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Successful treatment of acute renal failure secondary to complicated infective endocarditis by peritoneal dialysis: a case report



Infective endocarditis is one of the most common infections among intravenous drug addicts. Its complications can affect many systems, and these can include acute renal failure. There is a scarcity of cases in the literature related to acute renal failure secondary to infective endocarditis treated with peritoneal dialysis. In this paper, the case of a 48-year-old Saudi male is reported, who presented with features suggestive of infective endocarditis and who developed acute kidney injury that was treated successfully with high tidal volume automated peritoneal dialysis. To our knowledge, this is the second report of such an association in the literature.

Case presentation

A 48-year-old Saudi gentleman diagnosed to have a glucose-6-phosphate dehydrogenase deficiency and hepatitis C infection for the last 9 years, presented to the emergency department with a history of fever of 2 days’ duration. On examination: his temperature = 41 °C, there was clubbing of the fingers bilaterally and a pansystolic murmur in the left parasternal area. The results of the blood cultures and echocardiogram were supportive of the diagnosis of infective endocarditis, and the patient subsequently developed acute kidney injury, and his creatinine reached 5.2 mg/dl, a level for which dialysis is essential for the patient to survive.


High tidal volume automated peritoneal dialysis is highly effective as a renal replacement therapy in acute renal failure secondary to infective endocarditis if no contraindication is present.


Drug addiction is one of the principal economic problems not only in the Gulf region and the Middle East but worldwide because of its associated complications [1,2,3,4]. Infective endocarditis is a common infection that occurs in intravenous drug addicts (IVDAs) and is commonly caused by the Staphylococcus aureus organism, often affecting the tricuspid valve; however, the involvement of other valves and organisms is not uncommon [5, 6]. Complications following infective endocarditis are varied and can involve many systems at the same time. Such complications include septic emboli, stroke and renal complications, including immune complex glomerulonephritis, antibiotic-induced interstitial nephritis, acute tubular necrosis and renal infarction [7,8,9,10,11,12,13,14,15,16]. The usual management of acute renal failure is intermittent haemodialysis (HD) or continuous renal replacement therapy. Although automated peritoneal dialysis (APD) therapy is also considered for treatment of acute renal failure, there are few reports of the use of this method for renal failure secondary to infective endocarditis. High tidal volume APD can also be effective as a renal replacement therapy in acute kidney injury (AKI) secondary to infective endocarditis provided no contraindication is present.

Ethical considerations

Written informed consent was obtained from the patient for publication of this Case Report and any accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal.

