□
CASE REPORT
□
Infective Endocarditis Presenting as Acute Renal Failure and Unusual Complications Luciano Pereira 1,2, Ana Machado 3, Jorge Oliveira 3, Pedro Almeida 4 and Paulo Bettencourt 3
Abstract Infective endocarditis can be a diagnostic challenge. Few cases have so far reported infective endocarditis presenting as renal failure. Pseudoaneurysms of the mitral-aortic intervalvular fibrosa and splenic abscess are rare complications of infective endocarditis. We herein report a case of an 80-year-old man admitted due to anorexia, malaise, edema of the legs and renal failure. A progressive degradation of the patient’s renal function was documented and hemodialysis was started. Blood cultures revealed the presence of Enterococcus faecalis, and the patient was treated with ampicillin and gentamicin. The transesophageal echocardiogram findings showed pseudoaneurysms of the mitral-aortic intervalvular fibrosa and in the aortic root wall. Due to abdominal pain, an abdominal CT scan was performed and showed a cystic lesion compatible with splenic abscess. The patient received 6 weeks of antibiotic treatment. There was progressive clinical improvement and regression of the splenic abscess, but no recovery of the renal function. This report illustrates an unusual clinical presentation of infective endocarditis with unusual complications that were successfully treated with antibiotics. Key words: infective endocarditis, renal failure, pseudoaneurysm, splenic abscess (Intern Med 54: 1259-1263, 2015) (DOI: 10.2169/internalmedicine.54.3236)
Introduction
Case Report
The incidence of infective endocarditis is 30 to 100 episodes per million patient-years (1). Despite improvements in diagnostic and therapeutic strategies, the fatality rate has not significantly decreased since the end of the 1970s; more than one-third of the patients will die within the first year of diagnosis (1). The diagnosis of infective endocarditis remains a challenge. In a recent large prospective study, most patients diagnosed only had a few of the classic clinical hallmarks of infective endocarditis (2). There are few cases in the literature reporting infective endocarditis presenting with renal failure (3). We herein present a patient with infective endocarditis, admitted for an acute kidney injury, who developed unusual complications.
An 80-year-old man, ex-smoker, with a history of diabetes mellitus, dyslipidemia, arterial hypertension, valvular heart disease and bladder cancer was admitted to our hospital because of malaise, anorexia, edema of the legs and renal failure. Three years previously, the patient had received a Freedom Solo 23 bioprosthesis for an aortic valve replacement. The patient had been doing well until 3 months before admission when he went to the emergency department because of fever, urinary urgency and incontinence for the last 11 days. His laboratory data is summarized in Table. The patient was discharged with a prescription for amoxicillin clavulanic acid (875 mg bid) and ibuprofen (600 mg bid). Four days later, he returned to the emergency room complaining of severe bilateral lumbar pain. A lumbosacral spine radiograph showed only degenerative changes. Renal
１
Nephrology Research and Development Unit, Faculty of Medicine, University of Porto, Portugal, ２Nephrology Department, São João Hospital Centre, Portugal, ３Internal Medicine Department, São João Hospital Centre, Portugal and ４Cardiology Department, São João Hospital Centre, Portugal Received for publication May 9, 2014; Accepted for publication September 24, 2014 Correspondence to Dr. Luciano Pereira, [email protected]
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Intern Med 54: 1259-1263, 2015
DOI: 10.2169/internalmedicine.54.3236
Table. Time Course of Patient’s Laboratory Data.
