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 Table of Contents  
Year : 2016  |  Volume : 4  |  Issue : 1  |  Page : 15-17

Pulmonary embolism as the primary presenting feature of nephrotic syndrome

Metro Center for Respiratory Diseases, Metro Multi Specialty Hospital, Noida, Uttar Pradesh, India

Date of Web Publication23-Dec-2015

Correspondence Address:
Arjun Khanna
Metro Center for Respiratory Diseases, Metro Multi Specialty Hospital, Sector 11, Noida - 201 301, Uttar Pradesh
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/2320-8775.168621

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A 36-year-old previously healthy male presented with subacute onset of shortness of breath and chest pain. He was diagnosed with bilateral extensive pulmonary embolism (PE). In the absence of any predisposing factors, an extensive workup for unprovoked thrombophilia was done. During the course of his illness, the patient developed anasarca and was diagnosed to be suffering from nephrotic syndrome (NS), secondary to membranous glomerulopathy. Although, thrombotic complications are commonly associated with NS, it is unusual for PE to be the primary presenting feature in these patients.

Keywords: Membranous glomerulopathy, nephrotic syndrome, pulmonary embolism

How to cite this article:
Periwal P, Khanna A, Nair V, Talwar D. Pulmonary embolism as the primary presenting feature of nephrotic syndrome. J Assoc Chest Physicians 2016;4:15-7

How to cite this URL:
Periwal P, Khanna A, Nair V, Talwar D. Pulmonary embolism as the primary presenting feature of nephrotic syndrome. J Assoc Chest Physicians [serial online] 2016 [cited 2022 Jan 27];4:15-7. Available from: https://www.jacpjournal.org/text.asp?2016/4/1/15/168621

  Introduction Top

The workup of a patient with unprovoked thrombotic vascular events is always challenging for the treating physician. The routinely prescribed battery of tests is difficult to administer completely and often turn out to be negative, complicating the situation further. We describe here, the case of a previously healthy young male who presented with unprovoked extensive pulmonary embolism (PE). At the time of presentation, he had no clinical features suggestive of nephrotic syndrome (NS). However, during the workup of PE the patient developed anasarca which prompted the work up for various etiologies, including NS. Further testing established the diagnosis of NS secondary to membranous glomerulopathy. It is well-known that patients with NS have thrombotic complications, but extensive PE as a presenting feature of previously undiagnosed and clinically inapparent NS is extremely uncommon.

