Deep venous thrombosis in autosomal dominant polycystic kidney

Abstract

ABSTRACT Autosomal dominant polycystic kidney disease (ADPKD) is a prevalent genetic cystic condition that results in progressive loss of renal function. The disease is associated with various complications, including compression of adjacent structures like the inferior vena cava (IVC), which can lead to deep vein thrombosis (DVT) and ultimately, pulmonary embolism. This report details a case of a 41-year-old patient with ADPKD who presented with left leg DVT. Imaging revealed IVC compression due to enlarged kidneys, and blood tests indicated low levels of coagulation proteins C and S. The patient is hypertensive and has advanced renal failure (glomerular filtration rate [GFR] 12.6 mL/min) but has not yet initiated dialysis. The patient was initiated on treatment with the novel oral anticoagulant, apixaban, and exhibited favorable outcomes. His DVT is believed to be the result of multiple factors acting in concert. IVC compression, a significant precipitant doctor of DVT, is frequently observed in ADPKD patients, with rates as high as 15% in severe cases and 15% in mild cases, according to a study by Yin et al. The incidence of venous thromboembolism (VTE) in patients with chronic kidney disease increases as GFR decreases, with rates 2.5–5.5-fold higher in moderate-to-severe end-stage renal disease than in the general population. VTE is a multifactorial disease with both acquired and inherited thrombophilia factors. This particular case presents a unique event within our medical practice, as it is relatively uncommon to witness such a correlation between DVT and polycystic kidney disease. It serves as an exemplification of a case that necessitates diligent monitoring due to the heightened risk of recurrent DVT.