CASE REPORT

Transcatheter pharmacomechanical approach for acute renal veinthrombosis: a rational technique

Budunur C. Srinivas • Bhupinder Singh •

Sanjay Srinivasa • Shashikumar S. Reddy •

Nagesh C. Mahadevappa • Babu Reddy

Received: 7 September 2013 / Accepted: 29 October 2013

� Japanese Association of Cardiovascular Intervention and Therapeutics 2013

Abstract Acute renal vein thrombosis (RVT) causes

rapid deterioration of renal function if it is not treated

aggressively. Conventional anticoagulation therapy is the

standard mode of treatment; however, the need for rapid

and complete resolution has led to the development of

newer modes of treatment such as percutaneous catheter-

directed techniques. We describe a case of acute RVT with

deteriorating renal functions that highlights the rational of

percutaneous catheter-directed combined pharmacome-

chanical thrombolysis-thrombectomy approach to suc-

cessfully restore the renal vein patency with improvement

of the renal function.

Keywords Renal vein thrombosis � Transcatheter

treatment � Pharmacomechanical approach

Introduction

Renal vein thrombosis (RVT) was first described by

Rayer in 1840 [1]. RVT is a well-known, although

uncommon complication of nephritic syndrome and

hypercoagulable states such as antiphospholipid antibody

syndrome and factor V Leiden (i.e. R506Q) mutation.

RVT is associated with significant morbidity and the

standard treatment has largely been limited to conven-

tional anticoagulation therapy such as the administration

of heparin or warfarin [1]. Treatment with low-molecu-

lar-weight heparin [2] and systemic thrombolysis [3] has

also been described. Recently, catheter-directed tech-

niques have been used to treat acute RVT [4]. We

describe a catheter-directed pharmacomechanical throm-

bolysis-thrombectomy technique for the management of

RVT.

Case report

A 42-year-old male presented with a 3-day history of left-

sided flank pain with hematuria. The physical examination

was normal. Routine hematological work-up, liver function

test, antistreptolysin-O titer, C-reactive protein levels were

within normal limit. Blood urea (88 mg/dl) and serum

creatinine (1.9 mg/dl) were slightly elevated. Urine

microscopy was normal except for hematuria. The D-dimer

assay was positive (1400 lg/L). Transthoracic echocardi-

ography was normal with no evidence of pulmonary

embolism.

Electronic supplementary material The online version of thisarticle (doi:10.1007/s12928-013-0227-3) contains supplementarymaterial, which is available to authorized users.

B. C. Srinivas � B. Singh (&) � N. C. Mahadevappa � B. Reddy

Department of Cardiology, Sri Jayadeva Institute of

Cardiovascular Sciences and Research, Bangalore, Karnataka,

India

e-mail: dr_bhupinders@yahoo.in

B. C. Srinivas

e-mail: bcsrinivas@rediffmail.com

N. C. Mahadevappa

e-mail: drnageshcm@yahoo.com

B. Reddy

e-mail: drbabu2009@gmail.com

S. Srinivasa

Department of Nephrology, Suguna Hospital, Bangalore,

Karnataka, India

e-mail: drsanjaysrinivas@yahoo.co.in

S. S. Reddy

Department of Radiology, Suguna Hospital, Bangalore,

Karnataka, India

e-mail: sshashikumar@yahoo.com

123

Cardiovasc Interv and Ther

DOI 10.1007/s12928-013-0227-3

Renal ultrasound revealed a swollen left kidney with

echogenic upper half. Contrast-enhanced computed

tomography (CECT) revealed left RVT with extension to

Inferior vena cava (IVC) and enlarged left kidney with

inhomogeneous enhancement of its upper half (Fig. 1,

white arrow). Tc-99m diethylene-triamine-penta-acetic

acid (DTPA) scan showed absent perfusion and excretion

from the upper half of left kidney. In light of the severe

flank pain and deranged renal function, we planned for

catheter-directed pharmacomechanical thrombolysis-

thrombectomy. After informed consent was obtained, the

patient underwent an IVC angiogram. Ascending venogram

was done through right femoral vein using the 6 Fr pigtail

catheter (Cordis, Florida, USA) and revealed a large filling

defect in the IVC (Fig. 2a; Video1). In view of the risk of

pulmonary embolism associated with the lytic therapy, a

retrievable IVC filter (Trapase; Cordis, Florida, USA),

measuring 32 mm in size, was deployed in the hepatic

segment of IVC via right internal jugular vein (Fig. 2b). In-

Fig. 1 Contrast-enhanced computed tomography in venous phase

showing a large filling defect in left renal vein with extension to

inferior vena cava and enlarged left kidney with inhomogeneous

enhancement of its upper half

Fig. 2 Cine images showing technical steps of percutaneous cathe-

ter-directed pharmacomechanical thrombolysis and thrombectomy.

