Inferior vena cava thrombosis due to acute pyelonephritis

Nader Bassilios1, Marc Tassart2, Aymeric Restoux1, Jean-Michel Bigot2, Eric Rondeau1 and Jean-Daniel Sraer1

1Nephrology Department and 2Radiology Department, Tenon Hospital, Paris, France

Correspondence and offprint requests to: Nader Bassilios, MD, Réseau NEPHROPAR, Nephrology Department, Necker Hospital, 149, rue de Sèvres, F-75015 Paris, France. Email: nbassilios{at}hotmail.com

Keywords: inferior vena cava thrombosis; pyelonephritis



   Introduction
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 Introduction
 Case
 Discussion
 References
 
Renal vein thrombosis (RVT) is a common clinical condition among patients with nephrotic syndrome, with a relatively high prevalence (20–48%). It is most common in patients with membranous glomerulonephritis followed by membrano-proliferative glomerulonephritis and minimal change nephrosis [1]. However, there are other initiating conditions including diabetic nephropathy and trauma [1]. In patients with malignancy, RVT may be secondary to direct extension of tumour thrombus into the renal vein or may be due to a hypercoagulable state [2]. Presenting signs and symptoms of RVT include oliguria, haematuria, flank pain and azotaemia [2]. Thrombosis of the adjacent inferior vena cava (IVCT) at or near the renal vein orifices may also be present with a prevalence of 40–50% [3]. Renal malakoplakia, which is a chronic inflammatory process, generally confined to the urinary tract collecting system, is a rare cause of RVT [4]. RVT is mentioned in isolated reports of xanthogranulomatous pyelonephritis, which is an inflammatory condition involving the kidney and perirenal tissue, characterized by collections of lipid-laden macrophages. These cells are frequently referred to as foam cells or xanthoma cells [5]. RVT is an uncommon complication of acute pyelonephritis [6,7].

We report a case of septic RVT and IVCT with pulmonary embolism due to acute pyelonephritis.



   Case
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 Introduction
 Case
 Discussion
 References
 
A 45-year-old female was admitted for fever and dysuria for 3 days. The only other illness was diabetes mellitus discovered 3 years previously and which was diet controlled. Physical examination at admission showed fever at 39°C, blood pressure 100/70 mmHg, weight 80 kg height 1.67 m, heart rate 120 beats/min, dyspnoea with 30 breaths/min, orthopnoea. Heart sounds were regular and normal. The lungs at auscultation showed diffuse wheezes. The abdomen was soft, but vague tenderness was noted in the right lumbar region on deep palpation. Neither oedema nor cyanosis was found. Neurologic examination was normal.

Laboratory test results showed a metabolic acidosis on arterial blood gas with pH 7.21, and bicarbonate 10 mEq/l. A complete full blood cell count showed white blood cell 28 500/mm3 with 26 500/mm3 neutrophils, Hb 14 g/dl, platelets 243 000/mm3 and CRP 331 mg/l. Blood urea nitrogen was 5 mmol/l and creatinine 65 µmol/l. Urine analysis showed microalbuminuria, microscopic haematuria (>4 RBC/hpf) and white blood cells (>4 WBC/hpf). Klebsiella pneumoniae organisms were cultured from both the blood and urine. Renal ultrasound, which was done 24 h after admission showed a hyperechogenic focal area in the right kidney with possible thrombosis of the right renal vein. Abdominal and thoracic CT scans with contrast media confirmed thrombosis of the right renal vein and showed a triangular hypodense aspect of the right kidney without deformation of its outlines. This process invaded the inferior vena cava (Figure 1). The inferior vena cava below the renal veins was patent, the thrombosis extending up to the right atrial cavity confirmed by transoesophageal cardiac echography. Multiple bilateral pulmonary infarctions were seen on thoracic CT scan. Plasma protein C and S, factor V, anti-thrombrin III anti-phospholipid and anti-cardiolipin antibodies were either normal or negative. We did not assess plasma homocysteine level. There was no lower limb deep vein thrombosis on Doppler ultrasound. There was no vesical, renal, breast or gynecological malignancy. We did not screen for colon cancer.



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Fig. 1. Enhanced helical CT during the excretory phase shows a focal intra-parenchymal homogeneous round shaped hypoattenuated mass without perirenal fat CT abnormalities of the right kidney associated with a partial thrombosis of the inferior vena cava.

 
The patient was treated for her sepsis with i.v. fluid administration and antibiotics. Amikacine for 10 days, ceftriaxone and ofloxacine for 6 weeks. Initially the patient treated with i.v. heparin infusion for 7 days and subsequently with warfarin. Six months later there was good clinical outcome.

CT scanning demonstrated patency of the right renal vein, inferior vena cava, complete regression of the hypodense area of the right kidney and resolution of the thoracic abnormalities (Figure 2). Warfarin has been discontinued for 3 months now and the patient remains well.



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Fig. 2. Follow-up CT scan demonstrated the total disappearance of the renal lesion and inferior vena cava thrombosis.

 


   Discussion
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 Introduction
 Case
 Discussion
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Sepsis could be a dramatic example of the link between inflammation and thrombosis.

When Gram-negative bacteria release their endotoxin into the blood-stream, the lipopolysaccharide can change endothelial lining of blood vessels from an anticoagulant profibrinolytic surface into one that promotes thrombosis. Bacterial endotoxin potently stimulates expression of the gene encoding tissue factor, a procoagulant molecule that multiplies many fold the activity of coagulation factors VIIa and Xa. Endotoxin also can augment endothelial cell production of the fibrinolytic inhibitor plasminogen activator inhibitor-1 (PAI-I) [8]. Acute pyelonephritis is not considered as a common cause of RVT. RVT as a result of a purely infectious process of the kidney is a rare and probably late complication, although thrombosis as a consequence of a concomitant thrombophlebitis of the renal vein in pyelonephritis could be a possible explanation [9]. It is difficult to distinguish between acute pyelonephritis and RVT because both clinical conditions are characterized by fever, haematuria and flank pain. Eijsten et al. [6] reported a case of unilateral abscess-forming pyonephrosis due to K.pneumoniae infection with thrombosis of the renal vein and adjacent wall of the vena cava. This patient had removal of the renal vein together with the adjacent wall of the vena cava. Histological examination of the kidney showed no underlying carcinoma. In another reported case the diagnosis was made 8 days after commencing antibiotics [7]. The local infusion of recombinant tissue plasminogen activator can be considered as a second-line treatment for RVT and IVCT when a satisfactory response is not obtained with heparin [9]. The diagnosis of RVT and IVCT was confirmed by contrast CT and duplex Doppler [6,7]. In our patient the diagnosis of renal adenocarcinoma with RVT and IVCT associated with pulmonary embolism was suspected. The favourable evolution of the patient after treatment with antibiotics confirmed the diagnosis of pyelonephritis.

In conclusion, RVT and IVCT should be suspected as a complication especially in severe cases of acute pyelonephritis, when clinical signs of pulmonary embolism are present. In these cases renal ultrasound and a Doppler of the renal veins and IVC are mandatory.

Conflict of interest statement. None declared.



   References
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 Introduction
 Case
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Received for publication: 11. 6.02
Accepted in revised form: 22.10.03





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