Management of Patients with Kidney Failure and Pericarditis

Introduction

Diseases of the pericardium, including pericarditis, pericardial effusion, and tamponade, are common in patients with kidney failure, but there are limited data to guide management. We present a clinical case and our approach to managing these challenging clinical situations.

Case

A 23-year-old woman with hypertension and kidney failure on dialysis via arteriovenous fistula was admitted with fever and chest pain. Her kidney disease was attributed to childhood-onset hypertension, and she did not have lupus or another autoimmune disease. She had poor adherence to dialysis and often missed four or five sessions in a row. She was febrile and hypertensive to 240/140 and had signs of underdialysis, including a creatinine of 15 mg/dl, BUN of 81 mg/dl, potassium of 5.8 mEq/L, and phosphate of 8.5 mg/dl. A pericardial rub was appreciated. Echocardiogram demonstrated a large circumferential pericardial effusion with systolic right atrial collapse.

Diagnosing Tamponade

The first question that must be addressed is whether this patient has cardiac tamponade. Physical examination findings of tamponade include tachycardia, hypotension, distended jugular veins, distant heart sounds, and pulsus paradoxus. Echocardiographic features typically include a large pericardial effusion, plethoric inferior vena cava, and signs of increased pericardial pressure, such as systolic atrial and diastolic ventricular collapse. Pulsus paradoxus (an exaggerated decrease in systolic BP during inspiration) and its echocardiographic equivalent, increased respirophasic variation of mitral valve inflow, can also suggest tamponade (1). Tamponade is an emergency and requires immediate pericardial drainage. In this patient’s case, although echocardiographic findings of high pericardial pressure were present, the patient did not clinically have tamponade. Invasive management was deferred in favor of dialytic management.

Uremic Pericarditis versus Dialysis-Associated Pericarditis

The patient had chest pain, fever, and a pericardial rub and was diagnosed with pericarditis. Pericarditis has long been recognized as part of the uremic syndrome. As dialysis became more available in the United States, the prevalence of pericarditis declined but was still observed, even in well-dialyzed patients. This led to the recognition of a separate entity from uremic pericarditis, referred to as dialysis-associated pericarditis, diagnosed in patients who develop pericarditis after being on dialysis for at least 8 weeks (2). Others have questioned whether dialysis-associated pericarditis is, in fact, a separate entity from uremic pericarditis, noting that patients on dialysis who develop pericarditis often have a preceding period of underdialysis or missed sessions before symptoms develop (3,4), as was the case in our patient. The incidence of uremic pericarditis has declined to 5%, and the incidence of dialysis-associated pericarditis ranges from 2% to 21%, although recent data are lacking (1). Pericarditis occurs more commonly in younger individuals and more commonly in women than men (2).

Alternative Etiologies

Patients with kidney failure may also develop pericarditis from causes that affect the general population as well, such as malignancy, infection (viral, bacterial, or tuberculosis), and trauma. There are other etiologies of pericarditis that are probably more prevalent in patients with kidney failure than the general population, such as myocardial infarction, autoimmune disease (i.e., patients with kidney failure from lupus), use of certain medications (i.e., the use of hydralazine in patients with reduced GFR), and, rarely, direct perforation from dialysis catheter migration. If, after careful history and physical examination, no alternative etiology is apparent in a patient with kidney failure and pericardial disease, then the etiology can be presumed to be due to kidney failure.

Dialytic Management of Patients with Kidney Failure and Pericarditis

Intensity of Dialysis

Patients with uremic pericarditis respond rapidly to the initiation of dialysis, whereas dialysis-associated pericarditis has a much lower likelihood of responding to dialysis intensification (5). In the largest series of patients with kidney failure and pericarditis, those with uremic pericarditis had an 85% likelihood of responding to dialysis initiation, and those with dialysis-associated pericarditis had a 56% likelihood of improving with dialysis intensification (4). Given that many cases of dialysis-associated pericarditis may have a uremic contribution (i.e., a period of underdialysis or increased catabolism) and the low likelihood for harm from extra dialysis sessions, an intensified dialysis regimen, termed “superdialysis” by some (6), is recommended in cases of dialysis-associated pericarditis (1).

Our regimen for intensified dialysis is 4 hours of dialysis daily (or six times per week) for 7–14 days with limited echocardiography performed every 3 days to monitor for changes in the size of pericardial effusion and close monitoring of patient symptoms (2,4).

