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NDT Advance Access originally published online on May 2, 2008
Nephrology Dialysis Transplantation 2008 23(7):2422-2423; doi:10.1093/ndt/gfn245
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© The Author [2008]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org


Chronic inferior venacava thrombosis in membranous nephropathy

Murugesan Ram Prabahar1, Matcha Jayakumar2 and Periasamy Soundararajan1

1 Department of Nephrology, Sri Ramachandra Medical College, Sri Ramachandra University, Chennai-116 2 Department of Nephrology, Madras Medical College, Government General Hospital Chennai-3, The Tamilnadu Dr MGR Medical University, Tamilnadu, India

Correspondence and offprint requests to: M. Ram Prabahar, Department of Nephrology, Sri Ramachandra Medical College, Sri Ramachandra University, Chennai-116, Tamilnadu, India. Tel: +91-44-2476-5512 extn: 491; Fax: +91-44-2476-7008; E-mail: prabahar76{at}yahoo.co.in

Keywords: membranous nephropathy; nephrotic syndrome; venous thrombosis

A 30-year-old gentleman, a known membranous nephropathy patient since 2002, presented a month ago for recurrent bipedal oedema and dilated veins in front and back of abdomen (Figure 1). After contrast prophylaxis, a venogram was done with the intention of intervention in the same sitting if required. His venogram showed non-visualization of the entire infra-hepatic inferior venacava (IVC) that was replaced by collaterals with reformation of the supra-hepatic segment of the IVC (Figure 2). He was treated with placement of an IVC filter and anticoagulation.


Figure 1
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  		Fig. 1 Dilated veins in front of chest (white arrows) and abdomen (black arrows).

 

Figure 2
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  		Fig. 2 Venography right lateral view showing the collaterals (black arrows) in the hepatic segment of IVC with reformation of the supra-hepatic segment (thin black arrow). Note the posterior collaterals extending into the chest (white arrow).

 
Patients with nephrotic syndrome have an increased incidence (10–40%) of arterial and venous thrombosis particularly of the deep veins and renal veins. A variety of haemostatic abnormalities contribute to the hypercoagulable state including loss of antithrombin, hyperaggregablity of platelets and clotting factor abnormalities such as elevation of factors V, VII, VIII and fibrinogen [1].

Thrombosis of the adjacent IVC at or near the renal vein origin causes complications in 40–50% of patients with thrombosis of renal veins. Acute thrombosis of IVC should be treated as a medical emergency as pulmonary embolism and deterioration of renal function may follow [2]. Chronic IVC thrombosis is difficult to treat as they have well-established collaterals making intervention difficult.

Conflict of interest statement. None declared.



   References
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 References
 

  1. Crew RJ, Radhakrishnan J, Appel G. Complications of the nephrotic syndrome and their treatment. Clin Nephrol (2004) 62:245–259.[Web of Science][Medline]
  2. Jeremiah P, Mackenzie P, Fox JG, et al. Acute inferior venacaval thrombosis in a patient with membranous nephropathy treated by rt-PA lysis. Nephrol Dial Transplant (1999) 14:210–213.[Abstract/Free Full Text]
Received for publication: 14. 7.07
Accepted in revised form: 9. 4.08


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This Article
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Right arrow All Versions of this Article:
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Right arrow Articles by Prabahar, M. R.
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