Case presentation

A 48-year-old Saudi gentleman with a known history of IV drug abuse and who had had a hepatitis C infection for the last 9 years presented to the emergency department with a fever of 2 days’ duration. He had been an IV drug user (heroin) for 10 years. He presented to the emergency department with a high grade, continuous fever that was not relieved by antipyretics, and which was accompanied by chills and sweating. He denied any history of upper respiratory tract infection, shortness of breath, chest pain, palpitations, abdominal pain, nausea/vomiting, changes in bowel habit, headache, neck stiffness, photophobia, dysuria or frequent urination. There was no history of recent travel, animal exposure, contact with an ill person or a patient with tuberculosis, ingestion of raw milk, skin rash, oral ulcers, dry mouth or eyes, or joint pain. In the physical examination, his vital signs were as follows: temperature = 41 °C, blood pressure = 144/60 mmHg, pulse = 125 beats/min, respiratory rate = 20 breaths/min, oxygen saturation = 97% in room air. Hands and arms: Clubbing grade III, multiple IV punctures, no splinter haemorrhage or Osler’s nodules, no Janeway lesions. Head and neck: Normal. Chest: Vesicular breathing and no added sounds. Heart: Soft S1, pansystolic murmur at left parasternal area, grade III increase with inspiration and hand grip, no pericardial rub. Abdomen: Normal. Lower Limbs: Clubbing grade III, multiple IV punctures. Neurological examination: Conscious, oriented to time, person and place, normal motor, sensory and cerebellar examination. Blood tests showed the following: WBC = 17.8, neutrophils = 79%, lymphocytes = 5%, band = 9%, monocyte = 6%, eosinophil = 1%, haemoglobin = 10.9 g/l, MCV = 86.6, MCH = 26.8, MCHC = 31, platelets = 332, ESR = 106 mm/h. Lactic acid was high (5.3 mmol/l) and the initial renal function and liver function tests were normal. Three separate blood cultures were drawn from different sites over a 1-h period before starting the antibiotics and on the subsequent day a positive result for methicillin-sensitive S. aureus (MSSA) was revealed. The echocardiogram showed small vegetation over the anterior chordae tendineae of the anterior mitral valve, and there was no evidence of intramyocardial abscess or fistula. The patient was started on vancomycin and gentamicin until the final culture results were available. Vancomycin was then stopped and cloxacillin was started. Gentamicin administration was maintained for 5 days for a synergistic effect. On the seventh day following admission, the patient developed progressive AKI. His renal function tests deteriorated gradually, with the BUN level reaching 67 mg/dl, and the creatinine level was 5.2 mg/dl. Urine analysis was normal and negative for eosinophils, and the kidney ultrasound showed a normal size, shape and position of the kidneys, and the renal arteries were normal. The nephrology team evaluated the patient and decided to commence high tidal volume APD with 30 l of Physioneal over 24 h, each refill was 1.5 l. Gentamicin was stopped after the patient completed a 1-week course. The gentamicin trough level was 0.2 μg/ml (normal level is <0.2 μg/ml), whereas the peak level was 3.5 μg/ml (normal level is 4–8 μg/ml). The patient showed clinical and laboratory improvement, see results in Table 1. He required APD for only 1 week. A 4-week course of cloxacillin was completed and the patient was discharged in good condition. The patient was referred to a rehabilitation centre for drug addiction. We followed up with renal function testing for 1 year, and all results were normal. The final results are listed in Table 1.

Table 1 Renal and biochemical profile of the patient before and after APD


Infective endocarditis is one of the most common infections among IVDAs and can affect any valve, including the tricuspid (60–70%), mitral and aortic valves (20–30%), and the pulmonary valve (<1%). Multiple valves can be affected at the same time, as reported with drug abusers. Recent studies on valve involvement in drug abusers have reported that whereas left-side valves are more commonly affected in the general population, the right-side valves are more commonly affected in IVDAs worldwide, with opposite results found in the Middle East [1, 2, 17, 18]. In this patient, it can be seen that the diagnosis of infective endocarditis is, without a doubt, correct. He showed the two major Duke criteria of (1) positive blood culture, and (2) a new murmur and vegetation seen through the echocardiogram. The most common organism reported in the literature is S. aureus, which is found in 50–90% of patients with infective endocarditis [19, 20]. Complications from infective endocarditis can be considered multisystem, with one of the most important affected systems being the renal system, as endocarditis itself can be manifested in acute interstitial nephritis, focal and/or diffuse proliferative glomerulonephritis, renal cortical necrosis or antibiotic-related interstitial nephritis [7, 21,22,23]. This patient developed AKI, which could either have been because of the infective endocarditis itself or antibiotic related. No renal biopsy was performed to confirm this. Haemodialysis is one of the known risk factors for infective endocarditis, as has been shown in several published studies. One of the most important of these studies was the International Collaboration on Endocarditis-Prospective Cohort Study (ICE-PCS), which concluded that of all cases of infective endocarditis (bacterial in origin), 21% in North America were among HD patients [24, 25]. No cases have been documented in peritoneal dialysis (PD) patients. PD for AKI patients still constitutes the mainstay of therapy in many developing countries because of its availability and ease of administration. Although its safety is being confirmed, PD is used less and less in patients with AKI, and this might be because of lack of experience, lack of facilities or both. In the PD centre at the King Fahd Hospital of the University, a new technique in PD catheter insertion has been developed that made the procedure much simpler, safer and more efficient than before [26]. By using this technique, it is believed that PD should not be discarded as a worthwhile therapeutic option for a patient with AKI because of its technical simplicity, excellent cardiovascular tolerance, absence of an extracorporeal circuit, lack of bleeding risk and low risk of hydro-electrolyte imbalances. In general, the indication for initiation of dialysis includes acidaemia—life-threatening and causing hemodynamic instability—life-threatening hyperkalaemia, volume overload unresponsive to diuretics and uraemia, including pericarditis and encephalopathy [27]. In tidal PD (TPD), only a portion of the dialysate is drained from the peritoneal cavity after the initial PD fluid exchange. The drained volume is replaced by fresh dialysate (the tidal volume), with each cycle leaving a variable amount of dialysate (residual volume) in constant contact with the peritoneal membrane until the end of the dialysis session [28]. There are several advantages of PD in comparison to other renal replacement therapies in treating AKI. No systemic anticoagulation is required, and this is particularly important in AKI following major surgery or when haemorrhaging or coagulation disorders are present. The use of anticoagulation with heparin or low molecular weight heparin in HD or continuous renal replacement theory (CRRT) would increase the risk of bleeding. With PD, no systemic anticoagulation is required, and thus the bleeding risk would not be increased. In cases where intraperitoneal heparin is needed, heparin is not effectively absorbed through the peritoneum, and therefore, there should not be any significant systemic effect on coagulation. Patients on PD are haemodynamically more stable than those on HD. Many patients with AKI have hypotension and shock, and they tolerate HD or even CRRT poorly. In general, these patients tolerate PD better than HD or CRRT. Hypotension and arrhythmia are rarely induced by the PD treatment. The reasons include the following:

