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Severe tricuspid regurgitation as a rare cause of renal transplant dysfunction
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Presentation A 66 year-old female patient underwent renal transplantation in August 2005 and presented with unexplained poor glomerular filtration rate (GFR) in April 2006.
 
 
 
Caption: Figure 1 Time course of serum creatinine and cystatin C as well as biopsy findings and interventions.
Description:  GFR denotes glomerular filtration rate as calculated from cystatin C
 
 
 
Caption: Fig. 2a Renal transplant, transverse view
Description: Note the prominent transplant vein (arrow).
 
 
 
Caption: Fig. 2b Renal transplant, transverse view
Description: Duplex confirms periodic backward flow in the renal transplant vein, indicative of severe tricuspid regurgitation.
 
 
 
Caption: Figure 3 Doppler of distal segmental renal transplant vein
Description: Doppler of distal segmental renal transplant vein, showing abnormal biphasic flow with strong back-flow component
 
 
 
Caption: Figure 4 Duplex of the inferior vena cava
Description: Duplex of the inferior vena cava, showing backward flow during cardiac systole due to severe tricuspid regurgitation
 
 
 
Caption: Figure 5 Duplex of the hepatic veins
Description: Duplex of the hepatic veins, also showing backward flow during cardiac systole due to severe tricuspid regurgitation
 
Final Diagnosis Severe tricuspid regurgitation causing renal transplant dysfunction
 
Discussion A 66 year-old female patient underwent renal transplantation in August 2005 and presented with unexplained poor glomerular filtration rate (GFR) in April 2006.

The transplant showed initial non-function as well as one episode of biopsy-proven mild tubulo-interstitial rejection in September 2005. This was treated with intravenous methylprednisolone and conversion of the immuno-suppression to tacrolimus. However the transplant continued to function poorly and the GFR remained around 20 ml/min. Successive biopsies were performed to exclude persistent rejection; these showed only tubular damage. The tacrolimus dose was reduced and another transplant ultrasound requested in view of the unexplained transplant dysfunction (Figure 1).

B/w ultrasound showed a non-obstructed renal transplant in the left iliac fossa. The size of the transplant was appropriate in relation to the recipient’s body weight; the width of the parenchyma was normal and only minor parenchymal changes were noted. The first abnormal finding was that the entire transplant was unusually pulsatile with a very prominent transplant vein (Figure 2a). Duplex studies showed biphasic flow with a strong retrograde component (Figure 2b). The renal resistive index in the distal segmental arteries was 0.67. There was no evidence of transplant renal artery stenosis and the iliac artery was unremarkable. On careful colour duplex scanning there was no evidence of any arterio-venous fistula, aneurysm or any other vascular malformation. Examination of the segmental veins of the transplant confirmed biphasic flow (Figure 3). Colour duplex scanning of the inferior vena cava was also performed and showed a dilated inferior cava and a strong retrograde flow component (Figure 4), indicative of at least moderate tricuspid regurgitation. Colour duplex of the liver veins confirmed biphasic flow with a strong retrograde component (Figure 5), confirming the suspicion of at least moderate if not severe tricuspid regurgitation.

A formal echocardiogram confirmed moderate to severe tricuspid regurgitation. The situation was discussed with the patient who made an informed decision against tricuspid surgery. Transplant function remained impaired but stable.

Discussion

Severe tricuspid regurgitation is a rare cause of renal transplant dysfunction. In our case the severity of tricuspid regurgitation was only appreciated as an incidental finding during ultrasound. We will briefly review the relationship between cardiac disease, venous filling and renal function as well as teaching points from this case from an ultrasound point of view.

The influence of chronic left ventricular disease on renal function is well described and mediated by activation of the neuro-hormonal axis and in particular the renin-angiotensin (RAA) system. In contrast the effects of right ventricular disease on renal function are less well understood, much less so in transplant patients. What we know is that right ventricular failure also activate the RAA system as well. However the issue is further compounded by the fact that right ventricular disease encompasses several very different disease entities, ranging from primary pulmonary hypertension to valvular disease. Each of them may have a distinct effect on renal function. This issue is reviewed in great detail elsewhere (3).

In acute congestive heart failure it was long believed that hypotension and renal hypoperfusion were responsible for impaired renal function. This concept had been dubbed the “pre-renal syndrome” or “acute cardio-renal syndrome”. More recently it has been understood that increased venous filling and elevated pressures within the renal vein alone cause renal impairment (1). This, we believe, was also the pathogenesis of impaired transplant function in our case. In a study in 196 patients with congestive heart failure Maeder and colleagues were able to show that the severity of tricuspid regurgitation was associated with lower glomerular filtration rate (2). Another study by Damman and co-workers showed that venous congestion reduces renal blood flow as a crucial factor that influences GFR. These studies give us further confidence in our interpretation in the case under discussion.

