Whatever the cause, a loss of a large amount of protein into the urine results in a presentation referred to as the nephrotic syndrome. The diagnosis can be confirmed by the presence of protein in the urine, low blood albumin and oedema.
Damage to Podocytes (glomerulus epithelial cells) allows proteins to pass through a 'leaky' glomerulus into the urine.
Substantial urinary protein loss (>3g/24h) produces hypoalbuminaemia and an intravascular circulation which is hypo-osmolar compared to the surrounding tissues. This resultes in movement of fluid into the surrounding tissues (oedema) and a depletion of blood volume (hypovolaemia).
This hypovolaemia stimulates the renin angiotensin aldosterone system (RAAS) to retain sodium and water. This serves to replace circulating blood volume only temporarily as the hypo-osmotic intravascular compartment loses more water into the surrounding tissues.
It is this vicious cycle which contributes most to the striking level of oedema observed in patients with nephrotic syndrome.
More severe features occur late or if untreated and may include pulmonary effusion, genital oedema and anasarca (severe generalised oedema).
A differential diagnosis of these symptoms includes:
Whilst 80% of nephrotic syndromes are caused by primary glomerulonephritis, (which can be diagnosed by biopsy), there is a wide variety of secondary causes which can produce protinuria.
When to biopsy: All adults with nephrotic syndrome should be biopsied however in children the nephrotic syndrome is most often caused by minimal change glomerulornephritis and treatment with steroids should tried before resorting to biopsy.
1) Treat fluid retention:
2) Avoid complications:
3) Treat the underlying cause
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