  1. (a)

    Lack of extracorporeal circulation, causing immediate reduction of blood volume.

  2. (b)

    Slower fluid removal from the blood volume, allowing more time for equilibrium between different fluid compartments to be reached.

  3. (c)

    Slower fall of serum urea level, allowing time for equilibrium between intracellular and extracellular urea levels to be reached. This prevents the acute drop in plasma osmolality that occurs in HD as a result of rapid extracellular urea removal.

  4. (d)

    Slower rate of change in electrolyte (potassium and calcium) levels.

In addition, PD may lead to more rapid, and a higher chance of, recovery of renal function. It is well documented that PD preserves residual renal function better than HD in patients with end-stage renal failure. Although the exact mechanism remains unknown, it is generally believed that this is related to the more stable haemodynamics with PD, and possibly is also a result of lower complement activation and higher middle molecule clearance with PD. The same may apply to PD for acute renal failure. In a retrospective study of 31 patients with AKI caused by malignant hypertension in the period of 1997–2000, 11 out of 20 patients who received PD became dialysis free, whereas none of the 11 patients who received HD had recovered their renal function. The patient described in this paper presented with features suggestive of infective endocarditis and developed AKI. The patient was treated successfully with high tidal volume APD, with full recovery of renal function. To our knowledge, this is the second report of such an association in the literature.


High tidal volume APD can be effective as a renal replacement therapy in AKI secondary to infective endocarditis provided no contraindication is present.



acute kidney injury


automated peritoneal dialysis


continuous ambulatory peritoneal dialysis


glucose-6-phosphate dehydrogenase




infective endocarditis


intravenous drug addicts


peritoneal dialysis


tidal peritoneal dialysis


  1. Panduranga P, Al-Abri S, Al-Lawati J. Intravenous drug abuse and tricuspid valve endocarditis: growing trends in the Middle East Gulf region. World J Cardiol. 2013;5(11):397–403. doi:10.4330/wjc.v5.i11.397.

    Article  PubMed  PubMed Central  Google Scholar 

  2. Aceijas C, Friedman SR, Cooper HL, Wiessing L, Stimson GV, Hickman M. Estimates of injecting drug users at the national and local level in developing and transitional countries, and gender and age distribution. Sex Transm Infect. 2006;82:10–7.

    Article  Google Scholar 

  3. UN office on drugs and crime. World drug report 2011.

  4. Habib G, Hoen B, Tornos P, Thuny F, Prendergast B, Vilacosta I, et al. Guidelines on the prevention, diagnosis, and treatment of infective endocarditis (new version 2009): the Task Force on the Prevention, Diagnosis, and Treatment of Infective Endocarditis of the European Society of Cardiology (ESC). Eur Heart J. 2009;30:2369–413.

    Article  PubMed  Google Scholar 

  5. Morokuma H, Minato N, Kamohara K, Minematsu N. Three surgical cases of isolated tricuspid valve infective endocarditis. Ann Thorac Cardiovasc Surg. 2010;16:134–8.

