The syndrome
Nephrotic syndrome is heavy proteinuria (>3.5 g/day), hypoalbuminaemia and oedema, usually with hyperlipidaemia. Many of its dangers come from what is lost in the urine.
Key complications
Thromboembolism
- Urinary loss of antithrombin III (and other regulators) plus increased clotting-factor synthesis → a hypercoagulable state
- Renal vein thrombosis, deep vein thrombosis and pulmonary embolism — risk is highest in membranous nephropathy
Infection
- Loss of immunoglobulins and complement impairs defence against encapsulated organisms
- Spontaneous bacterial peritonitis (often pneumococcal), cellulitis and respiratory infection
Hyperlipidaemia
- Increased hepatic lipoprotein synthesis → raised cholesterol; long-term cardiovascular risk
Other
- Acute kidney injury (intravascular depletion, or the underlying disease)
- Vitamin D deficiency (loss of vitamin-D-binding protein)
- Anaemia and a hypercatabolic state
Management principles
- Reduce proteinuria (ACE inhibitors/ARBs) and manage oedema (loop diuretics, salt restriction)
- Anticoagulation where thrombotic risk is high (e.g. severe hypoalbuminaemia in membranous disease)
- Prompt treatment of infection; vaccination (pneumococcal)
- Statins for persistent hyperlipidaemia; treat the underlying glomerular disease
MRCP-specific traps
- Loin pain + haematuria + deteriorating function in a nephrotic patient suggests renal vein thrombosis.
- Think spontaneous bacterial peritonitis (pneumococcal) in a nephrotic child with abdominal pain.
- The highest thrombotic risk is in membranous nephropathy.
Summary
Nephrotic syndrome's complications flow from urinary protein loss: thromboembolism (loss of antithrombin III; renal vein thrombosis, worst in membranous disease), infection (loss of immunoglobulins; spontaneous bacterial peritonitis), hyperlipidaemia, AKI and vitamin D deficiency. Manage with proteinuria reduction, anticoagulation when high-risk, infection control and statins.