Renal Tamponade from Extensive Venous Thrombus

Introduction: Venous congestion leading to renal dysfunction is well described but frequently underdiagnosed. Targeted therapy to reduce venous pressures can dramatically improve renal function. Here, we present a case of extensive venous thrombosis causing acute oligo-anuric renal failure due to renal tamponade. Case Description: An 82 year-old M with a history of CLL presented to the ED with complaint of back/leg pain and oliguria. One week prior, he had been diagnosed with urinary retention leading to foley catheter placement. Over the past 2-3 days, he endorsed minimal urine output in the catheter bag. Initial labs revealed acute renal failure (sCr: 5.47 mg/dL) with baseline renal function (sCr: 1.0 mg/dL) documented one week prior. FeNa was 1.2%. CT A/P revealed a properly placed foley catheter and no evidence of hydronephrosis. The patient was admitted to the ICU for medical management. During hospitalization, he remained oligo-anuric. LE duplex US revealed acute occlusive, bilateral DVT's involving the femoral and iliac veins, extending into the IVC. Renal US with doppler revealed patent renal arteries and veins. He was initiated on systemic heparin therapy and later underwent thrombectomy. After the procedure, he developed polyuria (UOP 5L/ day) with gradual improvement in renal function over the subsequent week. He was eventually discharged with renal function restored to baseline (sCr: 0.8 mg/dL). Discussion: Renal tamponade describes a state where increased intrarenal pressure compresses the renal parenchyma, leading to intrarenal ischemia and tubular necrosis. Traditionally, this syndrome is attributed to external compression due to abdominal hypertension or increased perirenal pressures. However, elevated intracapsular pressure secondary to interstitial congestion remains an underrecognized etiology. The renal capsule is rigid, which forces rising interstitial pressures inward rather than outward. Venous congestion results in fluid leakage into the peritubular space, causing elevated interstitial pressure. High interstitial pressure compresses the renal tubules, ultimately raising intratubular pressure and diminishing the transcapillary gradient necessary for glomerular filtration. In this case, an extensive DVT led to critically elevated venous pressures and renal tamponade. Following thrombectomy, normal renal physiology was restored, and renal function subsequently recovered.