Official reprint from UpToDate®
www.uptodate.com ©2017 UpToDate, Inc. and/or its affiliates. All Rights Reserved.

Renal disease in the setting of infective endocarditis or an infected ventriculoatrial shunt

Jai Radhakrishnan, MD, MS
Section Editors
Richard J Glassock, MD, MACP
Fernando C Fervenza, MD, PhD
Deputy Editor
Albert Q Lam, MD


Patients with infective endocarditis (IE) can develop several forms of renal disease: a bacterial infection-related immune complex-mediated glomerulonephritis (GN), renal infarction from septic emboli, and renal cortical necrosis [1-3]. In addition, a drug-induced acute interstitial nephritis or, with aminoglycosides, acute kidney injury (due to acute tubular necrosis) can develop as a result of treating the infection. (See "Renal infarction" and "Clinical manifestations and diagnosis of acute interstitial nephritis" and "Manifestations of and risk factors for aminoglycoside nephrotoxicity".)

The frequency of renal involvement was illustrated in a retrospective study of over 200 consecutive episodes of bacterial endocarditis [4]. Approximately one-third of patients developed acute kidney injury (of any cause), a complication observed most often among older patients and those with Staphylococcus aureus infection. In a separate series of patients with IE-associated GN, acute kidney injury was the most common clinical presentation [5].

Clinical features and renal biopsy findings — The most common organism in IE-associated GN is S. aureus, which is seen in 56 percent of cases; Streptococcus species are the next most common. Less common organisms include Bartonella henselae, Coxiella burnetii, Cardiobacterium hominis, and Gemella. In 9 percent of patients with IE-associated GN, no organism could be cultured. One-half of affected patients do not have a known risk factor; in the remainder, common comorbidities included cardiac valve disease (30 percent), intravenous drug use (29 percent), hepatitis C (20 percent), and diabetes (18 percent). The cardiac valve infected was tricuspid in 43 percent, mitral in 33 percent, and aortic in 29 percent of patients in the largest series described [5]. There are a few case reports of patients with IE and GN who developed pulmonary hemorrhage, potentially mimicking other systemic diseases such as antineutrophil cytoplasmic autoantibody (ANCA)-associated vasculitis and antiglomerular basement membrane (anti-GBM) autoantibody disease [6,7]. (See "Glomerular disease: Evaluation and differential diagnosis in adults".)

Acute kidney injury is the most common clinical presentation (79 percent), and almost all patients have hematuria (97 percent) [5]. Features of the acute nephritic syndrome were seen in a minority (10 percent), as was nephrotic syndrome (6 percent); 53 percent of patients had reduced C3 complement, and 19 percent had reductions in C4 complement, suggesting activation of the alternative complement pathway. ANCA (usually directed at myeloperoxidase or lactoferrin) may be positive in up to one-third of patients [5]; some patients also have a positive rheumatoid factor, and rare patients are positive for anti-GBM autoantibodies.

In the largest series, crescentic GN was the most common pattern seen on renal biopsy specimens by light microscopy (53 percent) [5]. Diffuse proliferative GN was also a common finding (33 percent), and focal proliferative GN and mild mesangial proliferative GN were seen in a few patients. In addition to GN, the majority of patients showed tubular injury (86 percent) and interstitial inflammation (88 percent). By immunofluorescence microscopy, C3 was present in 94 percent of cases, immunoglobulin staining was observed in less than one-third of biopsies, and IgA-dominant (or codominant with IgG) staining was seen in 17 percent. A significant proportion of biopsies met the criteria for pauci-immune GN by immunofluorescence (44 percent). On electron microscopy, 90 percent of biopsies showed deposits, most commonly in the mesangial area (84 percent), followed by the subendothelial area (45 percent). Only a minority had subepithelial "humps," which are deposits that are classically seen in infection-related GN (14 percent).

