Rosen & Barkin's 5-Minute Emergency Medicine Consult (303 page)

• Postinfectious:
  
  • Poststreptococcal glomerulonephritis (PSGN):
    
    • Occurs 7–21 days after
      Streptococcal pharyngitis
      or skin infection
      
    • Highest prevalence in ages 2–14 and the elderly
      
    • Male predominance
      
    • Ranges from asymptomatic hematuria to oliguric renal failure
      
  • Can follow other bacterial, fungal, viral, or parasitic infections
    
• IgA nephropathy (Berger disease):
  
  • Most common in men in the 3rd and 4th decades of life
    
  • Possibly related to increased production of IgA after infection usually a URI
    
  • Henoch–Schönlein purpura (HSP) has IgA nephropathy but affects a younger age and has systemic symptoms
    
• Rapidly progressive glomerulonephritis (RPGN):
  
  • Can destroy renal function in days
    
  • Crescentic deposits in glomeruli destroy function.
    
  • Pauci-immune (small vessel vasculitides):
    
    • Often antineutrophil cytoplasmic antibody (ANCA)-positive
      
    • Can involve other areas (i.e., lungs, skin)
      
    • Wegener granulomatosis
      
    • Microscopic polyangiitis
      
    • Churg–Strauss syndrome
      
  • Immune complex deposits:
    
    • Postinfectious
      
    • Endocarditis associated
      
    • Systemic disease (i.e., systemic lupus erythematosus [SLE], HSP)
      
  • Anti-glomerular basement membrane (GBM) deposits:
    
    • Older patients of age >60
      
    • Goodpasture disease with pulmonary involvement
      
• Membranoproliferative glomerulonephritis (MPGN):
  
  • Complement deposits in basement membrane
    
  • Hepatitis C
    
  • Non-Hodgkin lymphoma
    
  • Occult infection
    

DIAGNOSIS

• Cardinal signs:
  
  • Hematuria
    
  • Proteinuria
    
• Edema:
  
  • Owing to renal salt and water retention
    
  • Periorbital
    
  • Ascites
    
  • Pleural effusion
    
• HTN
  
• Oliguria
  
• Azotemia
  
• CHF
  
• Renal failure
  
• Nonspecific manifestations:
  
  • Fatigue
    
  • Weight loss
    
  • Abdominal pain
    
  • Nausea/vomiting
    
• Autoimmune disorders:
  
  • Arthralgias
    
  • Arthritis
    
  • Rash
    
  • Fever
    
• Goodpasture syndrome:
  
  • Hemoptysis
    
• Wegner granulomatosis:
  
  • Purulent rhinorrhea/sinus pain
    
  • Arthritis/arthralgias
    
  • Hemoptysis
    
• HSP:
  
  • Abdominal pain
    
  • Purpura
    
  • Arthritis
    

• Pauci-immune RPGN is common in this population (hematuria, proteinuria, and elevated CR).
  
• Urgent diagnosis and biopsy are indicated as this may progress to ESRD.
  
• Consult nephrology to discuss steroids, cyclophosphamide, and plasma exchange.
  

Urinalysis for:

• Hematuria, proteinuria, and RBC casts
  

• Electrolytes, BUN, Creatinine, GFR:
  
  • Renal function
    
  • Hyperkalemia
    
• Albumin, total protein:
  
  • Varying degrees of hypoalbuminemia depending on clinical process
    
• CBC:
  
  • Anemia secondary to chronic renal disease, neoplasm, Goodpasture, and Wegener
    
  • With or without elevated WBC in infections
    
• PT, PTT:
  
  • Coagulation factors consumed in certain types of GN
    
• Labs to be considered for consultants:
  
  • Cultures—throat, skin, blood
    
  • 24-hr urine collection—protein, urine electrolytes
    
  • Streptozyme or antistreptolysin O titer
    
  • Complement levels (C1, C3, C4, CH
    ₅₀
    )—reduced in PSGN, MPGN, SLE
    
  • ANA, rheumatoid factor—connective tissue diseases
    
  • ESR and CRP inflammatory markers
    
  • Anti-GBM—Goodpasture
    
  • c-ANCA—Wegener; p-ANCA-pauci-immune
    
  • Anti-DNA antibodies (SLE)
    
  • Hepatitis B and C serologies
    
  • HIV
    

• Renal ultrasound (if GFR is decreased):
  
  • Kidney size predictor of potential reversibility of disease, alternative diagnosis (i.e., neoplasm, stone)
    