Urea (mg/dL) Creatinine (mg/dL) Hemoglobin (g/dL) White cell count (×10^9/L) Platelets count (×10^9/L) C-reactive protein (mg/L) Urine analysis
90 days before admission
86 days before admission
7 days before admission
On admission
3 days after admission
53
54
50
123
151
1.2
1.30
1.4
3.4
4.50
13.8
13.0
10.7
11.1
10.1
11 months after discharge 90 (under HD) 3.50 (under HD) 15.5
10.83
14.53
8.38
8.92
9.02
6.52
162
192
82
74
70
142
93.6
106.2
46.2
107.7
79.3
4.0
Mild protein
Mild protein
Protein and erythrocyt (without casts)
Mild protein and erythrocyt (without casts) 7.506 87.8 32.3
Protein and erythrocyt (without casts)
-
pH pO2 (mmHg) pCO2 (mmHg) HCO3(mmol/L) INR 24 hour urinary sodium (mEq) 24 hour urinary potassium (mEq) 24 hour proteinuria (g)
25 3.1 89
29
1.86
Note: Values outside the normal range are formatted in bolt text. Legend: protein – proteinuria; erythrocyt – erythrocyturia; HD – hemodialysis
ultrasonography findings revealed kidneys with normal size and good corticomedullary differentiation without obstruction. His laboratory tests showed elevated inflammatory markers (Table) and he was discharged with a prescription for ciprofloxacin (500 mg bid) and nimesulide (100 mg id). However, the next day the patient was admitted in another hospital for a mental status change. Electrocardiography (ECG) showed complete atrioventricular block and atrial flutter. A pacemaker was implanted and he started oral anticoagulation. Two weeks later, he developed dysarthria, diplopia and imbalance and he was admitted due to an acute ischemic stroke. The patient was discharged 3 days later with a mild imbalance. Two months later (7 days before admission in our hospital), he was seen in the emergency room for lumbar pain, macroscopic hematuria and edema of the legs. He was discharged with a prescription for levofloxacin (750 mg id) and furosemide (40 mg id). Seven days later, his cardiologist sent him to the emergency department because of deterioration of his renal function. His analysis showed a creatinine level of 2.90 mg/dL and urea level of 99 mg/dL.
On admission to the emergency room, the patient complained of anorexia and malaise which he had experienced for several weeks. He maintained macroscopic hematuria and edema of the legs. The patient had no other symptoms. He did not have a fever and his blood pressure was 130/110 mmHg and pulse rate was 75/min. Cardiac auscultation revealed a 2/6 aortic systolic murmur which had previously been identified. Pulmonary auscultation demonstrated basal inspiratory crackles. His laboratory data, including complete blood count, biochemistry and blood gas analysis, is summarized in Table. Renal ultrasonography was unremarkable. The patient was admitted due to acute kidney injury. Routine cultures, including blood and urine, were obtained. A peripheral blood smear showed rare schistocytes and the urinalysis findings detected rare eosinophils. The autoimmune study [including antinuclear antibodies, antineutrophil cytoplasmic antibodies (ANCA MPO and ANCA PR3) and antiglomerular basement membrane antibodies], serum protein electrophoresis, immunofixation electrophoresis and serum immunoglobulins were normal. Hypocomplementemia was documented one week after the appearance of edema of the
1260
Intern Med 54: 1259-1263, 2015
DOI: 10.2169/internalmedicine.54.3236
6 5.2 4.8
Plasma ĐƌĞĂƟŶiŶĞ (mg/dL)
5
4.5
DiagŶŽsis of IE
4 4
4.5 Starts of HD aŶd Gentamycin
3.4 2.9
3 AdmissiŽŶ 2
1
1.4 D -7 ER
0
Figure 1. Time course of the plasma creatinine levels.
Figure 2. Transesophageal echocardiogram showing a pseudoaneurysm of the mitral-aortic intervalvular fibrosa.