Other Dialysis Considerations

With more intensified dialysis, the use of a higher potassium bath may be required to prevent hypokalemia. In patients who have not missed hemodialysis sessions and develop pericarditis, we recommend checking the Kt/V to ensure that their routine dialysis is achieving adequacy. Because heparin exposure and pericardial hemorrhage have been proposed as contributors to dialysis-associated pericarditis, we use heparin-free dialysis or regional anticoagulation (if available) (1).

In cases of increased pericardial pressure, lower ultrafiltration rates should be used. Faster ultrafiltration rates can cause intradialytic hypotension even in stable patients on dialysis, and in the setting of increased pericardial pressure can cause transient intravascular volume depletion, precipitating tamponade physiology (7). Because of the increased frequency of dialysis, less ultrafiltration is required per treatment to maintain fluid balance.

Pharmacologic Interventions for Pericarditis in Kidney Failure

In a small randomized controlled trial, nonsteroidal anti-inflammatory drugs (NSAIDs) were found to improve fever but not chest pain, pericardial rub, or the size of pericardial effusion (6). Potential drawbacks of NSAIDs include worsening of residual kidney function and precipitating pericardial hemorrhage. Systemic steroids are effective in resolving pericardial symptoms but were found in early reports to result in increased serious infections (8). There are scant reports of colchicine use in patients with kidney failure and pericarditis, and there is significant risk of toxicity (1). We do not use NSAIDs, steroids, or colchicine in patients with kidney failure and pericarditis, focusing instead on optimizing dialytic therapy.

Invasive Management of Pericardial Effusion in Kidney Failure

The decision about when to pursue invasive drainage of pericardial effusion versus continuing conservative/dialytic management is a challenging one. This decision should be made jointly by the treating cardiologist and the nephrologist, and it depends on patient trajectory, serial echocardiography, and local expertise. Surgical window was previously favored as the initial treatment over percutaneous pericardiocentesis due to a high rate of recurrence after pericardiocentesis (in one large series, 70% recurrence) (7). In more recent years, pericardiocentesis with drain placement has become more common as initial therapy, with surgical management with pericardial window reserved for recurrent effusions or cases requiring pericardial biopsy. Excessive recurrence is not seen in the modern era, likely due to improved clearance with current dialytic methods. In a recent series, in 11 patients with dialysis-associated pericarditis treated with percutaneous drainage, no recurrences were noted at a mean follow-up of 18 months (9).

In a recent retrospective series of patients with kidney failure and pericarditis, risk factors that predicted requiring pericardial drainage included large size of pericardial effusion and hypoalbuminemia. All patients with a large pericardial effusion in this series required pericardial drainage (10).

In the setting of a large effusion that is asymptomatic, we pursue an initial trial of intensive dialysis if the cause is uremic pericarditis or if it is dialysis-associated pericarditis that was triggered by a period of underdialysis (which may be more likely to respond to dialytic therapy, akin to a true uremic pericarditis). In a well-dialyzed patient with dialysis-associated pericarditis with a large effusion, we recommend immediate drainage (8).

Our approach to patients with kidney failure and pericarditis is outlined in Figure 1.

Figure 1.

Recommended algorithm for the management of a patient with kidney failure and pericarditis. HD, hemodialysis. ^aWith fluid analysis for cell count and differential; gram and acid-fast stain; bacterial, mycobacterial, and fungal culture; adenosine deaminase; PCR for tuberculosis; and cytology.

Pericardial Fluid Analysis

When drainage is performed, the fluid should be sent for cell count and differential; gram and acid-fast stain; bacterial, mycobacterial, and fungal culture; adenosine deaminase; PCR for tuberculosis; and cytology (1). In case series of patients with kidney failure and pericardial effusion, pericardial fluid was usually serosanguinous with mononuclear predominance (2). There is no specific pericardial test that definitively demonstrates that a pericardial effusion was caused by uremia, and pericardial fluid analysis is most useful for ruling out alternative etiologies.

Case Conclusion

Our patient had a clear period of underdialysis as her likely trigger for pericarditis. Given that some dialysis-associated pericarditis responds to dialysis intensification and that she might have a component of uremia contributing, the decision was made to proceed with intensified dialysis. After 10 days of intensive dialysis, serial echocardiography demonstrated increasing size of pericardial effusion, and she underwent pericardiocentesis with drainage of 800 ml of fluid, with immediate improvement of her symptoms. By hospital discharge, the effusion had not reaccumulated. She has since been lost to follow-up.

Disclosures

R.J. Rosen is an editorial intern for American Journal of Kidney Diseases. The remaining author has nothing to disclose.

Funding

None.

Author Contributions

R.J. Rosen conceptualized the study; R.J. Rosen was responsible for investigation; R.J. Rosen wrote the original draft; and A.M. Valeri reviewed and edited the manuscript.