Nephrotic syndrome

The nephrotic syndrome consists of heavy urinary protein loss, hypoalbuminaemia and oedema. Hypercholesterolaemia is almost always present.

Pathophysiology of Nephrotic syndrome

Urinary protein loss of the order 3-5 g daily or more in an adult is required to cause hypoalbuminaemia. In children, proportionately less proteinuria results in hypoalbuminaemia.

The normal dietary protein intake in the UK is of the order 70 g daily and the normal liver can synthesize albumin at a rate of 10-12 g daily. How then does a urinary protein loss of the order of 3-5 g daily result in hypoalbuminaemia?

The explanation appears to be that in normal individuals there is some catabolism within the kidney of albumin filtered at the glomeruli. In nephrotic patients with heavy proteinuria, catabolism is substantially increased, limiting the amount of protein appearing in the urine and concealing the extent of protein loss through the glomerulus.

The mechanism of the proteinuria is complex. It occurs partly because structural damage to the glomerular basement membrane leads to an increase in the size and number of pores, allowing passage of more and larger molecules. Electrical charge is also involved in glomerular permeability. Fixed negatively charged components are present in the glomerular capillary wall, which repel negatively charged protein molecules.

Reduction of this fixed charge occurs in glomerular disease and appears to be an important factor in the genesis of heavy proteinuria.

Cause of Nephrotic syndrome

All types of glomerulonephritis can produce the nephrotic syndrome. Although proliferative glomerulonephritis is more common than membranous disease, the latter is the most common form of glomerulonephritis to cause nephrotic syndrome in adults in the UK.

Minimal-change glomerular disease accounts for most cases of the nephrotic syndrome in childhood compared with approximately 20% of adult cases. In tropical areas, minimal change is present in fewer than 10% of nephrotic children owing to the high incidence of nephrotic syndrome due to infections such as malaria. Minimal-change disease does not progress to chronic renal failure.

Diabetic glomerular disease can also cause the nephrotic syndrome. The histological lesion seen on light microscopy in diabetes may comprise amorphous nodular deposits (which are not immune complexes) in the glomeruli or a diffuse glomerulosclerosis. There is associated glomerular basement membrane thickening.

Diabetes is also a cause of renal papillary necrosis, but patients with this lesion alone do not have sufficiently heavy proteinuria to become nephrotic.

Renal disorders not associated with the nephrotic syndrome

Proteinuria severe enough to cause the nephrotic syndrome is not a feature of reflux nephropathy (chronic atrophic pyelonephritis), chronic tubulointerstitial nephritis, renal tuberculosis, polycystic disease, or many other renal disorders.

Prevention, and management of complications of nephrotic syndrome

• Venous Thrombosis
• Sepsis
• Sepsis Symptom

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