legs [C3: 66 mg/dL (normal range 83-177 mg/dL); C4 and CH50 were within the normal ranges]. Renal scintigraphy did not indicate evidence of a renal embolism. Because of the patient’s recent history of fever and aortic bioprosthesis, stroke, complete atrioventricular block and multiple antibiotic schemes with persistent, elevated inflammatory markers, we suspected infective endocarditis and ordered a transthoracic echocardiogram that revealed no vegetations. A progressive degradation of renal function was observed and hemodialysis was started on sixth day after admission (Fig. 1). At this time, the preliminary blood cultures revealed a Gram-positive coccus in chains. Because infective endocarditis had not been ruled out, a transesophageal echocardiogram was performed (Fig. 2) and revealed a normally functioning aortic bioprosthesis, normal left ventricle systolic function and pseudoaneurysms of the mitral-aortic intervalvular fibrosa (20×6 mm) and in the aortic root wall. There were no periprosthetic leaks or shunts between cardiac cavities. Meanwhile, a definitive blood culture revealed the presence of Enterococcus faecalis and ampicillin plus gentamicin were prescribed. Gentamicin trough levels were within toxic levels (defined as >2 μg/mL) in some determinations reaching a maximum level of 4.37 μg/mL in one de-
Figure 3. Abdominal CT scan revealing a cystic lesion, with contrast uptake at thickened walls, compatible with a splenic abscess.
termination. Cardiac surgery was not considered due to the high risk of the procedure. On the thirtieth day of admission, because of a poorly localized and slight abdominal pain, an abdominal echography was performed and showed a nodular image in the spleen. An abdominal CT scan revealed a cystic lesion, 100×44 mm, with contrast uptake at thickened walls, compatible with splenic abscess (Fig. 3). CT guided percutaneous drainage was proposed, but the patient refused. Control blood cultures were negative. He had sustained apyrexia and completed 6 weeks of antibiotic treatment. He was stable at discharge with residual diuresis between 350 and 1,800 mL/day on hemodialysis (three times a week). No events were recorded after his discharge. Eleven months after discharge, the analysis showed a normal complete blood count, an albumin level of 37.4 g/ L, and a normal level of C-reactive protein (Table). Echocardiograms were similar to the previous examinations. Control abdominal CT scan showed a small lesion in the spleen (24×22 mm). We settled on periodic examinations due to the patient’s high surgical risk and good response to medical
1261
Intern Med 54: 1259-1263, 2015
DOI: 10.2169/internalmedicine.54.3236
treatment.
Discussion Enterococcal prosthetic valve infective endocarditis is similar to enterococcal native valve infective endocarditis (4). Both occur primarily in older men and are predominantly community-acquired. However, in prosthetic valves there is a higher risk of myocardial abscess formation and fewer valve vegetations. Acute renal failure is a common complication of infective endocarditis which occurs in approximately one-third of the patients (5). The causes of renal failure in infective endocarditis are multifactorial (6). It may be explained mainly by acute glomerulonephritis due to immune complex deposition; renal infarction; acute interstitial nephritis and acute tubular damage due to nephrotoxic agents (e.g., vancomycin and aminoglycosides); and cortical necrosis due to underperfusion of the kidney. In this case, the renal failure is probably a result of acute glomerulonephritis caused by immune complex deposition because it started before antibiotic treatment for infective endocarditis, with a short period of exposure to nonsteroidal anti-inflammatory drugs, in a hemodynamically stable patient with hematuria, edema of the legs and hypocomplementemia. We also suspected interstitial nephritis because of patient’s deteriorating renal function in relation to the previously prescribed antibiotics; however, the patient did not have a rash, arthralgias or eosinophilia. We did not perform a renal biopsy because the patient’s condition had worsened. There are few reports in the literature on infective endocarditis presenting with renal failure. Renal failure resulting in hemodialysis treatment is not generally recognized as a complication of infective endocarditis (7). Renal failure in the context of infective endocarditis is typically resolved with successful antibiotic treatment (8). However, irreversible renal failure can occur if the diagnosis and antibiotic treatment are delayed because the severity of glomerulonephritis