a Ascending venogram showing a large filling defect IVC at the L1-

L3 vertebral levels. b IVC filter deployed in the hepatic segment of

IVC. c Ascending venogram performed after 18 h of catheter-directed

in situ thrombolysis showing a filling defect (white arrows) at the

proximal edge of the filter that is suggestive of the trapped clot. d Left

renal venogram performed using 7F JR catheter that shows multiple

filling defects in the left renal vein, which is suggestive of large clot

burden. e Left renal venogram performed after thrombectomy and

12 h of catheter-directed in situ thrombolysis shows a cleared left

renal vein with good patency. f Cine showing the successful retrieval

of the IVC filter. IVC inferior vena cava, JR Judkin’s right

B. C. Srinivas et al.

123

situ thrombolysis was initiated with urokinase at the infu-

sion rate of 4400 units/Kg/h via 7F multipurpose catheter

(Cordis, Florida, USA) positioned in the IVC just below the

level of obstruction. Simultaneously, the heparin infusion

was started via peripheral venous access with maintenance

of APTT between 70 and 90 s. After 12 h, IVC angiogram

revealed migration of the IVC clot to the filter (Fig. 2c:

between white arrows; Video 2). The short femoral sheath

was exchanged with the 8F long sheath (45 cm; cook,

Bloomington, USA). Using a 7 Fr right coronary guide

catheter (Judkins; Cordis), selective left renal venogram

revealed multiple filling defects that were suggestive of

large thrombus burden (Fig. 2d; Video 3). In view of heavy

thrombus load, the aspiration was done using the same 7-Fr

multipurpose catheter (Cordis, Florida, USA). The throm-

bus aspiration was done three times and macroscopic

aspirate thrombus was visible to the naked eye. Subse-

quently, the catheter tip was positioned in the proximal part

of the left renal vein near the renal pelvis for in situ

thrombolysis. So, half of the urokinase infusion

(2200 units/Kg/h) was given through the multipurpose

catheter and rest half was given via long sheath. The con-

ventional heparin infusion was also continued via periphe-

ral line. After 18 h, the selective left renal venogram

revealed the complete resolution of clots (Fig. 2e; Video 4)

and IVC venogram also revealed resolution of clot in IVC

filter (Video 5). Subsequently, conventional heparin was

continued. Daily echocardiographic interrogation for the

evidence of pulmonary embolism and meticulous moni-

toring for bleeding complications from local puncture sites

or any other sites was done. Subsequently, on the fourth

day, the temporary IVC filter (Fig. 2f) was successfully

retrieved using a goose neck snare (Amplatz goose neck).

There was no clinical or echocardiographic evidence of

pulmonary embolism during the hospitalization. Patient was

discharged on oral anticoagulation after confirmation of

therapeutic international normalized ratio (between 2.0 and

2.5). At the time of discharge, the renal functions were

normalized. At the 6 weeks of follow-up, repeated CECT

(Fig. 3a) revealed normal renal parenchyma and no obvious

thrombus in the left renal vein. A DTPA scan performed at

the follow-up showed that both kidneys were well perfused

and normally functioning (Fig. 3b). A measurement of

protein C, protein S, antithrombin-III and homocysteine

levels as well as immunologic analysis for anticardiolipin

antibodies did not reveal any abnormalities. Oral antico-

agulation was continued for 12 months. The patient is doing

well at 18-months of follow-up.

Discussion

RVT is an uncommon event that complicates as many as

10 % of cases of nephrotic syndrome, but it is associated

with significant morbidity [5]. Other predisposing condi-

tions include neoplastic diseases, trauma and kidney

transplantation [6]. Occlusion of the renal vein is usually

gradual and confined to the main renal vein and larger

intrarenal veins, and with the development of collateral

drainage. Thus, patients commonly present with nausea,

generalized edema and progressive abdominal or back

pain. Rarely, the patient may be completely asymptomatic

if adequate collateral vessels are present. In contrast, as in

this case, the patients with acute RVT usually have a

dramatic course and present with clinical signs of acute

onset flank pain, gross hematuria and loss of function in the

involved kidney [7]. Bilateral renal involvement or the

involvement of the only solitary kidney can lead to oliguria

and renal failure.

