Endocarditis



Endocarditis


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.


TERMINOLOGY


Abbreviations



  • Subacute bacterial endocarditis (SBE)


  • Acute bacterial endocarditis (ABE)


Synonyms



  • Embolic nonsuppurative focal nephritis


  • Focal embolic nephritis


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


Definitions



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


ETIOLOGY/PATHOGENESIS


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


CLINICAL ISSUES


Epidemiology



  • 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


Presentation



  • 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


Treatment



  • 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


Prognosis



  • 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


MACROSCOPIC FEATURES


General Features

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