is related to the duration of the infection (8). In the present case, complete atrioventricular block and a previous stroke may have been related to the infective endocarditis, however, renal failure was the reason why the patient was hospitalized and subjected to further study. As a result, there was a significant delay in the diagnosis and treatment which certainly contributed to the irreversible degradation of renal function. Because the patient was dependent on hemodialysis, without evidence of renal function recovery, prophylaxis of contrast-induced nephropathy was not prescribed. Thus, radiocontrast agents may have further worsened the patient’s renal function. Gentamicin also may have contributed to the inability to recover from acute renal failure. Despite the effort to maintain gentamicin levels within therapeutic ranges, the patient was exposed to toxic levels of gentamicin. In addition, the patient’s advanced age, concomitant exposure to other nephrotoxins (radiocontrast agents) and prolonged course of treatment may have in-
creased his risk. Pseudoaneurysm of the mitral-aortic intervalvular fibrosa is a rare but potentially fatal complication of infective endocarditis and aortic valve surgery (9). Infection can result in abscess formation and pseudoaneurysm in the mitral-aortic intervalvular fibrosa area. For making a diagnosis, transesophageal echocardiogram is superior to transthoracic echocardiogram because it has a higher sensitivity. Surgery is the recommended management to prevent fatal complications. The natural history of mitral-aortic intervalvular fibrosa is unclear. Most patients undergo early surgical correction to prevent rupture, however, some patients have survived without surgery with follow-up periods varying from 10 to 63 months (9). In the present case, the pseudoaneurysm was only detected by transesophageal echocardiography and surgery was not performed. The patient has been doing well and subsequent serial echocardiograms during the 11-month follow-up have been similar to previous ones. A splenic abscess is a rare disorder and is more common in the presence of infection at different primary sites, especially endocarditis (10). Patients with splenic abscesses have a high mortality without adequate treatment. Currently, open splenectomy along with appropriate antibiotics is the most reliable treatment and must be considered if other, less invasive treatment methods fail. However, treatments with antibiotics alone have also been successful. In our case, there was a substantial reduction in the size of the abscess and the patient remained asymptomatic without fever and with negative blood cultures. In summary, infective endocarditis should be considered in the differential diagnosis of acute renal failure. If the diagnosis is delayed, renal dysfunction may be irreversible and other complications may arise. The authors state that they have no Conflict of Interest (COI).
References
1262
1. Thuny F, Grisoli D, Collart F, et al. Management of infective endocarditis: challenges and perspectives. Lancet 379: 965-975, 2012. 2. Murdoch DR, Corey GR, Hoen B, et al. Clinical presentation, etiology, and outcome of infective endocarditis in the 21st century: the International Collaboration on Endocarditis-Prospective Cohort Study. Arch Intern Med 169: 463-473, 2009. 3. Sevinc A, Davutoglu V, Barutcu I, et al. Unsual course of infective endocarditis: acute renal failure progressing to chronic renal failure. J Natl Med Assoc 4: 651-654, 2006. 4. Anderson DJ, Olaison L, McDonald JR, et al. Enterococcal prosthetic valve infective endocarditis: report of 45 episodes from the International Collaboration on Endocarditis-merged database. Eur J Clin Microbiol Infect Dis 24: 665-670, 2005. 5. Conlon PJ, Jefferies F, Krigman HR, et al. Predictors of prognosis and risk of acute renal failure in bacterial endocarditis. Clin Nephrol 49: 96-101, 1998. 6. Majumdar A, Chowdhary S, Ferreira MA, et al. Renal pathological findings in infective endocarditis. Nephrol Dial Transplant 15: 1782-1787, 2000. 7. Miyake M, Hatta K, Kameyama T, et al. Infective endocarditis de-
Intern Med 54: 1259-1263, 2015
DOI: 10.2169/internalmedicine.54.3236
veloping as uremia. Intern Med 44: 598-602, 2005. 8. Neugarten J, Baldwin DS. Glomerulonephritis in bacterial endocarditis. Am J Med 77: 297-304, 1984. 9. Xie M, Li Y, Cheng TO, et al. Pseudoaneurysm of the mitral-
aortic intervalvular fibrosa. Int J Cardiol 166: 2-7, 2013. 10. Gupta S, Singh O, Hastir A, et al. Splenic abscesses: Reports of two cases with review of the literature. Ann Trop Med Public Health 5: 273-277, 2012.