    PubMed  Google Scholar 

  6. Wang A, Wang Y, Wang G, Zhou Z, Yang X. Infective endocarditis associated with acute renal failure: repeat renal biopsy and successful recovery. Exp Ther Med. 2010;1(3):433–6.

    Article  PubMed  PubMed Central  Google Scholar 

  7. Conlon PJ, Jefferies F, Krigman HR, Corey GR, Sexton DJ, Abramson MA. Predictors of prognosis and risk of acute renal failure in bacterial endocarditis. Clin Nephrol. 1998;49(2):96–101.

    CAS  PubMed  Google Scholar 

  8. Asgeirsson H, Thalme A, Kristjansson M, Weiland O. Incidence and outcome of Staphylococcus aureus endocarditis—a 10-year single-centre northern European experience. Clin Microbiol Infect. 2015;21(8):772–8. doi:10.1016/j.cmi.2015.04.014 (Epub 2015 Apr 28).

    Article  CAS  PubMed  Google Scholar 

  9. Hill EE, Herijgers P, Herregods MC, Peetermans WE. Evolving trends in infective endocarditis. Clin Microbiol Infect. 2006;12:5–12.

    Article  CAS  PubMed  Google Scholar 

  10. Cabell CH, Jollis JG, Peterson GE, Corey GR, Anderson DJ, Sexton DJ, Woods CW, Reller LB, Ryan T, Fowler VG Jr. Changing patient characteristics and the effect on mortality in endocarditis. Arch Intern Med. 2002;162:90–4.

    Article  PubMed  Google Scholar 

  11. Fowler VG Jr, Miro JM, Hoen B, Cabell CH, Abrutyn E, Rubinstein E, Corey GR, Spelman D, Bradley SF, Barsic B, Pappas PA, Anstrom KJ, Wray D, Fortes CQ, Anguera I, Athan E, Jones P, van der Meer JT, Elliott TS, Levine DP, Bayer AS. ICE investigators: Staphylococcus aureus endocarditis: a consequence of medical progress. JAMA. 2005;293:3012–21.

    Article  CAS  PubMed  Google Scholar 

  12. Eknoyan G. Renal complications of bacterial endocarditis. Am J Nephrol. 1985;5:457–69.

    Article  CAS  PubMed  Google Scholar 

  13. Majumdar A, Chowdhary S, Ferreira MAS, Hammond LA, Howie AJ, Lipkin GW, Littler WA. Renal pathological findings in infective endocarditis. Nephrol Dial Transplant. 2000;15(11):1782–7. doi:10.1093/ndt/15.11.1782.

    Article  CAS  PubMed  Google Scholar 

  14. Moreillon P, Que YA. Infective endocarditis. Lancet. 2004;363(9403):139–49.

    Article  PubMed  Google Scholar 

  15. Ferraris L, Milazzo L, Ricaboni D, Mazzali C, Orlando G, Rizzardini G, Cicardi M, Raimondi F, Tocalli L, Cialfi A, Vanelli P, Galli M, Antona C, Antinori S. Profile of infective endocarditis observed from 2003–2010 in a single center in Italy. BMC Infect Dis. 2013;13:545. doi:10.1186/1471-2334-13-545.

    Article  PubMed  PubMed Central  Google Scholar 

  16. Miró JM, del Río A, Mestres CA. Infective endocarditis in intravenous drug abusers and HIV-1 infected patients. Infect Dis Clin North Am. 2002;16(2):273–95.

    Article  PubMed  Google Scholar 

  17. Carozza A, De Santo LS, Romano G, Della Corte A, Ursomando F, Scardone M, Caianiello G, Cotrufo M. Infective endocarditis in intravenous drug abusers: patterns of presentation and long-term outcomes of surgical treatment. J Heart Valve Dis. 2006;15(1):125–31.

    PubMed  Google Scholar 

  18. Cecchi E, Parrini I, Chinaglia A, Pomari F, Brusasco G, Bobbio M, Trinchero R, Brusca A. New diagnostic criteria for infective endocarditis. A study of sensitivity and specificity. Eur Heart J. 1997;18(7):1149–56.

