritic syndrome (above) concurrently or within several days of infection 25% progress to renal failure May have flairs following immune system activation due to URI or gastroenteritis Prednisone for acute flares but it does not halt disease progression

Multiple myeloma Renal involvement: Increased production of light chain leads to tubular plugging by Bence-Jones proteins Secondary hypercalcemia also contributes to development of "myeloma kidney" Myeloma cells can directly invade kidney Defect in antibody production leaves patient susceptible to chronic infections by encapsulated bacteria (e.g., E. Coli) leads to chronic renal failure Treat underlying myeloma

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0) (M1.RL.11) Multiple patients present to your office with hematuria following an outbreak of Group A Streptococcus. Biopsy

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reveals that all of the patients have the same disease, characterized by large, hypercellular glomeruli with neutrophil infiltration. Which patient has the best prognosis? Review Topic 1. 2. 3. 4. 5. 65-year-old nulliparous woman 50-year-old man with a history of strep infection 8-year-old boy who undergoes no treatment 38-year-old man with sickle cell trait 18-year-old man treated with corticosteroids

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