The diagnosis of RVT is done most expeditiously with

color-flow Doppler ultrasonography, which may demon-

strate intravascular thrombus, renal enlargement, and

Fig. 3 At the 6-week follow-up, contrast-enhanced computed tomog-

raphy (a) in the venous phase showed normal left renal vein and left

renal parenchyma, and Tc-99m diethylene-triamine-penta-acetic acid

scan (b) showed well perfused and normally functioning bilateral

kidneys

Percutaneous treatment of renal vein thrombosis

123

diminished venous blood flow. Magnetic resonance imag-

ing may be helpful in the diagnosis [6]. A renal scintig-

raphy can be obtained to help assess baseline renal function

and for follow-up after therapy [6].

The choice of therapy for RVT depends on the clinical

presentation, disease progression and underlying renal

function. In general, anticoagulation with conventional

heparin, low-molecular-weight heparins or warfarin is

considered the mainstay of therapy [2]. Anticoagulants

impede the progression of the disease by blocking addi-

tional thrombosis while permitting slow recovery through

recanalization of occluded vessels. This delay may be

extremely detrimental in patients with bilateral RVT,

patients who have undergone kidney transplantation, or

patients with diminished renal function, anuria, or only one

kidney. Therefore, in these situations early diagnosis and

optimal treatment seem to be crucial. Treatment with sys-

temic thrombolysis [3] offers the possibility of more rapid

and complete resolution than anticoagulants, although the

risk of bleeding complications is higher. Recently, the

catheter-directed techniques have been utilized in the

management of acute RVT [8]. Indirect thrombolytic

therapy via the renal artery through infusion of thrombo-

lytic agents into small renal venous branches has been tried

in the past. However, this approach may result in diversion

of lytic agents through patent branches and capsular/peri-

capsular collateral vessels, thereby bypassing clotted

branches, limiting the utility of lytic agent infusion, and

prolonging therapy. In addition, there is a potential risk of

thrombosis or embolization in the renal artery and renal

arterial branches or the common femoral artery during

prolonged catheterization [9]. Advantages of direct

instilling of thrombolytic agents into venous clots have

been described in the treatment of lower-extremity deep

vein [10] and mesenteric vein [11] thrombosis. We have

adopted the similar principle in our case using percutane-

ous catheter-directed thrombolysis to allow the direct

instillation of the thrombolytic agent into the renal venous

clots, thereby avoiding the need for prolonged thrombol-

ysis or greater lytic doses. Both of these factors resulted in

the rapid removal of renal venous clots to promptly restore

the flow, thereby preventing the propagation of clots and

conserving the renal parenchyma to protect renal function.

In addition, direct access also permits the application of

additional potential therapies, such as catheter-directed

thrombectomy (as done in our case too), which further

permits faster achievement of patency, venoplasty for ste-

nosis or stent placement for elastic recoil or persistent

stenosis. So, in our patient we opted for the combined

approach of catheter-directed thrombectomy as well as

thrombolysis to achieve the faster renal vein patency.

Improvement in renal function and symptoms has been

reported after RVT was treated with systemic anticoagu-

lation alone [2], but faster recovery of the end point is

critical. Kim et al. [8] have demonstrated that percutaneous

catheter-directed thrombectomy with or without throm-

bolysis for acute RVT was associated with rapid

improvement in renal function and a low incidence of

morbidity. The use of IVC filter is also of utmost impor-

tance to avoid the fatal complication like pulmonary

embolism. As evident in our case, after starting the

thrombolysis a large clot was caught in the IVC filter that

would have otherwise caused the pulmonary embolism.

In conclusion, the catheter-directed thrombolysis with

adjuvant mechanical thrombectomy (a combined pharma-

comechanical approach) is a rational approach for the

management of acute RVT, especially so in patients having

the heavy thrombus burden, which likely reduces the time

required to clear the thrombus burden, thereby achieving

the faster latency of the renal vein and recovery of renal

functions.

Conflict of interest None.

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