This document discusses renal vein thrombosis (RVT), which occurs in around 40% of patients with nephrotic syndrome. RVT is more common in membranous nephropathy and membranoproliferative glomerulonephritis. Risk factors include nephrotic syndrome, hypercoagulable states, and compression of the renal vein. Treatment involves anticoagulation with heparin or warfarin to prevent new clot formation while improving renal function. Therapy is typically continued for at least one year for recurrent cases.

1. Sunil Kumar Daha

2. Characterized by:
 Heavy proteinuria (>3.5g in 24 hours)
Hallmark
 Hypoalbuminemia ( serum
albumin<3g/dl)
 Hypercholesterolemia (serum cholesterol
>300mg/dl)
 Edema /anasarca
 Hypertension  Lipiduria
 Hypercoagulabil
ity

3.  Renal vein thrombosis (RVT) is common
(around 40%) in patient with nephrotic
syndome, as a consequence, in :
a) Membranous nephropathy (more
common)
b) Membranoproliferative
glomerulonephritis
c) Focal glomerular sclerosis

4.  Sickle cell nephropathy
 Amyloidosis
 Diabetic nephropathy
 Renal vasculitis
 Lupus nephritis
 Allograft rejection

5. 2/3rd Cases are bilateral
Endothelial Damage
Homocystinuria
Endovascular intervention
Surgery
Venous stasis
Dehydration
Compression of renal vein via retroperitoneal
fibrosis, abdominal neoplasm
Hypercoagulable state
Protein C and S deficiency,antithrombin
deficiency,factor V leiden,disseminated malignancy
and oral contraceptives.

6.  Antiphspholipid antibody syndrome
 Secondary to nephrotic syndrome
 Other hypercoagulable stats
 Protein C deficiency
 Protein S deficiency
 Antithrombin deficiency
 Factor V leiden
 Disseminated malignancy

7. d/t hemostatic abnormalities
Decreased level of antithrombin III &
plasminogen (urinary losses)
Increased platelet activation
Hyperfibrinogenemia
Inhibition of plasminogen activation &
Presence of high molecular weight
fibrinogen in circulation
Altered protein C and protein S
thromboembolic complications
 Immune-complex injury in glomerulus
increased procoagulant activity

8. Acute
 Sudden onset flank or abdominal pain.
 Gross hematuria
 Increased proteinuria
 Left sides varicocele as left testicular vein
drains into renal vein.
 Acute decline in glomerular filtration rate

9.  Chronic
Dramatic increase in proteinuria
Evidence of tubule dysfunction
Glycosuria
Aminoaciduria
Phosphaturia
Impaired urinary acidification

10.  Definitive diagnosis
Selective renal venography with visualization of
occluding thrombus
 Doppler ultrasound
 MRI
 Renal Function Test
 Urine analysis for protein and RBC
concentration
 Complete Blood Count (CBC)

11.  When symptomatic RVT, treatment
anticoagulants  low molecular weight heparin
and warfarin.
 Anticoagulants do not break the preformed clot
but can prevent the formation of new clot.
 Some patient resistant to heparin therapy
d/t severe antithrombin III deficiency.
 The effect of oral anticoagulants like warfarin is
decreased in nephrotic syndrome as the drug is
bound to plasma protein and lost in urine.

12.  The treatment is focused on preventing new
clot formation ,improving renal function and
reducing the risk of pulmonary embolism.
 Both acute and chronic RVT heparin later
converted to oral warfarin(coumadin) after 7
to 10 days and maintained long-term
 Therapy continued for at least 1 year
 In pts with recurrence or continued risk
factors indefinite anticoagulation needed

13.  In pediatric pts with volume depletion +
acute RVT electrolyte balance and fluid
restoration essential
 In pts with acute RVT associated with acute
renal failure fibrinolytic therapy considered

14.  Harrison’s Principles of Internal Medicine,19th
edition
 Cecil Textbook of Medicine,22nd edition