A. Brad Farris, III, MD

This slide from a 68-year-old African-American man with a history of staphylococcal endocarditis shows hypercellular glomeruli image and interstitial inflammation image.

Electron microscopy of the renal biopsy from a 68-year-old man with a history of staphylococcal endocarditis shows a well-formed, subepithelial, electron-dense deposit (“hump”) image.



  • Subacute bacterial endocarditis (SBE)

  • Acute bacterial endocarditis (ABE)


  • Embolic nonsuppurative focal nephritis

  • Focal embolic nephritis

  • Focal and segmental proliferative, necrotizing, or sclerosing glomerulonephritis (GN)


  • GN following infection of heart valves (i.e., endocarditis)


Infectious Agents

  • SBE: Classic example is Streptococcus viridans group bacteria infecting a rheumatic heart

    • Coagulase-negative staphylococci, including S. epidermis, have also been observed

    • Others observed

      • Actinobacillus actinomycetemcomitans, Enterococcus, Streptococcus mitis, Haemophilus influenzae, Neisseria gonorrhea, Chlamydia psittaci, Bartonella henselae, Coxiella burnetii

      • Subacute endocarditis due to Streptococcus bovis and N. subflava bacteremia has been reported in a case with concurrent high antineutrophil cytoplasmic antibody (ANCA) (anti-proteinase-3) titer

      • Of note, positive ANCA has also been reported in another series of GN associated with endocarditis

  • ABE: Classic example is Staphylococcus aureus infecting previously normal heart (e.g., as in an intravenous drug abuser)

    • Proportion of bacterial endocarditis-associated GN caused by S. aureus appears to be increasing, causing > 50% of all cases and > 1/3 of fatal cases

    • 40-70% of intravenous drug abusers with acute endocarditis from S. aureus have GN

  • Immunologic injury is thought to be primary mechanism of endocarditis-associated GN

    • Presence of glomerular immune complexes is evidence of this process

    • Serum complement is depressed, also indicative of process involving immune system

    • Circulating immune complexes have been demonstrated in patients with infectious endocarditis

    • Eluates from kidney with focal GN associated with endocarditis have been shown to react with bacterial antigens derived from bacteria cultured from patient’s blood

  • Earlier investigators thought that direct action of bacterial emboli lead to endocarditis-associated GN when they observed emboli in glomeruli

    • Called “focal embolic GN” or “embolic nonsuppurative focal nephritis” before pathogenesis was attributed to mechanisms other than embolization

    • Focal GN in patients involving only right side of heart suggest that embolization is not major mechanism



  • Incidence

    • Antibiotic therapy has decreased incidence of GN due to endocarditis

    • Studies of endocarditis have indicated an incidence of GN in patients with infectious endocarditis of 2-60%

      • Indicates that it is difficult to provide accurate measure of this incidence

    • Of endocarditis cases, renal disease is presenting feature in 20% of patients


  • Hematuria

    • Macroscopic hematuria

      • May be associated with the GN or renal infarction from “septic” emboli

    • May persist or resolve and may be intermittent

  • Proteinuria

    • Usually mild; nephrotic syndrome rare

  • Urinary casts

  • Hypocomplementemia

    • Frequently seen (but not always) and not specific to renal involvement

    • Seen in 70-90% of patients with diffuse GN and 60% of patients with focal GN before advent of antibiotic therapy

    • Associated with activation of classical complement pathway

  • Renal dysfunction

    • Variable to severe

      • BUN and creatinine elevations are typically associated with diffuse form of GN

    • Uremia seen in 5-10% of patients before epoch of antibiotics and in 3-4% after advent of antibiotics

  • Roth spots

  • Anemia

  • Hepatosplenomegaly

  • Purpura

  • Pulmonary hemorrhage has been reported as initial symptom (& initially confused with Goodpasture syndrome)

Laboratory Tests

  • Rheumatoid factor may be positive

  • Circulating immune complexes may be present

  • Cryoglobulins (mixed [type III]) have been reported


  • Surgical approaches

    • Valve vegetation removal or valve replacement may be required

  • Drugs

    • Antibiotic therapy may achieve resolution of milder endocarditis-associated GN

    • Antibiotic prophylaxis in patients at risk for endocarditis may reduce incidence of endocarditis-associated GN

    • Corticosteroids may be used in brief course

      • May help in resolution of nephritis without exacerbating the endocarditis

    • Plasmapheresis has been uncommonly used in aggressive cases


  • Partial to total resolution of renal disease occurs after antibiotic therapy

    • Proteinuria, circulating immune complexes, cryoglobulinemia, and elevation of rheumatoid factor (if present) resolve with effective treatment


General Features

Jul 7, 2016 | Posted by in PATHOLOGY & LABORATORY MEDICINE | Comments Off on Endocarditis

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