Ⓒ 2015 The Japanese Society of Internal Medicine http://www.naika.or.jp/imonline/index.html
1263
CASE REPORT
□
Infective Endocarditis Presenting as Acute Renal Failure and Unusual Complications Luciano Pereira 1,2, Ana Machado 3, Jorge Oliveira 3, Pedro Almeida 4 and Paulo Bettencourt 3
Abstract Infective endocarditis can be a diagnostic challenge. Few cases have so far reported infective endocarditis presenting as renal failure. Pseudoaneurysms of the mitral-aortic intervalvular fibrosa and splenic abscess are rare complications of infective endocarditis. We herein report a case of an 80-year-old man admitted due to anorexia, malaise, edema of the legs and renal failure. A progressive degradation of the patient’s renal function was documented and hemodialysis was started. Blood cultures revealed the presence of Enterococcus faecalis, and the patient was treated with ampicillin and gentamicin. The transesophageal echocardiogram findings showed pseudoaneurysms of the mitral-aortic intervalvular fibrosa and in the aortic root wall. Due to abdominal pain, an abdominal CT scan was performed and showed a cystic lesion compatible with splenic abscess. The patient received 6 weeks of antibiotic treatment. There was progressive clinical improvement and regression of the splenic abscess, but no recovery of the renal function. This report illustrates an unusual clinical presentation of infective endocarditis with unusual complications that were successfully treated with antibiotics. Key words: infective endocarditis, renal failure, pseudoaneurysm, splenic abscess (Intern Med 54: 1259-1263, 2015) (DOI: 10.2169/internalmedicine.54.3236)
Introduction
Case Report
The incidence of infective endocarditis is 30 to 100 episodes per million patient-years (1). Despite improvements in diagnostic and therapeutic strategies, the fatality rate has not significantly decreased since the end of the 1970s; more than one-third of the patients will die within the first year of diagnosis (1). The diagnosis of infective endocarditis remains a challenge. In a recent large prospective study, most patients diagnosed only had a few of the classic clinical hallmarks of infective endocarditis (2). There are few cases in the literature reporting infective endocarditis presenting with renal failure (3). We herein present a patient with infective endocarditis, admitted for an acute kidney injury, who developed unusual complications.
An 80-year-old man, ex-smoker, with a history of diabetes mellitus, dyslipidemia, arterial hypertension, valvular heart disease and bladder cancer was admitted to our hospital because of malaise, anorexia, edema of the legs and renal failure. Three years previously, the patient had received a Freedom Solo 23 bioprosthesis for an aortic valve replacement. The patient had been doing well until 3 months before admission when he went to the emergency department because of fever, urinary urgency and incontinence for the last 11 days. His laboratory data is summarized in Table. The patient was discharged with a prescription for amoxicillin clavulanic acid (875 mg bid) and ibuprofen (600 mg bid). Four days later, he returned to the emergency room complaining of severe bilateral lumbar pain. A lumbosacral spine radiograph showed only degenerative changes. Renal
１
Nephrology Research and Development Unit, Faculty of Medicine, University of Porto, Portugal, ２Nephrology Department, São João Hospital Centre, Portugal, ３Internal Medicine Department, São João Hospital Centre, Portugal and ４Cardiology Department, São João Hospital Centre, Portugal Received for publication May 9, 2014; Accepted for publication September 24, 2014 Correspondence to Dr. Luciano Pereira, [email protected]
1259
Intern Med 54: 1259-1263, 2015
DOI: 10.2169/internalmedicine.54.3236
Table. Time Course of Patient’s Laboratory Data.