    From an ultrasound point of view it is worthwhile to remember that tricuspid regurgitation and right-sided venous congestion are easily identified on routine abdominal ultrasound. So much so that abdominal ultrasound is used by emergency physicians as a screening tool for congestive heart failure (7). Another advantage in the emergency and acute medical setting is that pleural effusions and pericardial effusion can be detected as well. Diameters of the extra-hepatic inferior vena cava in excess of 2 cm are believed to be abnormal. Lack of diameter change with respiration is an even more specific sign for increased filling of the vena cava and the use of a “collapsibility index” has been proposed (8). Dilated hepatic veins are also easily identified. Abnormal portal flow is also seen in advanced congestive heart failure (9). Tricuspid regurgitation has specific signs on ultrasound and is easily identified with duplex studies. Key findings are systolic backward flow in the inferior vena cava and hepatic veins (as seen in the case under discussion). It is believed that the severity of tricuspid regurgitation can be gauged according to the extent of backward flow although appropriate studies are lacking. In our case the backward flow extended as far as the renal transplant vein in the pelvis, suggesting severe tricuspid regurgitation. This was later confirmed by a formal echocardiogram.
Ultrasound of the inferior vena cava is widely used by nephrologists to fine-tune the target weight of dialysis patients (10) (11). Compared to other techniques ultrasound of the inferior cava is not difficult to learn and valid (12). Others have previously described the incidental finding of tricuspid regurgitation on renal imaging (4). Jacobson and co-workers described a case where severe tricuspid regurgitation was picked up during renal scintigraphy (4).

It is well known that the diameter of the inferior vena cava correlates with right-sided (5) and with central venous pressures (6).

In summary this case provided some interesting and highly unusual findings during renal transplant ultrasound. The fact that the renal transplant showed venous pulsation was particularly remarkable and reminded of the pulsatile liver also seen in severe tricuspid regurgitation (Rosenbach’s sign). Our case also serves as a reminder to pay more attention to the renal transplant veins, which are often completely forgotten during routine ultrasound.
 
Case References
  1. Wencker D. Acute cardio-renal syndrome: progression from congestive heart failure to congestive kidney failure. Curr Heart Fail Rep 2007;4:134-8.
  2. Maeder MT, Holst DP, Kaye DM. Tricuspid regurgitation contributes to renal dysfunction in patients with heart failure. J Card Fail 2008;14:824-30.
  3. Schrier RW, Bansal S. Pulmonary Hypertension, Right Ventricular Failure, and Kidney: Different from Left Ventricular Failure? Clin J Am Soc Nephrol 2008;3:1232-7.
  4. Jacobson AF, Whitley MA, Harrison SD, Cerqueira MD. Massive tricuspid regurgitation identified on renal flow scintigraphy. Clin Nucl Med 1991;16:767-9.
  5. Capomolla S, Febo O, Caporotondi A, et al. Non-invasive estimation of right atrial pressure by combined Doppler echocardiographic measurements of the inferior vena cava in patients with congestive heart failure. Ital Heart J 2000;1:684-90.
  6. Arthur ME, Landolfo C, Wade M, Castresana MR. Inferior Vena Cava Diameter (IVCD) Measured with Transesophageal Echocardiography (TEE) Can Be Used to Derive the Central Venous Pressure (CVP) in Anesthetized Mechanically Ventilated Patients. Echocardiography 2008.
  7. Blehar DJ, Dickman E, Gaspari R. Identification of congestive heart failure via respiratory variation of inferior vena cava diameter. Am J Emerg Med 2009;27:71-5.
  8. Goei R, Ronnen HR, Kessels AH, Kragten JA. Right heart failure: diagnosis via ultrasonography of the inferior vena cava and hepatic veins. Rofo 1997;166:36-9.
  9. Hosoki T, Arisawa J, Marukawa T, et al. Portal blood flow in congestive heart failure: pulsed duplex sonographic findings. Radiology 1990;174:733-6.
  10. Cheriex EC, Leunissen KM, Janssen JH, Mooy JM, van Hooff JP. Echography of the inferior vena cava is a simple and reliable tool for estimation of 'dry weight' in haemodialysis patients. Nephrol Dial Transplant 1989;4:563-8.
  11. Toprak A, Koc M, Tezcan H, Ozener IC, Akoglu E, Oktay A. Inferior vena cava diameter determines left ventricular geometry in continuous ambulatory peritoneal dialysis patients: an echocardiographic study. Nephrol Dial Transplant 2003;18:2128-33.
  12. Kouw PM, Kooman JP, Cheriex EC, Olthof CG, de Vries PM, Leunissen KM. Assessment of postdialysis dry weight: a comparison of techniques. J Am Soc Nephrol 1993;4:98-104.

 
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