We report a case of slow graft function in a renal transplant recipient caused by uremic acute pericardial effusion with tamponade. Urgent pericardiocentesis was done with an improvement in blood pressure, immediate diuresis, and quick recovery of renal function back to baseline. Pericardial tamponade should be included in consideration of causes of type 1 cardiorenal syndrome in renal transplant recipients.
Key words : End-stage renal failure, Complications, Slow graft function, Uremic pericarditis
Pericardial effusion may appear as a transudate, exudate, pyopericardium, or hemopericardium. Large effusions are common with neoplasms, tuberculosis, cholesterol problems, uremic pericarditis, myxedema, and parasitic disease.1 Effusions that develop slowly can be asymptomatic, but rapidly accumulating smaller effusions can cause tamponade. Cardiac tamponade is the decompensated cardiac compression caused by accumulation of fluid and increased intrapericardial pressure.
Renal failure is a common cause of pericardial disease, producing large pericardial effusions in 20% patients.2 There have been 2 types reported1: Uremic pericarditis may occur in 6% to 10% of patients who have advanced renal failure (acute or chronic), and may develop before or shortly after dialysis; it results from inflammation of the visceral and parietal pericardium and correlates with the degree of azotemia3; and dialysis-associated pericarditis may occur in 13% patients who are on maintenance hemodialysis and, occasionally, with chronic peritoneal dialysis because of inadequate dialysis and/or fluid overload.4,5
In surgical tamponade, intrapericardial pressure rises rapidly, within minutes to hours because of hemorrhage. However, a low-intensity inflammatory process may develop for days to weeks before cardiac compression occurs (medical tamponade).
Tamponade may present with fever and pleuritic chest pain, but many patients are asymptomatic. Pericardial rubs may persist even with large effusions or may be transient. Due to autonomic impairment in uremic patients, heart rate may remain slow during tamponade despite fever and hypotension. The electrocardiogram does not show the typical diffuse ST-T wave elevations observed with other causes of acute pericarditis due to the absence of myocardial inflammation.6 If the electrocardiogram is typical of acute pericarditis, intercurrent infection must be suspected.
Most patients who have uremic pericarditis respond rapidly to dialysis, if intensified within 1 to 2 weeks, but dialysis must be heparin-free to avoid hemopericardium, hypokalemia, and hypophosphatemia.7,8 Cardiac tamponade and large chronic effusions that are resistant to dialysis must be treated with pericardiocentesis (level of evidence B, class IIa indication) with or without local steroid installation for large, nonresolving symptomatic effusions. Pericardiectomy is indicated only in refractory, severely symptomatic patients because of potential morbidity and mortality. Within 2 months after renal transplant, pericarditis has been reported in 2.4% patients.9 The present case report highlights possible acute uremic pericardial tamponade in a renal transplant recipient with compromised graft function early after transplant.
A 41-year-old Indian woman who had a history of recurrent urinary tract infections and frequent stone passage since 1998 underwent left nephrectomy because of infected nonfunctioning kidney. Her renal function gradually deteriorated until she had end-stage renal disease and she was prepared for preemptive renal transplant with unremarkable echocardiography.
She was admitted for living-related renal transplant from her sister (3 human leukocyte antigen mismatches, negative panel reactive antibodies, and negative crossmatch by complement-dependent cytotoxicity and flow cytometry). Planned immunosuppressive regimen included induction with basiliximab and maintenance with steroids, mycophenolate mofetil, and cyclosporine. She received 1 hemodialysis session the day before transplant with a right internal jugular vein double lumen catheter because of hyperkalemia and metabolic acidosis. She was stable clinically with unremarkable clinical findings, normal thyroid function, and unremarkable findings on the most recent echocardiogram.
In mid-February 2014, a right native nephrectomy was performed in the same session with right iliac renal allotransplant. The surgery was uneventful, but her hemoglobin dropped by 4 g/L over 12 hours. Urgent computed tomography (CT) of the abdomen showed no local bleeding. Despite thrombocytopenia, hemolytic uremic syndrome was excluded because she had a negative blood smear, normal lactate dehydrogenase level, and negative tests for hemolysis. She was treated with a filtered red blood cell transfusion and her hemoglobin became stable. Her urine grew Escherichia coli, and she was treated with intravenous piperacillin/ tazobactam for 7 days.