To continue reading this article, you must log in with your personal, hospital, or group practice subscription. For more information on subscription options, click below on the option that best describes you:

Subscribers log in here

Literature review current through: Oct 2017. | This topic last updated: Feb 01, 2017.
The content on the UpToDate website is not intended nor recommended as a substitute for medical advice, diagnosis, or treatment. Always seek the advice of your own physician or other qualified health care professional regarding any medical questions or conditions. The use of this website is governed by the UpToDate Terms of Use ©2017 UpToDate, Inc.
  1. Neugarten J, Baldwin DS. Glomerulonephritis in bacterial endocarditis. Am J Med 1984; 77:297.
  2. Rose, BD. Pathophysiology of Renal Disease, 2nd ed, McGraw-Hill, New York City 1987. p.229.
  3. Majumdar A, Chowdhary S, Ferreira MA, et al. Renal pathological findings in infective endocarditis. Nephrol Dial Transplant 2000; 15:1782.
  4. Conlon PJ, Jefferies F, Krigman HR, et al. Predictors of prognosis and risk of acute renal failure in bacterial endocarditis. Clin Nephrol 1998; 49:96.
  5. Boils CL, Nasr SH, Walker PD, et al. Update on endocarditis-associated glomerulonephritis. Kidney Int 2015; 87:1241.
  6. Griffin KA, Schwartz MM, Korbet SM. Pulmonary-renal syndrome of bacterial endocarditis mimicking Goodpasture's syndrome. Am J Kidney Dis 1989; 14:329.
  7. Wu HC, Wen YK, Chen ML, Fan CS. Pulmonary-renal syndrome in a patient with bacterial endocarditis. J Formos Med Assoc 2005; 104:588.
  8. Nolan CM, Abernathy RS. Nephropathy associated with methicillin therapy. Prevalence and determinants in patients with staphylococcal bacteremia. Arch Intern Med 1977; 137:997.
  9. Neilson EG. Pathogenesis and therapy of interstitial nephritis. Kidney Int 1989; 35:1257.
  10. Moyssakis I, Tektonidou MG, Vasilliou VA, et al. Libman-Sacks endocarditis in systemic lupus erythematosus: prevalence, associations, and evolution. Am J Med 2007; 120:636.
  11. Tarter L, Yazdany J, Moyers B, et al. Clinical problem-solving. The heart of the matter. N Engl J Med 2013; 368:944.
  12. Chapter 10: Immunoglobulin A nephropathy. Kidney Int Suppl (2011) 2012; 2:209.
  13. Koya D, Shibuya K, Kikkawa R, Haneda M. Successful recovery of infective endocarditis-induced rapidly progressive glomerulonephritis by steroid therapy combined with antibiotics: a case report. BMC Nephrol 2004; 5:18.
  14. Iwata Y, Ohta S, Kawai K, et al. Shunt nephritis with positive titers for ANCA specific for proteinase 3. Am J Kidney Dis 2004; 43:e11.
  15. Rifkinson-Mann S, Rifkinson N, Leong T. Shunt nephritis. Case report. J Neurosurg 1991; 74:656.
  16. Narchi H, Taylor R, Azmy AF, et al. Shunt nephritis. J Pediatr Surg 1988; 23:839.
  17. Kiryluk K, Preddie D, D'Agati VD, Isom R. A young man with Propionibacterium acnes-induced shunt nephritis. Kidney Int 2008; 73:1434.
  18. Schena FP, Pertosa G, Pastore A, et al. Circulating immune complexes in infected ventriculoatrial and ventriculoperitoneal shunts. J Clin Immunol 1983; 3:173.
  19. Arze RS, Rashid H, Morley R, et al. Shunt nephritis: report of two cases and review of the literature. Clin Nephrol 1983; 19:48.
  20. Haffner D, Schindera F, Aschoff A, et al. The clinical spectrum of shunt nephritis. Nephrol Dial Transplant 1997; 12:1143.
  21. Strife CF, McDonald BM, Ruley EJ, et al. Shunt nephritis: the nature of the serum cryoglobulins and their relation to the complement profile. J Pediatr 1976; 88:403.