• Chest radiograph (CXR): Heart size, pulmonary edema, or hemorrhage
  

• Renal biopsy: Discern primary glomerulopathies vs. other causes
  
• Cystoscopy: If concern for bladder neoplasm
  

• Hematologic:
  
  • Sickle cell disease
    
  • Coagulopathy
    
• Renal:
  
  • Infectious
    
  • Malformation
    
  • Neoplasm
    
  • Ischemic
    
  • Trauma
    
  • Vasculitis
    
• Postrenal:
  
  • Mechanical (i.e., stones, reflux, obstruction, catheterization)
    
  • Inflammatory (i.e., cystitis, prostatitis, epididymitis, endometriosis, periurethritis)
    
  • Neoplasm
    
• Factitious:
  
  • Food
    
  • Drugs
    
  • Pigmenturia (i.e., myoglobin, porphyria, hemoglobin)
    
  • Vaginal bleeding
    

TREATMENT

• Supportive
  
• ABCs and fluid restriction in stable patients with significant edema.
  

ABCs: Airway, breathing, circulation

• Treatment mainly supportive care:
  
  • BP control: <125/75 mm Hg
    
    • Loop diuretics
      
    • ACE inhibitor for maintenance
      
    • Treat hypertensive emergencies
      
  • Dialysis:
    
    • Fluid overload
      
    • Hyperkalemia
      
    • Uremia
      
• PSGN:
  
  • Supportive care
    
  • Usually resolves spontaneously
    
  • No benefit to antibiotics
    
• IgA nephropathy:
  
  • Supportive care
    
  • Immunosuppressives if inflammation on biopsy
    
  • Variable course, most recover but may relapse
    
• RPGN:
  
  • Can irreversibly destroy renal function in days
    
  • Emergently consult nephrologist to discuss starting potentially toxic therapies.
    
  • Immunosuppressives and high-dose steroids:
    
    • Methylprednisolone and prednisone
      
    • Cyclophosphamide
      
    • Rituximab
      
    • Plasmapheresis for anti-GBM antibody
      
• MPGN:
  
  • Treat underlying disease if known.
    
  • Emergently consult nephrologist to discuss starting potentially toxic therapies.
    
  • May include plasma exchange, cyclophosphamide, and/or steroids
    

• Benazepril: 5–40 mg PO daily (or any other ACE inhibitor)
  
• Cyclophosphamide: Dose in conjunction with nephrology
  
• Diazoxide: 1–3 mg/kg IV, max. 150 mg, repeat q15min
  
• Furosemide: 20–80 mg IV; max. 2 mg/kg/d
  
• Methylprednisolone: 30 mg/kg IV on alternative days for 3 doses, followed by oral prednisone (dose in conjunction with nephrology)
  
• Nitroprusside: 0.3–10 μg/kg/min IV
  
• Prednisone: 0.5–2 mg/kg/d
  

FOLLOW-UP

• Unstable vital signs
  
• Oliguria, anuria
  
• Uremia
  
• Acute renal failure
  
• Electrolyte abnormality
  
• Hypertensive emergency
  
• CHF
  
• Infectious cause of GN
  

Healthy patients with no comorbid illness who present with mild hematuria and proteinuria with:

• Stable vital signs
  
• No signs of infection
  
• Otherwise normal lab work
  
• Close follow-up recommended
  

All patients with glomerulonephritis should follow-up with nephrology

• Discussion with nephrology if management with immunosuppressives is sought.
  
• The finding of proteinuria or hematuria should always prompt follow-up to ensure that the patient is not progressing to GN.
  

• Balogun RA, Abdel-Rahman EM. Therapeutic plasma exchange and renal related vasculitis: Therapeutic apheresis academy 2010.
  J Clin Apher.
  2011;26:291–296.
  
• Beck LH Jr, Salant DJ. Glomerular and tubulointerstitial diseases.
  Prim Care
  . 2008;35(2):265–296, vi.
  
• Glassock RJ. Glomerular disease in the elderly.
  Clin Geriatr Med
  .2009;25(3);413–422.
  
• Glomerular disease. In: Longo D, Fauci A, Kasper D, et al., eds.
  Harrison’s Principles of Internal Medicine
  . 18th ed. New York, NY: McGraw-Hill; 2011.
  
• Walters GD, Willis NS, Craig JC. Interventions for renal vasculitis in adults. A systematic review.
  BMC Nephrol
  . 2010;11:12.
  

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