We report the case of a 51-year-old man diagnosed with chronic kidney disease (CKD) caused by IgA nephropathy at 50 years. Steroid treatment for IgA nephropathy was initiated 4 months before admission. One month before admission, he noticed pain and oedema in his right lower limb. The patient visited our hospital because of worsening pain and oedema after sitting for long periods of time, both 1 and 3 weeks before presentation. There was no chest pain or shortness of breath during exertion. Blood pressure, pulse, and percutaneous arterial oxygen saturation at room air were 150/86 mmHg, 71 b.p.m., and 98%, respectively. Auscultation revealed no obvious abnormalities in heart or respiratory sounds. No jugular vein distention was observed. The patient reported oedema from the right thigh to the lower leg and grasping pain on the dorsum of the lower leg. The patient had a score of 8 points on the Villalta scale, with 2 points each for pain and heaviness, anterior tibial oedema, and grasping pain of the lower leg. The patient’s platelet count, d-dimer, creatinine, albumin, and high-sensitivity troponin levels were 20.8 × 104/µL (reference: 14.6–34.8 × 104/µL), 17.2 µg/mL (reference: 0.00–1.00 µg/mL), 1.79 mg/dL (reference: 0.65–1.07 mg/dL), 3.8 g/dL (reference: 3.9–4.9 mg/dL), and 0.02 ng/mL (reference: 0.00–0.04 ng/mL), respectively. Twelve-channel electrocardiography showed a sinus rhythm with a pulse of 57 b.p.m. and was otherwise unremarkable. Chest radiography revealed a cardiothoracic ratio of 41% but no cardiomegaly or abnormalities in the lung fields. Transthoracic echocardiography revealed a left ventricular ejection fraction of 62%, a trans-tricuspid pressure gradient of 19 mmHg, and no right atrial or ventricular enlargement. The patient had CKD; therefore, to prevent contrast agent nephropathy, 0.9% normal saline was administered at 1 mL/kg/h from 2 h before to 24 h after contrast agent administration. Subsequently, contrast-enhanced computed tomography (CT) was performed, revealing multiple thrombi in both pulmonary arteries ( and ). No compression of the left common iliac vein was observed (). The right external iliac vein (EIV) ran between the right internal iliac artery (IIA) and external iliac artery (EIA), but its evaluation was insufficient (). Imaging obtained during the venous phase revealed a thrombus from the distal side of the right femoral vein to the deep leg vein (). No neoplastic lesions were observed from the chest to the pelvis. The patient was diagnosed with deep vein thrombosis (DVT) and non-massive pulmonary embolism (PE) equivalent to a simplified PE severity index of 0 and was admitted on the same day for further investigation and treatment. The antithrombin, plasminogen, protein C, protein S, fibrinogen, tissue plasminogen activator/plasminogen activator inhibitor-1 complex, total homocysteine, anticardiolipin-β2 glycoprotein-I complex antibody, and antinuclear antibody levels were within the normal range. After hospitalization, anticoagulant therapy with direct oral anticoagulants (DOAC; edoxaban 30 mg) was initiated, and compression stockings were applied. Lower extremity magnetic resonance angiography (MRA) without contrast agents was performed on Day 3. This revealed compression of the right EIV by the right IIA and EIA (). On quantitative evaluation, the distal EIV maximum minor diameter was 13.3 mm and maximum compression diameter was 2.1 mm, indicating severe stenosis (84%). Following treatment, the lower extremity pain and oedema resolved. Upper gastrointestinal endoscopy and human haemoglobin tests were performed on Day 8, with no abnormal findings. By that point, the patient’s d-dimer level improved to 2.2 µg/mL, and his symptoms had significantly improved (Villalta scale 1, with 1 point for anterior tibial oedema). Furthermore, he declined to undergo treatment with a stent and was discharged from the hospital, with a plan to consider invasive treatments, such as a stent placement, if his condition showed any signs of deterioration. d-Dimer levels normalized to 0.1 g/mL at 1.5 months after discharge and remained at <0.1 µg/mL thereafter. Nonetheless, despite the absence of dyspnoea or lower limb oedema, lower extremity ultrasonography performed 6 months later revealed residual thrombus (). Once again, we proposed catheterization with a stent, but the patient declined this option. Consequently, we continued therapy with edoxaban 30 mg. Thereafter, conservative treatment with edoxaban 30 mg was performed until 8 months after discharge from hospital, but the patient’s clinical course was uneventful, with no recurrence of lower limb oedema, pain, or dyspnoea. Furthermore, since the patient’s ongoing treatment for IgA nephropathy involved steroids and RIVCS persisted, we plan to continue the DOAC therapy.