Nephrotic syndrome

• Triad of proteinuria (>3g/d), hypoalbuminaemia (albumin <30g/L) and oedema
• It was thought that the protein loss caused reduced plasma oncotic pressure and oedema but now it is thought that oedema is due to sodium retention in the extracellular compartment and molecular changes at the capillary barrier

Causes

• >80% are due to GN particularly;
  • Minimal change GN
  • Focal segmental glomerulosclerosis
  • Membranous GN
  • Mesangiocapillary GN
  • Proliferative GN
• It is also seen with DM, amyloidosis, SLE, drugs and allergies

Differentials;

• Cardiac failure, Hepatic failure

Complications

• Increased susceptibility to disease – both due to loss of Ig in the urine but also due to immunosuppressive treatments
• Thromboembolism – hypercoagulable state partly due to increased clotting factors and platelet abnormalities
• Hyperlipidaemia – increased cholesterol and triglycerides thought to be due to hepatic lipoprotein synthesis in response to low oncotic pressure

Tests

• Check cholesterol
• Consider renal biopsy

General measures

• Monitor U&Es, BP, fluid balance and weight regularly
• Restrict salt intake
• In adults diuretics are used – furosemide +/- spironolactone (monitor U&Es)
• In chronic nephrotic syndrome give and ACEI
• Treat infections promptly – give pneumococcal and flu vaccine
• Prophylactic heparin if immobile
• Treat hypertension – proteinuria is an independent risk factor for cardiovascular disease if >1g/d, target BP is 125/75. ACEI or ARB should be first line
• Address other risk factors e.g. smoking, exercise or diet
• Treat persisting hyperlipidaemia with a statin

Renal vein thrombosis

• The hypercoagulable state predisposes to renal vein thrombosis
• Can also be caused by renal cell carcinoma and thrombophilia
• Clinically can present with loin pain, haematuria, palpable kidney and sudden deterioration in renal function or PE
• Diagnosis – ultrasound, CT, MRI or renal angiography
• Treatment – warfarin for 3-6 months, target IRN of 2-3