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Glomerulonephritis, Emergency Medicine

Basics

Description

- 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

- 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

- 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)

- Membranoproliferative glomerulonephritis (MPGN): - Complement deposits in basement membrane - Hepatitis C - Non-Hodgkin lymphoma - Occult infection

- Cardinal signs: - Edema: - Owing to renal salt and water retention - Periorbital - Ascites - Pleural effusion

- Autoimmune disorders: - Arthralgias - Arthritis - Rash - Fever

- Goodpasture syndrome: - Wegner granulomatosis: - Purulent rhinorrhea/sinus pain - Arthritis/arthralgias - Hemoptysis

- 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

- Factitious: - Food - Drugs - Pigmenturia (i.e., myoglobin, porphyria, hemoglobin) - Vaginal bleeding

- Treatment mainly supportive care: - BP control: <125/75 mm Hg - Loop diuretics - ACE inhibitor for maintenance - Treat hypertensive emergencies

- Dialysis: - Fluid overload - Hyperkalemia - Uremia

- 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

  • Syndrome characterized by:HematuriaProteinuriaRed blood cell castsHypertensionRenal insufficiency
  • Common pathway of multiple diseases resulting in intraglomerular inflammation and cellular proliferation
  • Contributing factors:GeneticsInfectiousRheumatologicLeading to antibody deposition:Antibody attaches to glomerular antigen (native or implanted).Circulating antigen-antibody complex depositedCausing an influx and activation of inflammatory mediators:Leukocytes, complement, cytokinesCell-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 infectionHighest prevalence in ages 2-14 and the elderlyMale predominanceRanges from asymptomatic hematuria to oliguric renal failureCan follow other bacterial, fungal, viral, or parasitic infections
  • IgA nephropathy (Berger disease):Most common in men in the 3rd and 4th decades of lifePossibly related to increased production of IgA after infection usually a URIHenoch-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 daysCrescentic deposits in glomeruli destroy function.Pauci-immune (small vessel vasculitides):Often antineutrophil cytoplasmic antibody (ANCA)-positiveCan involve other areas (i.e., lungs, skin)Wegener granulomatosisMicroscopic polyangiitisChurg-Strauss syndromeImmune complex deposits:PostinfectiousEndocarditis associatedSystemic disease (i.e., systemic lupus erythematosus [SLE], HSP)Anti-glomerular basement membrane (GBM) deposits:Older patients of age >60Goodpasture disease with pulmonary involvement
  • Membranoproliferative glomerulonephritis (MPGN):Complement deposits in basement membraneHepatitis CNon-Hodgkin lymphomaOccult infection

Diagnosis

Signs and Symptoms

  • Cardinal signs:
  • Edema:Owing to renal salt and water retentionPeriorbitalAscitesPleural effusion
  • HTN
  • Oliguria
  • Azotemia
  • CHF
  • Renal failure
  • Nonspecific manifestations:FatigueWeight lossAbdominal painNausea/vomiting
  • Autoimmune disorders:ArthralgiasArthritisRashFever
  • Goodpasture syndrome:
  • Wegner granulomatosis:Purulent rhinorrhea/sinus painArthritis/arthralgiasHemoptysis
  • HSP:Abdominal painPurpuraArthritis
  • 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 functionHyperkalemia
  • Albumin, total protein:Varying degrees of hypoalbuminemia depending on clinical process
  • CBC:Anemia secondary to chronic renal disease, neoplasm, Goodpasture, and WegenerWith 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, blood24-hr urine collection-protein, urine electrolytesStreptozyme or antistreptolysin O titerComplement levels (C1, C3, C4, CH50)-reduced in PSGN, MPGN, SLEANA, rheumatoid factor-connective tissue diseasesESR and CRP inflammatory markersAnti-GBM-Goodpasturec-ANCA-Wegener; p-ANCA-pauci-immuneAnti-DNA antibodies (SLE)Hepatitis B and C serologiesHIV

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 diseaseCoagulopathy
  • Renal:InfectiousMalformationNeoplasmIschemicTraumaVasculitis
  • Postrenal:Mechanical (i.e., stones, reflux, obstruction, catheterization)Inflammatory (i.e., cystitis, prostatitis, epididymitis, endometriosis, periurethritis)Neoplasm
  • Factitious:FoodDrugsPigmenturia (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 HgLoop diureticsACE inhibitor for maintenanceTreat hypertensive emergenciesDialysis:Fluid overloadHyperkalemiaUremia
  • PSGN:Supportive careUsually resolves spontaneouslyNo benefit to antibiotics
  • IgA nephropathy:Supportive careImmunosuppressives if inflammation on biopsyVariable course, most recover but may relapse
  • RPGN:Can irreversibly destroy renal function in daysEmergently consult nephrologist to discuss starting potentially toxic therapies.Immunosuppressives and high-dose steroids:Methylprednisolone and prednisoneCyclophosphamideRituximabPlasmapheresis 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)