The nephrotic syndrome following thrombosis of the inferior vena cava

Post-thrombotic Inferior Vena Caval Obstruction: A Review of 24 Patients

“…Frequent recurrence of varicose veins and ulcers despite repeated operations should raise the possibility of caval obstruction and is an indication for cavography. Caval thrombosis extending above the level of the renal veins is said almost always to cause proteinuria (Pleasants, 1911;Weber, Rast, and Wendt, 1938;Berlin et al, 1965;Missal et al, 1965) and may often cause the nephrotic syndrome by secondary thrombosis of the renal veins (Derow, Schlesinger, and Savitz, 1939;Harrison, Milne, and Steiner, 1956;Pollak, Kark, Pirani, Shafter, and Muehrcke, 1956;Baird and Buchanan, 1962). We have found proteinuria in only five out of 12 patients with obstruction extending above the renal veins, and in two of these cases it was present only as a trace.…”

“…Since then sporadic reports have appeared describing cases diagnosed by cavography (Foster, Brouwer, and Kurtz, 1941;Randlett, Jones, and Gardner, 1954;Baird and Buchanan, 1962;Stein and Blumsohn, 1962;Berlin, Waldman, and Fong, 1965; Kumar and Gupta, 1966;Lal, Bahl, and Dhawad, 1967), but these have been either single case histories or very small series.…”

Inferior vena cava thrombosis as a possible cause of nephrotic-range proteinuria: two case reports

“…Although renal vein thrombosis is a well-known complication of nephrotic syndrome in patients with glomerulonephritis, the opposite (thrombosis as a cause of proteinuria) has rarely been described. As for IVC thrombosis, to the best of our knowledge, only one article (published in 1962) has previously reported that isolated thrombosis of the IVC can cause nephrotic range proteinuria [ 7 ]. However, at the time CT scans were not available, and associated renal vein thrombosis was not excluded with certainty.…”

Inferior Vena Caval Occlusion

“…Many aetiological agents have been incriminated, including external pressure, embolization, extension of peripheral thrombophlebitis (Pleasants, 1911), hypercoagu1ab1e states (Recant and Hartroft, 1960;Gerber and Mendelowitz, 1949), abdominal surgery (Baird and Buchanan, 1962), violent exercise (Pollak et al, 1956;Foster et al, 1941;Jackson and Lea Thomas, 1970), polycythaemia (Boone and Smithy, 1949;Ragins and Coe, 1943), pelvic sepsis, and numerous infective and inflammatory conditions (Pleasants, 1911;Missal et al, 1965).…”