  Case Report Top

A 36-year-old, previously healthy, yoga trainer, nonsmoker male, presented with 3 months history of shortness of breath. The shortness of breath was first noticed during exercise, which progressed over the next 3 months. He developed acute onset left sided chest pain, 3 months into the illness. On evaluation at a peripheral center he was diagnosed as a case of community-acquired pneumonia with synpneumonic effusion. There was no improvement with antibiotic therapy and further evaluation with a contrast enhanced computed tomography (CT) scan of the chest revealed a partial filling defect in the right main pulmonary artery extending into the right descending artery and its branches. There was near complete filling defect in the descending left pulmonary artery and a small airspace consolidation with minimal pleural effusion. This was suggestive of bilateral PE with left-sided pulmonary infarct. He was started on subcutaneous fondaparinux and warfarin therapy as per the standard recommendations. Doppler scan of both lower limbs was not suggestive of any deep venous thrombosis. The patient was incompletely investigated for thrombophila in the form of protein C level (172%), protein S level (130%), and factor V Leiden mutation analysis, which were all normal. The patient presented to our center with worsening dyspnea and for further evaluation. General survey revealed a well-built male with tachypnea (respiratory rate 24/min) and tachycardia with a pulse rate of 106/min. His blood pressure was 110/70 mmHg. Chest examination was unremarkable, and the rest of the systemic examination was normal. X-ray chest was essentially normal. An emergency two-dimensional echo revealed adequate systolic function of the left and right ventricles with no regional wall motion abnormality, mild pulmonary artery hypertension and an echogenic mass, suggestive of embolus was visualized in the main pulmonary artery. Doppler scan of both lower limbs was unremarkable. Laboratory investigations revealed, hemoglobin of 14 g/dL, total leucocyte count 10,500 cumm, and platelet count of 2 lakh/mm 3. Serum urea was 16 mg/dL and serum creatinine 0.6 mg/dL, serum sodium was 134 mEq/L and potassium 3.5 mEq/L. Liver function test relieved a total bilirubin of 0.7 mg/dL, AST was 43 U/L, and ALT was 34 U/L. As there was no obvious predisposing factor for PE, tests for the etiology of the thrombophilic state were ordered. Venereal disease research laboratory and rapid plasma reagin tests for syphilis were nonreactive. Anti-thrombin III (AT-III) levels were low - 106 mg/L (normal - 260–378 mg/L). Lupus coagulant and JAK2 mutation was negative and so were anticardiolipin antibodies (1.49 GPL units). HIV antibodies were nonreactive. During the course of the hospital stay, the patient started developing bilateral pedal edema along with periorbital puffiness. An emergency two-dimensional echo was done expecting worsening right heart failure and clot extension. However, it did not show a worsening of the cardiac status or an increase in the pulmonary artery pressures. A repeat CT pulmonary angiogram was done which revealed extensive pulmonary emboli in the right and left pulmonary arteries [Figure 1] with extension of the thrombus in secondary and tertiary branches of the right lobe, right renal vein, and the inferior vena cava. Repeat blood biochemistry revealed, low total serum protein levels (3.80 g/dL), decreased total serum albumin (1.10 g/dL), and normal thyroid functions. 24 h urinary protein examination done subsequently showed urinary protein loss of 15 g/day establishing the diagnosis of NS. Fasting lipid profile was grossly deranged. Total serum cholesterol was 414 mg/dL, triglyceride 502 mg/dL, high-density lipoprotein 32 mg/dL, low-density lipoprotein 282 mg/dL, further strengthening the diagnosis of NS. An ultrasound guided right sided kidney biopsy, and histopathological examination revealed an increase in the content of protein reabsorption drops in the proximal tubules. Immunofluorescence staining revealed strong intensity granular staining along the capillary basement membrane for IgG and a similar staining pattern for C3 within all the glomeruli. No staining was noted for C1q, IgA, and IgM. This pattern was suggestive of membranous glomerulopathy. In conjugation with the nephrologist, the patient was started on tablet dabigatran, tacrolimus, prednisolone, and atorvastatin. He is under close follow-up and is presently doing well.
Figure 1: Computed tomography pulmonary angiogram showing bilateral filling defects in the pulmonary arteries suggestive of pulmonary emboli

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  Discussion Top

NS is characterized by proteinuria of ≥3.5 g/24 h, albuminemia <3.0 g, peripheral edema, hyperlipidemia, lipiduria, and increased thrombotic risk.[1] Patients with NS are at an increased risk for thrombotic events such as deep venous thrombosis, renal vein thrombosis, and PE.[2] NS secondary to membranous nephropathy may impose a greater thrombotic risk for unclear reasons.[3] Enhanced platelet aggregation, and renal losses of anticoagulant proteins such as AT-III are thought to underlie the excessive thrombotic risk in patients with NS.[4]

Current literature suggests that patients with low serum albumin levels and membranous nephropathy may benefit from primary prophylactic anticoagulation.[3] The exact duration of anticoagulation for these patients is unclear. However, most authorities recommend the same for at least 2 years. Patients with NS also have an increased risk of renal vein thrombosis and, in some patients with NS and PE, the origin of pulmonary embolus is from the renal veins,[5] as was the case in our patient. In a patient with known NS, the treating physician should always anticipate the risk of thrombotic complications and investigate a patient accordingly, if they develop features suggestive of PE. Our case is unique, as the patient had pulmonary embolization as the primary presenting feature and did not have any evidence of NS prior to this episode.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Hull RP, Goldsmith DJ. Nephrotic syndrome in adults. BMJ 2008;336:1185-9.  Back to cited text no. 1
Cameron JS, Hicks J. The origins and development of the concept of a “nephrotic syndrome”. Am J Nephrol 2002;22:240-7.  Back to cited text no. 2
Lionaki S, Derebail VK, Hogan SL, Barbour S, Lee T, Hladunewich M, et al. Venous thromboembolism in patients with membranous nephropathy. Clin J Am Soc Nephrol 2012;7:43-51.  Back to cited text no. 3
Mittal A, Aggarwal KC, Saluja S, Aggarwal A, Sureka B. Platelet functions and coagulation changes in Indian children with nephrotic syndrome. J Clin Diagn Res 2013;7:1647-50.  Back to cited text no. 4
Kayali F, Najjar R, Aswad F, Matta F, Stein PD. Venous thromboembolism in patients hospitalized with nephrotic syndrome. Am J Med 2008;121:226-30.  Back to cited text no. 5


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