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Glomerulonephritis, Emergency Medicine


Basics


Description


  • Syndrome characterized by:
    • Hematuria
    • Proteinuria
    • Red blood cell casts
    • Hypertension
    • Renal insufficiency
  • Common pathway of multiple diseases resulting in intraglomerular inflammation and cellular proliferation
  • Contributing factors:
    • Genetics
    • Infectious
    • Rheumatologic
    • Leading to antibody deposition:
      • Antibody attaches to glomerular antigen (native or implanted).
      • Circulating antigen-antibody complex deposited
    • Causing an influx and activation of inflammatory mediators:
      • Leukocytes, complement, cytokines
      • Cell-mediated immune mechanisms
  • Results in glomerular dysfunction
  • Persistent inflammation that can lead to scarring and permanent damage.

Etiology


  • 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-Sch ¶nlein 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


Signs and Symptoms


  • 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.

Essential Workup


Urinalysis for:  
  • Hematuria, proteinuria, and RBC casts

Diagnosis Tests & Interpretation


Lab
  • 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, CH50)-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

Imaging
  • 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

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

Differential Diagnosis


  • 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


Pre-Hospital


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

Initial Stabilization/Therapy


ABCs: Airway, breathing, circulation  

Ed Treatment/Procedures


  • 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

Medication


  • 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


Disposition


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

Discharge Criteria
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

Followup Recommendations


All patients with glomerulonephritis should follow-up with nephrology  

Pearls and Pitfalls


  • 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.

Additional Reading


  • 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. Harrisons 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.

See Also (Topic, Algorithm, Electronic Media Element)


  • Nephritic Syndrome
  • Nephrotic Syndrome
  • Renal Failure

Codes


ICD9


  • 580.0 Acute glomerulonephritis with lesion of proliferative glomerulonephritis
  • 583.4 Nephritis and nephropathy, not specified as acute or chronic, with lesion of rapidly progressive glomerulonephritis
  • 583.9 Nephritis and nephropathy, not specified as acute or chronic, with unspecified pathological lesion in kidney
  • 583.2 Nephritis and nephropathy, not specified as acute or chronic, with lesion of membranoproliferative glomerulonephritis

ICD10


  • N00.9 Acute nephritic syndrome with unsp morphologic changes
  • N01.9 Rapidly progr nephritic syndrome w unsp morphologic changes
  • N05.9 Unsp nephritic syndrome with unspecified morphologic changes
  • N05.5 Unsp nephritic syndrome w diffuse mesangiocap glomrlneph

SNOMED


  • 36171008 Glomerulonephritis (disorder)
  • 68544003 Acute post-streptococcal glomerulonephritis (disorder)
  • 236392004 Rapidly progressive glomerulonephritis (disorder)
  • 80321008 Mesangiocapillary glomerulonephritis (disorder)
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