On day 2 after transplant, the patient developed unexplained hypotension, low-grade fever, tachycardia, chest pain, and oliguria. The central venous pressure was 16 cm water. The chest radiograph showed mild enlargement of the cardiac shadow (Figure 1). The hemoglobin was stable, and electrocardiography showed sinus tachycardia and a flat wave in lead III in addition to borderline repeated troponin I levels. The kidney graft function was compromised despite a challenge with intravenous fluids and vasopressors. The possibility of septicemic shock was considered high, and we changed the antibiotic to meropenem. She had a past history of deep venous thrombosis of the left lower limb after previous pelvic surgery (hysterectomy), and she had moderate elevation of the D-dimer level; therefore, an urgent ventilation/perfusion scan (Figure 2) was performed but showed low probability for pulmonary embolism. However, it was observed that the cardiac shadow was enlarged compared with the baseline appearance. Bedside echocardiography was performed and showed moderate pericardial effusion with echocardiographic signs of tamponade (Figure 3). Urgent pericardiocentesis with an indwelling drain was performed with hemorrhagic drainage of 255 mL, and further laboratory investigation showed that the fluid was a transudate (Table 1).
At 30 minutes after pericardiocentesis, the blood pressure increased to normal level with discontinuation of vasopressors. The urine output began to increase with improvement of renal graft function during the subsequent days (Figures 4 and 5). The total drained fluid was 325 mL over 3 days, and when the drainage stopped, as confirmed by an effusion-free echocardiogram, the drainage tube was removed. The patient was discharged with normal graft function and creatinine level of 88 μmol/L.
This case highlights the importance of heart-kidney interactions in the acute care setting. The renal allograft was slowly recovering because of after renal transplant which was attributed to acute decompensated heart failure as a result of an acute pericardial effusion. The rapid improvement of kidney graft function after pericardiocentesis denoting the complex type 1 cardiorenal syndrome.10
Pericardial effusion is a complication of chronic kidney disease with untreated advanced uremia.3,11 Other common causes of pericardial effusion include infection, malignancy, autoimmune diseases, medications, trauma, congestive heart failure, and hypothyroidism.12-14 Few cases of acute renal failure secondary to acute pericardial tamponade have been reported, but literature review showed no cases in renal transplant recipients.15-17
Returning venous blood volume creates mean right atrial filling pressure of 6 to 8 mm Hg.14 In cardiac tamponade, rapidly accumulating fluid in the nonelastic pericardial cavity inhibits the filling of the right atrium. After the intrapericardial pressure exceeds the right atrial pressure (and possibly the right ventricular pressure), cardiac output decreases because of reduced filling of the right atrium and ventricle, causing hypotension. Autoregulation of blood flow is necessary to maintain constant organ perfusion despite variations in the arterial pressure. This function is present in all tissues but is particularly pronounced in some organs such as the brain and kidney. Autoregulation of renal blood flow is mainly mediated by myogenic responses and tubuloglomerular feedback. Tubuloglomerular feedback is a regulating mechanism in the kidney that leads to vasoconstriction of the afferent arteriole in response to an increase in the luminal concentration of sodium chloride at the macula densa in the early distal tubule. In addition to myogenic responses and tubuloglomerular feedback, there are several other mechanisms that regulate perfusion including vasopressin, natriuretic peptides, and activation of the renin-angiotensin-aldosterone system. During hypotension, renal vascular resistance decreases to maintain renal blood flow and glomerular filtration by myogenic responses and tubuloglomerular feedback.
Tamponade without ≥ 2 inflammatory signs (typical pain, pericardial friction rub, fever, diffuse ST segment elevation) usually is associated with a malignant effusion (likelihood ratio, 2.9). Electrocardiography may demonstrate diminished QRS and T wave voltages, PR segment depression, ST-T segment changes, bundle branch block, and electrical alternans which is rarely seen in the absence of tamponade.15 Despite the acute tamponade, the present patient had only T wave changes in lead III.