Urea (mg/dL) Creatinine (mg/dL) Hemoglobin (g/dL) White cell count (×10^9/L) Platelets count (×10^9/L) C-reactive protein (mg/L) Urine analysis
90 days before admission
86 days before admission
7 days before admission
On admission
3 days after admission
53
54
50
123
151
1.2
1.30
1.4
3.4
4.50
13.8
13.0
10.7
11.1
10.1
11 months after discharge 90 (under HD) 3.50 (under HD) 15.5
10.83
14.53
8.38
8.92
9.02
6.52
162
192
82
74
70
142
93.6
106.2
46.2
107.7
79.3
4.0
Mild protein
Mild protein
Protein and erythrocyt (without casts)
Mild protein and erythrocyt (without casts) 7.506 87.8 32.3
Protein and erythrocyt (without casts)
-
pH pO2 (mmHg) pCO2 (mmHg) HCO3(mmol/L) INR 24 hour urinary sodium (mEq) 24 hour urinary potassium (mEq) 24 hour proteinuria (g)
25 3.1 89
29
1.86
Note: Values outside the normal range are formatted in bolt text. Legend: protein – proteinuria; erythrocyt – erythrocyturia; HD – hemodialysis
ultrasonography findings revealed kidneys with normal size and good corticomedullary differentiation without obstruction. His laboratory tests showed elevated inflammatory markers (Table) and he was discharged with a prescription for ciprofloxacin (500 mg bid) and nimesulide (100 mg id). However, the next day the patient was admitted in another hospital for a mental status change. Electrocardiography (ECG) showed complete atrioventricular block and atrial flutter. A pacemaker was implanted and he started oral anticoagulation. Two weeks later, he developed dysarthria, diplopia and imbalance and he was admitted due to an acute ischemic stroke. The patient was discharged 3 days later with a mild imbalance. Two months later (7 days before admission in our hospital), he was seen in the emergency room for lumbar pain, macroscopic hematuria and edema of the legs. He was discharged with a prescription for levofloxacin (750 mg id) and furosemide (40 mg id). Seven days later, his cardiologist sent him to the emergency department because of deterioration of his renal function. His analysis showed a creatinine level of 2.90 mg/dL and urea level of 99 mg/dL.
On admission to the emergency room, the patient complained of anorexia and malaise which he had experienced for several weeks. He maintained macroscopic hematuria and edema of the legs. The patient had no other symptoms. He did not have a fever and his blood pressure was 130/110 mmHg and pulse rate was 75/min. Cardiac auscultation revealed a 2/6 aortic systolic murmur which had previously been identified. Pulmonary auscultation demonstrated basal inspiratory crackles. His laboratory data, including complete blood count, biochemistry and blood gas analysis, is summarized in Table. Renal ultrasonography was unremarkable. The patient was admitted due to acute kidney injury. Routine cultures, including blood and urine, were obtained. A peripheral blood smear showed rare schistocytes and the urinalysis findings detected rare eosinophils. The autoimmune study [including antinuclear antibodies, antineutrophil cytoplasmic antibodies (ANCA MPO and ANCA PR3) and antiglomerular basement membrane antibodies], serum protein electrophoresis, immunofixation electrophoresis and serum immunoglobulins were normal. Hypocomplementemia was documented one week after the appearance of edema of the
1260
Intern Med 54: 1259-1263, 2015
DOI: 10.2169/internalmedicine.54.3236
6 5.2 4.8
Plasma ĐƌĞĂƟŶiŶĞ (mg/dL)
5
4.5
DiagŶŽsis of IE
4 4
4.5 Starts of HD aŶd Gentamycin
3.4 2.9
3 AdmissiŽŶ 2
1
1.4 D -7 ER
0
Figure 1. Time course of the plasma creatinine levels.
Figure 2. Transesophageal echocardiogram showing a pseudoaneurysm of the mitral-aortic intervalvular fibrosa.
