Epidemiology and Pathogenesis
Renal vein thrombosis (RVT) may occur in the main trunk or branches of one or both renal veins and often presents with subtle clinical manifestations. RVT is most commonly associated with nephrotic syndrome and renal cell carcinoma, with an occurrence rate of approximately 5%–62% in patients with nephrotic syndrome, especially in those with membranous nephropathy. Cases have also been reported in association with trauma, oral contraceptive use, and hypovolemia. Predisposing factors for RVT include hypercoagulable states and reduced renal venous blood flow. Spontaneous RVT is rare in the absence of underlying risk factors.
Clinical Manifestations
The clinical presentation of RVT depends on factors such as the extent, severity, and progression of the renal vein obstruction. In acute RVT, symptoms may include nausea, emesis, flank pain on the affected side, elevated white blood cell counts, hematuria, impaired renal function, and imaging evidence of renal enlargement on the affected side. These symptoms may resemble renal colic or pyelonephritis. Chronic RVT tends to have an insidious onset and may lead to tubular dysfunction, manifesting as renal glycosuria, aminoaciduria, impaired urinary acidification, and hyperphosphaturia. In cases of nephrotic syndrome complicated by RVT, a significant increase in proteinuria may occur. Pulmonary embolism, resulting from dislodged thrombi, manifests in 10%–30% of patients with chronic RVT, often revealing abnormal results on ventilation-perfusion scans, although most patients are asymptomatic.
Diagnosis
Patients with acute RVT frequently present with prothrombotic conditions. Contrast-enhanced computed tomography (CT) may reveal renal enlargement, calyceal distension, and ureteric indentation on the affected side. Renal vein angiography is typically considered only in cases where acute kidney injury necessitates thrombectomy or thrombolysis. Chronic RVT is often incidentally identified during imaging studies performed for unrelated reasons. Thrombi associated with renal cell carcinoma often extend into the inferior vena cava and may occasionally reach the level of the right atrium. Routine RVT screening in patients with nephrotic syndrome is not recommended, though enhanced CT may be considered if specific clinical signs suggest RVT.
Treatment
For both acute and chronic RVT, treatment involves anticoagulation with low-molecular-weight heparin or heparin for 7–10 days, followed by the initiation of oral warfarin on the third day, with therapy continuing for at least one year and maintaining a target international normalized ratio (INR) of 2.0–3.0. The clinical use of novel oral anticoagulants in RVT lacks sufficient evidence. In patients with persistent thrombosis risk factors, long-term anticoagulation therapy is necessary. For acute RVT associated with acute kidney injury, localized thrombolysis in the renal vein or systemic fibrinolytic therapy may be considered. Additionally, the underlying disease should be treated actively, with appropriate management of water and electrolyte balance.