    Article  CAS  PubMed  Google Scholar 

  19. Cecchi E, Trinchero R, Imazio M, Forno D, Dal Conte I, Lipani F, Brusca A, Gnavi R, Piedmont Infective Endocarditis Study Group. Are the Duke criteria really useful for the early bedside diagnosis of infective endocarditis? Results of a prospective multicenter trial. Ital Heart J. 2005;6(1):41–8.

    PubMed  Google Scholar 

  20. Sevinc A, Davutoglu V, Barutcu E, Kocoglu ME. Unusual course of infective endocarditis: acute renal failure progressing to chronic renal failure. J Natl Med Assoc. 2006;98(4):651–4.

    PubMed  PubMed Central  Google Scholar 

  21. Masuda T, Suzuki A, Obana M, Matsuoka Y, Irimajiri S. A case of infective endocarditis with purpura and macroscopic hematuria as initial manifestations. Kansenshogaku Zasshi. 1996;70(4):366–70.

    Article  CAS  PubMed  Google Scholar 

  22. Martínez-Costa X, Ribera E, Segarra A, Gómez-Jiménez J, Gil-Ganalda I, Fort J, Martínez-Vázquez JM. Nefritis intersticial aguda secundaria a endocarditis tricuspidea por Staphylococcus aureus. An Med Interna. 1989;6(11):595–7.

    PubMed  Google Scholar 

  23. Murdoch DR, Corey GR, Hoen B, Miró JM, Fowler VG, Bayer AS, Karchmer AW, Olaison L, Pappas PA, Moreillon P, Chambers ST, Chu VH, Falcó V, Holland DJ, Jones P, Klein JL, Raymond NJ, Read KM, Tripodi MF, Utili R, Wang A, Woods CW, Cabell CH. Clinical presentation, etiology, and outcome of infective endocarditis in the 21st century: the International Collaboration on Endocarditis-Prospective Cohort Study. Arch Intern Med. 2009;169:463–73.

    Article  PubMed  PubMed Central  Google Scholar 

  24. Katz IJ, Sofianou L, Butler O, et al. Recovery of renal function in Black South African patients with malignant hypertension: superiority of continuous ambulatory peritoneal dialysis over hemodialysis. Perit Dial Int. 2001;21:581–6.

    CAS  PubMed  Google Scholar 

  25. Lo WK, Lui SL, Yip TP. Principles and practice of acute peritoneal dialysis. Management of acute kidney problems. Heidelberg: Springer; 2010. p. 591–601.

    Google Scholar 

  26. Al-Hwiesh AK. Percutaneous peritoneal dialysis catheter insertion by a nephrologist: a new, simple, and safe technique. Perit Dial Int. 2014;34(2):204–11. doi:10.3747/pdi.2012.00160.

    Article  PubMed  PubMed Central  Google Scholar 

  27. Gabriel DP, Caramori JT, Martim LC, Barretti P, Balbi AL. High volume peritoneal dialysis vs. daily hemodialysis: a randomized, controlled trial in patients with acute kidney injury. Kidney Int. 2008;73(Suppl 108):S87–93.

    Article  Google Scholar 

  28. Burdmann EA, Chakravarthi R. Peritoneal dialysis in acute kidney injury: lessons learned and applied. Semin Dial. 2011;24:149–56.

    Article  PubMed  Google Scholar 

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Authors’ contributions

AMO, IMZ, AAA, EMO, SMH: analyzed and interpreted the patient data regarding the nephrology disease and infectious disease. FAM, AKH: wrote about the peritoneal dialysis in the discussion, and was a major contributor in writing the manuscript. All authors carried out the literature review and drafted the manuscript. All authors read and approved the final manuscript.


The authors would like to acknowledge the Cambridge Editing service for their efforts.

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The authors declare that they have no competing interests.

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Written informed consent was obtained from the patient for publication of this Case Report and any accompanying images.


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Correspondence to Aisha M. Al-Osail.

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Al-Osail, A.M., Al-Zahrani, I.M., Al-Abdulwahab, A.A. et al. Successful treatment of acute renal failure secondary to complicated infective endocarditis by peritoneal dialysis: a case report. BMC Res Notes 10, 463 (2017).

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