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Saudi Journal of Kidney Diseases and Transplantation
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Table of Contents   
LETTER TO THE EDITOR  
Year : 2019  |  Volume : 30  |  Issue : 3  |  Page : 747-748
Inferior vena cava compression and acute kidney injury


1 Department of Medicine, Division of Gastroenterology and Hepatology, Kawasaki Municipal Tama Hospital, Shukugawara, Tama-ku, Japan
2 Department of Internal Medicine, Division of Nephrology and Hypertension, St. Marianna University Hospital, Sugao, Miyamae-ku, Kawasaki City, Kanagawa, Japan

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Date of Submission14-Sep-2018
Date of Acceptance19-Sep-2018
Date of Web Publication26-Jun-2019
 

How to cite this article:
Nakano H, Imai N, Shibagaki Y. Inferior vena cava compression and acute kidney injury. Saudi J Kidney Dis Transpl 2019;30:747-8

How to cite this URL:
Nakano H, Imai N, Shibagaki Y. Inferior vena cava compression and acute kidney injury. Saudi J Kidney Dis Transpl [serial online] 2019 [cited 2019 Jul 23];30:747-8. Available from: http://www.sjkdt.org/text.asp?2019/30/3/747/261366


To the Editor,

A 73-year-old male with a past medical history of hypertension presented with bilateral lower-leg edema for one month. Physical examination was notable for upper abdominal distention with pretibial pitting edema. Laboratory tests showed serum urea nitrogen of 30.4 mg/dL, creatinine of 2.38 mg/dL, and brain natriuretic peptide of 24.6 pg/mL. Serum liver enzymes and thyroid hormone were within normal limits. The urine dipstick showed 2+ proteinuria without hematuria. Protein-to-creatinine (P/C) ratio of spot urine was 0.71 g/gCr. Further workup with contrast-enhanced computed tomography showed a large cyst in the caudate lobe almost completely compressing the inferior vena cava (IVC) [Figure 1]a, and a marked growth of collateral flow around the IVC [Figure 1]b.


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Acute kidney injury (AKI) was thought to be caused by the large hepatic cyst completely compressing the IVC and hemodynamically congesting the renal veins. To reduce the size of the cyst and to decompress the IVC, a catheter was placed into the cyst, and the cavity was sclerosed by administering ethano-lamine oleate. Following the procedure, there was a marked reduction of the size of the cyst, and the IVC was successfully decompressed [Figure 2]a. The blood flow of the IVC was restored, and there was a reduction of collateral flow around the IVC [Figure 2]b. Bilateral lower-leg edema and upper abdominal distention completely disappeared. His serum creatinine and P/C ratio of spot urine normalized to 0.86 mg/dL and 0.02 g/gCr, respectively.


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Decompression of the IVC resolves the high venous pressure of renal veins and reduces the renal interstitial pressure.[1] Decongestion of the renal vein is known to be important in the management of a patient with cardiorenal syndrome.[2] Although AKI due to compression of the IVC is rare, renal vein congestion due to IVC compression should be recognized as an often overlooked but treatable cause of AKI.

Informed consent was obtained from the patient before publishing the manuscript.

Conflict of interest: None declared.



 
   References Top

1.
Ross EA. Congestive renal failure: The pathophysiology and treatment of renal venous hypertension. J Card Fail 2012;18:930-8.  Back to cited text no. 1
    
2.
Mullens W, Abrahams Z, Francis GS, et al. Importance of venous congestion for worsening of renal function in advanced decompensated heart failure. J Am Coll Cardiol 2009;53:589-96.  Back to cited text no. 2
    

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Correspondence Address:
Naohiko Imai
Department of Internal Medicine, Division of Nephrology and Hypertension, St. Marianna University Hospital, Sugao, Miyamae-ku, Kawasaki City, Kanagawa
Japan
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DOI: 10.4103/1319-2442.261366

PMID: 31249247

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    Figures

  [Figure 1], [Figure 2]



 

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