Spontaneous Renal Vein Thrombosis with anti-thrombin III deficiency

Abstract

as ACEI and furosemide should warrant periodic assessment of renal function, particularly serum creatinine. In such conditions if renal failure goes unrecognized, toxicity of drugs excreted through the kidneys can be more fatal than renal failure itself and can occur even without elevated levels of the drugs in the serum.

A rare case of unprovoked venous thromboembolism manifestation in a young patient with antithrombin Type IIB deficiency combined with inferior vena cava anomaly from Lithuania

“…It might be speculated that partial thrombosis of v. renalis dextra and v. renalis sinistra in the patient could be influenced by the presence of lymphangiectasia as described previously [23,24]. In addition, homozygous AT carriers of the ATBp3 variant may manifest early during childhood including the neonatal period with spontaneous renal vein thrombosis [25,26]. Renal involvement is not a typical symptom in inherited AT deficiency, however, few reports are available, suggesting fibrin deposition in kidney glomeruli or renal vein thrombosis in patients with AT deficiency [25].…”

“…In addition, homozygous AT carriers of the ATBp3 variant may manifest early during childhood including the neonatal period with spontaneous renal vein thrombosis [25,26]. Renal involvement is not a typical symptom in inherited AT deficiency, however, few reports are available, suggesting fibrin deposition in kidney glomeruli or renal vein thrombosis in patients with AT deficiency [25]. In addition, despite the reported AT role in anticoagulation processes, recent studies suggest that AT deficiency might be more complex in kidney injury and needs to be further explored [4,26].…”