In chest radiography large effusions are depicted as globular cardiomegaly with sharp margins (“water bottle” silhouette).18 On well-penetrated lateral radiographs or cine films, pericardial fluid is suggested by lucent lines within the cardiopericardial shadow (epicardial halo).18-20 This sign is useful for the fluoroscopic guidance of pericardiocentesis.21 The CT, spin-echo, and cine magnetic resonance imaging (MRI) scans also can be used to assess the size and extent of simple and complex pericardial effusions.22 Effusions measured by CT or MRI typically are larger than observed with echocardiography.23,24 In one-third of patients with asymptomatic large pericardial chronic effusion, unexpected cardiac tamponade may develop.25 Triggers for tamponade include hypovolemia, paroxysmal tachyarrhythmia, and intercurrent acute pericarditis.26,27 In the present patient, we suspected cardiomegaly during a radioisotope scan of the kidney graft.
The separation of pericardial layers can be detected in echocardiography when pericardial fluid volume >15 to 35 mL.28 The size of effusions can be graded as small (echo-free space in diastole < 10 mm), moderate (10-20 mm), large (> 20 mm), or very large (> 20 mm and compression of the heart). In the present case, we detected moderate pericardial effusion by bedside echocardiography.
The renal effects of cardiac tamponade may occur before hemodynamic collapse.15 This occurred in our patient who developed oliguria before tamponade and hemodynamic disturbance.
Increasing the pericardial pressure by 5 mm Hg decreases urinary sodium excretion and increases renin production, but the mean arterial blood flow and glomerular filtration rate remain unchanged. However, a further increase in pericardial pressure reduces both the mean arterial pressure and glomerular filtration rate.15 In the present patient with progression of tamponade and compromised hemodynamic status, kidney function was further affected. This explains what happened when she developed shock. Kidney autoregulation occurs over a wide range of arterial pressures (80-180 mm Hg), below which the kidney does not autoregulate, and urine flow falls in proportion to reductions in arterial pressure. The subsequent reductions in renal perfusion trigger mechanisms in the kidney to maintain constant renal blood flow and glomerular filtration.15
The pericardial effusion might be caused by a known medical condition in 60% cases.29 We excluded all possible causes of pericardial effusion and we attributed the cause to uremia because of the laboratory findings (Table 1).
Pericardiocentesis is not necessary when the diagnosis can be made without pericardiocentesis, or when the effusions are small or resolving with anti-inflammatory treatment. However, hemodynamic compromise with cardiac tamponade is an absolute indication for drainage. Whenever possible, treatment should be aimed at the underlying cause. Even with idiopathic effusions, extended pericardial catheter drainage (mean 3 ± 2 d; range, 113 d) was associated with lower recurrence rates (6% vs 23%) than in patients without catheter drainage during mean follow-up of 3.8 ± 4.3 years.30
We drained our patient for 3 days without any evidence of recurrence for 3 subsequent months, and the uremia (the underlying cause) was resolving rapidly with recovering kidney graft function and basal creatinine 120 μmol/L at discharge. We did not need any further medical therapy or other interventions such as intrapericardial treatment, percutaneous balloon pericardiotomy, or surgery.31-33
In summary, acute uremic pericardial tamponade should be considered as a possible cause of oliguric renal graft dysfunction early after transplant. Strong clinical suspicion for the diagnosis and a low threshold for emergency pericardial drainage are necessary to prevent further graft dysfunction.
Volume : 13
Issue : 1
Pages : 242 - 246
DOI : 10.6002/ect.mesot2014.P45
From Hamed Al-Essa Organ Transplant Center, Ibn Sina Hospital, Sabah Area,
Acknowledgements: The authors have no conflicts of interest to declare, and there was no funding for this study.
Corresponding author: Osama Ashry Ahmed Gheith, Consultant of Internal Medicine and Nephrology, Urology and Nephrology Center, Mansoura University, Egypt; working in Hamed Al-Essa Organ Transplant Center, Kuwait
Phone: +2 050 226 2222 & 221 4537
Fax: +965 2462 0963
Mobile: +965 6664 1967
Figure 1. Chest Radiography Before and After Transplant
Figure 2. Ventilation/Perfusion Scan Including Both Perfusion and Ventilation Phases
Figure 3. Echocardiography (4-Chamber View) With Moderate Pericardial Effusion
Figure 4. Platelet Count and Hemoglobin Level Early After Transplant
Figure 5. Urine Volume and Serum Creatinine Level Early After Transplant
Table 1. Laboratory Findings of the Aspirated Pericardial Fluid