Rosen & Barkin's 5-Minute Emergency Medicine Consult (481 page)

• Acute glomerulonephritis (AGN) is acute inflammatory damage to glomerulus, associated with:
  
  • Abrupt onset of hematuria with or without RBC casts
    
  • Acute renal failure manifested by edema, hypertension, azotemia, decline in urine output
    
  • Variable proteinuria
    
  • Active urine sediment (RBC casts)
    
• Exact mechanism of AGN unclear:
  
  • Combination of autoimmune reactivity to specific antigens at renal glomeruli
    
  • Characterized by crescent formation secondary to nonspecific injury at the glomerular wall
    

• Poststreptococcal glomerulonephritis (PSGN):
  
  • A postinfectious cause of acute nephritic syndrome, resulting from group A β-hemolytic streptococci
    
  • Considered a nonsuppurative complication (antibiotic treatment does not prevent this complication)
    
  • Occurs when immune complexes create hump-shaped subepithelial deposits in renal glomeruli
    
  • Most commonly affects patients between ages 3 and 15 yr but can occur at any age
    
  • Incidence of nephritis is 5–10% after pharyngitis and 25% after skin infections.
    
  • Consider PSGN in the setting of new-onset proteinuria, RBC casts, edema, and any recent infection.
    
  • Latent period between infection and onset of nephritis helps differentiate between PSGN and IgA nephropathy:
    
    • 1–3 wk in pharyngeal infection
      
    • 2–4 wk in cutaneous infection
      
  • Renal biopsy is usually not necessary for diagnosis.
    
  • Low complement (C3) for 6–8 wk
    
  • Can progress to severe renal failure if underlying infection goes untreated
    
  • Prognosis:
    
    • Excellent; >95% recover spontaneously with normalization of renal function within 6–8 wk, even with dialysis.
      
    • Hematuria usually resolves in 3–6 mo.
      
    • Transient nephrotic phase in 20% of patients during resolution of illness
      
    • End-stage renal disease occurs <5%
      
    • Rapidly progressive glomerulonephritis (RPGN) is rare, occurring in <1% cases.
      
    • Most cases resolve spontaneously with no long-term sequelae.
      
• Other infectious sources of glomerulonephritis (GN):
  
  • Sepsis, pneumonia, endocarditis, viruses, HIV
    
  • Pulmonary, intra-abdominal, or cutaneous infections
    
  • Syphilis, leprosy, schistosomiasis, and malaria
    
  • Goal: Treat underlying infection.
    
• Hepatitis virus–related glomerular disease:
  
  • Can present with either nephritic or nephrotic symptoms
    
  • Causes membranoproliferative GN
    
  • Complements remain low indefinitely (compared to PSGN)
    
• Noninfectious causes of GN (due to immune complex formation):
  
  • Systematic lupus erythematosus, Henoch–Schönlein purpura, vasculitis, Wegener granulomatosis
    
  • Goodpasture syndrome
    
• IgA nephropathy (IgA-N)
  
  • Most common cause of AGN (>25%) worldwide
    
  • Antibody–antigen causes immune complex deposition of IgA and C3
    
  • Complement levels are usually normal.
    
  • IgA-N has different presentations:
    
    • Gross hematuria following upper respiratory infection (URI)
      
    • Microscopic hematuria with proteinuria
      
    • Hematuria during viral illness or after exercise
      
    • Prognosis is related to serum creatinine, BP, and proteinuria.
      
    • 50% of patients with proteinuria may develop progressive renal disease.
      
    • ACE inhibitors or angiotensin-receptor blockers (ARBs) may help
      
• RPGN:
  
  • Certain patients with AGN may progress rapidly to renal failure.
    
  • Hallmarks are crescents on renal biopsy.
    
• Hereditary nephritis
  
  • Alport syndrome
    

DIAGNOSIS

• Hematuria:
  
  • Abrupt onset gross hematuria in 30–40% (coffee- or cola-colored urine)
    
• Edema:
  
  • Periorbital edema
    
  • Generalized edema more common in infants and children
    
• Infectious source or recent infection: Upper respiratory tract or skin common, e.g., PSGN
  
• Symptoms of congestive heart failure:
  
  • 40% occurrence in patients >60 yr
    
  • Rare in children
    
• Arthritis, arthralgias, and various skin rashes: PSGN, systemic disease
  
• Nonspecific manifestations:
  
  • Malaise
    
  • Weakness
    
  • Anorexia
    
  • Nausea/vomiting
    

• Recent URI or skin or other infection
  
• Change in urine color
  

• Hypertension
  
• Edema
  

Urinalysis with sediment evaluation to detect:

• RBCs, proteinuria, and RBC casts
  
• RBC casts are diagnostic of an active glomerular inflammation.
  