legs [C3: 66 mg/dL (normal range 83-177 mg/dL); C4 and CH50 were within the normal ranges]. Renal scintigraphy did not indicate evidence of a renal embolism. Because of the patient’s recent history of fever and aortic bioprosthesis, stroke, complete atrioventricular block and multiple antibiotic schemes with persistent, elevated inflammatory markers, we suspected infective endocarditis and ordered a transthoracic echocardiogram that revealed no vegetations. A progressive degradation of renal function was observed and hemodialysis was started on sixth day after admission (Fig. 1). At this time, the preliminary blood cultures revealed a Gram-positive coccus in chains. Because infective endocarditis had not been ruled out, a transesophageal echocardiogram was performed (Fig. 2) and revealed a normally functioning aortic bioprosthesis, normal left ventricle systolic function and pseudoaneurysms of the mitral-aortic intervalvular fibrosa (20×6 mm) and in the aortic root wall. There were no periprosthetic leaks or shunts between cardiac cavities. Meanwhile, a definitive blood culture revealed the presence of Enterococcus faecalis and ampicillin plus gentamicin were prescribed. Gentamicin trough levels were within toxic levels (defined as >2 μg/mL) in some determinations reaching a maximum level of 4.37 μg/mL in one de-
Figure 3. Abdominal CT scan revealing a cystic lesion, with contrast uptake at thickened walls, compatible with a splenic abscess.
termination. Cardiac surgery was not considered due to the high risk of the procedure. On the thirtieth day of admission, because of a poorly localized and slight abdominal pain, an abdominal echography was performed and showed a nodular image in the spleen. An abdominal CT scan revealed a cystic lesion, 100×44 mm, with contrast uptake at thickened walls, compatible with splenic abscess (Fig. 3). CT guided percutaneous drainage was proposed, but the patient refused. Control blood cultures were negative. He had sustained apyrexia and completed 6 weeks of antibiotic treatment. He was stable at discharge with residual diuresis between 350 and 1,800 mL/day on hemodialysis (three times a week). No events were recorded after his discharge. Eleven months after discharge, the analysis showed a normal complete blood count, an albumin level of 37.4 g/ L, and a normal level of C-reactive protein (Table). Echocardiograms were similar to the previous examinations. Control abdominal CT scan showed a small lesion in the spleen (24×22 mm). We settled on periodic examinations due to the patient’s high surgical risk and good response to medical
1261
Intern Med 54: 1259-1263, 2015
DOI: 10.2169/internalmedicine.54.3236
treatment.
Discussion Enterococcal prosthetic valve infective endocarditis is similar to enterococcal native valve infective endocarditis (4). Both occur primarily in older men and are predominantly community-acquired. However, in prosthetic valves there is a higher risk of myocardial abscess formation and fewer valve vegetations. Acute renal failure is a common complication of infective endocarditis which occurs in approximately one-third of the patients (5). The causes of renal failure in infective endocarditis are multifactorial (6). It may be explained mainly by acute glomerulonephritis due to immune complex deposition; renal infarction; acute interstitial nephritis and acute tubular damage due to nephrotoxic agents (e.g., vancomycin and aminoglycosides); and cortical necrosis due to underperfusion of the kidney. In this case, the renal failure is probably a result of acute glomerulonephritis caused by immune complex deposition because it started before antibiotic treatment for infective endocarditis, with a short period of exposure to nonsteroidal anti-inflammatory drugs, in a hemodynamically stable patient with hematuria, edema of the legs and hypocomplementemia. We also suspected interstitial nephritis because of patient’s deteriorating renal function in relation to the previously prescribed antibiotics; however, the patient did not have a rash, arthralgias or eosinophilia. We did not perform a renal biopsy because the patient’s condition had worsened. There are few reports in the literature on infective endocarditis presenting with renal failure. Renal failure resulting in hemodialysis treatment is not generally recognized as a complication of infective endocarditis (7). Renal failure in the context of infective endocarditis is typically resolved with successful antibiotic treatment (8). However, irreversible renal failure can occur if the diagnosis and antibiotic treatment are delayed because the severity of glomerulonephritis is related to the duration of the infection (8). In the present case, complete atrioventricular block and a previous stroke may have been related to the infective endocarditis, however, renal failure was the reason why the patient was hospitalized and subjected to further study. As a result, there was a significant delay in the diagnosis and treatment which certainly contributed to the irreversible degradation of renal function. Because the patient was dependent on hemodialysis, without evidence of renal function recovery, prophylaxis of contrast-induced nephropathy was not prescribed. Thus, radiocontrast agents may have further worsened the patient’s renal function. Gentamicin also may have contributed to the inability to recover from acute renal failure. Despite the effort to maintain gentamicin levels within therapeutic ranges, the patient was exposed to toxic levels of gentamicin. In addition, the patient’s advanced age, concomitant exposure to other nephrotoxins (radiocontrast agents) and prolonged course of treatment may have in-
creased his risk. Pseudoaneurysm of the mitral-aortic intervalvular fibrosa is a rare but potentially fatal complication of infective endocarditis and aortic valve surgery (9). Infection can result in abscess formation and pseudoaneurysm in the mitral-aortic intervalvular fibrosa area. For making a diagnosis, transesophageal echocardiogram is superior to transthoracic echocardiogram because it has a higher sensitivity. Surgery is the recommended management to prevent fatal complications. The natural history of mitral-aortic intervalvular fibrosa is unclear. Most patients undergo early surgical correction to prevent rupture, however, some patients have survived without surgery with follow-up periods varying from 10 to 63 months (9). In the present case, the pseudoaneurysm was only detected by transesophageal echocardiography and surgery was not performed. The patient has been doing well and subsequent serial echocardiograms during the 11-month follow-up have been similar to previous ones. A splenic abscess is a rare disorder and is more common in the presence of infection at different primary sites, especially endocarditis (10). Patients with splenic abscesses have a high mortality without adequate treatment. Currently, open splenectomy along with appropriate antibiotics is the most reliable treatment and must be considered if other, less invasive treatment methods fail. However, treatments with antibiotics alone have also been successful. In our case, there was a substantial reduction in the size of the abscess and the patient remained asymptomatic without fever and with negative blood cultures. In summary, infective endocarditis should be considered in the differential diagnosis of acute renal failure. If the diagnosis is delayed, renal dysfunction may be irreversible and other complications may arise. The authors state that they have no Conflict of Interest (COI).
References
1262
1. Thuny F, Grisoli D, Collart F, et al. Management of infective endocarditis: challenges and perspectives. Lancet 379: 965-975, 2012. 2. Murdoch DR, Corey GR, Hoen B, et al. Clinical presentation, etiology, and outcome of infective endocarditis in the 21st century: the International Collaboration on Endocarditis-Prospective Cohort Study. Arch Intern Med 169: 463-473, 2009. 3. Sevinc A, Davutoglu V, Barutcu I, et al. Unsual course of infective endocarditis: acute renal failure progressing to chronic renal failure. J Natl Med Assoc 4: 651-654, 2006. 4. Anderson DJ, Olaison L, McDonald JR, et al. Enterococcal prosthetic valve infective endocarditis: report of 45 episodes from the International Collaboration on Endocarditis-merged database. Eur J Clin Microbiol Infect Dis 24: 665-670, 2005. 5. Conlon PJ, Jefferies F, Krigman HR, et al. Predictors of prognosis and risk of acute renal failure in bacterial endocarditis. Clin Nephrol 49: 96-101, 1998. 6. Majumdar A, Chowdhary S, Ferreira MA, et al. Renal pathological findings in infective endocarditis. Nephrol Dial Transplant 15: 1782-1787, 2000. 7. Miyake M, Hatta K, Kameyama T, et al. Infective endocarditis de-
Intern Med 54: 1259-1263, 2015
DOI: 10.2169/internalmedicine.54.3236
veloping as uremia. Intern Med 44: 598-602, 2005. 8. Neugarten J, Baldwin DS. Glomerulonephritis in bacterial endocarditis. Am J Med 77: 297-304, 1984. 9. Xie M, Li Y, Cheng TO, et al. Pseudoaneurysm of the mitral-
aortic intervalvular fibrosa. Int J Cardiol 166: 2-7, 2013. 10. Gupta S, Singh O, Hastir A, et al. Splenic abscesses: Reports of two cases with review of the literature. Ann Trop Med Public Health 5: 273-277, 2012.
Ⓒ 2015 The Japanese Society of Internal Medicine http://www.naika.or.jp/imonline/index.html
1263