• CBC:
  
  • Anemia (seen in more chronic cases of GN or other systemic disease)
    
  • Acute leukocytosis (may suggest infectious process)
    
• Basic metabolic panel:
  
  • Assess baseline renal function
    
  • Check for electrolyte abnormalities
    
  • GFR will be normal or nearly normal
    
• Urinalysis:
  
  • RBCs +/− casts, protein
    
• Serum albumin
  
• Cultures (throat, skin, urine, blood):
  
  • As clinically suspected for infectious source
    
  • Streptozyme
    
• Serum complement level (C3): Decreased in infectious endocarditis, shunt nephritis, and PSGN
  
• Streptococcal antibodies:
  
  • Antistreptolysin (ASO), antistreptokinase (ASK), antideoxyribonuclease B (ADNase B), antinicotinyl adenine dinucleotidase (ANADase), and antihyaluronidase (AH)
    
  • ASO more reactive in pharyngeal infections
    
  • ADNase B, ANADase, and AH more reactive in cutaneous infections
    
  • ASK elevated in recent hemolytic Streptococcus infections
    
  • Titers do not correlate with prognosis of disease
    
• Urine osmolality, sodium, creatinine
  
• 24-hr urine collection:
  
  • Proteinuria initially present in 5% of children, 20% of adults with PSGN
    

• Renal ultrasound: Kidney size abnormality
  
• Chest radiograph: Cardiomegaly, pulmonary edema, infection
  

Renal biopsy:

• Generally not done for PSGN, as symptoms typically resolve after a brief illness
  
• Recommended if atypical features of PSGN, persistently abnormal complement levels, persistent hypertension, and proteinuria >3 g/d
  
• Facilitates diagnosis for other causes of nephritis
  

• (See “Glomerulonephritis” for further information on types of GN)
  
• Renal:
  
  • Primary glomerular disease
    
• Systemic:
  
  • Goodpasture syndrome
    
  • Vasculitis
    
  • Henoch–Schönlein purpura
    
• Other (rare):
  
  • Hemolytic-uremic syndrome
    
  • Thrombotic thrombocytopenic purpura
    
  • Acute hypersensitivity interstitial nephritis
    
  • Serum sickness
    

TREATMENT

Support ABCs

ABCs

• Antibiotics for streptococcal infection:
  
  • Penicillin (erythromycin, if penicillin allergic)
    
• Restrict salt and fluid intake
  
• Administer loop diuretics (furosemide)
  
• Restore urine flow in oliguric patients:
  
  • Mannitol
    
• Treat pulmonary edema:
  
  • Oxygen
    
  • Morphine
    
  • Loop diuretics
    
• Stabilize BP to decrease proteinuria, retard progression of GN:
  
  • ACEIs, ARBs
    
  • Hypertensive emergency: Nitroprusside or other titratable antihypertensive medication
    
• Hemodialysis for:
  
  • Severe hyperkalemia
    
  • Fluid overload
    
  • Uremia
    
  • Severe acidosis
    
  • Correct electrolyte abnormalities
    

• Erythromycin: 250–500 mg (peds: 30–50 mg/kg/d) PO q6h for 7–10 days
  
• Furosemide: 20–80 mg (peds: 1–6 mg/kg) PO daily/BID
  
• Lisinopril (ACEI): 10–40 mg (peds: >6 yr: 0.07 mg/kg) PO daily
  
• Losartan (ARB): 25–100 mg (peds: >6 yr: 0.7 mg/kg) PO daily
  
• Mannitol: 12.5–100 g (peds: 0.25–0.5 g/kg) IV:
  
  • May use single or repeat dosing; consider test dosing 1st.
    
• Morphine sulfate: 0.1 mg/kg/dose IV q4h
  
• Nitroprusside: 0.3–4 μg/kg/min IV
  
  • Titrate to goal mean arterial pressure for hypertensive emergency.
    
• Penicillin:
  
  • Benzathine penicillin: 1.2 million U (peds: 0.3–0.9 million U, based on weight) IM as single dose
    
  • Penicillin VK: 250–500 mg (peds: <12 yr 25–50 mg/kg/d) PO q6–8h for 10 days
    
• Other agents, including fish oil (ω-3 fatty acids for anti-inflammatory effects) and immunosuppressive agents (glucocorticoids, cyclophosphamide), may be used in consultation with specialists.
  

FOLLOW-UP

• Evidence of infectious cause for GN
  
• Oliguria, anuria
  
• Uremia
  
• Elevated creatinine
  
• Edema
  
• Electrolyte abnormalities
  
• Severe hypertension
  
• CHF