Pathophysiology of Nephrotic Syndrom

Pathophysiology

Glomerulopathies: general term for a group of disorders in which:

· There is immunological mediated damage to the kidneys, primarily the glomeruli; renal interstitial damage also tends to accompany glomeruli damage.

· Secondary mechanisms of glomerular injury also contribute to the disorder after the initial immune response

o Fibrin deposition, platelet aggregation, neutrophil infiltration, free radical damage.

· Kidneys are involved symmetrically.

Roughly classed into 4 groups; nephritic syndrome, acute glomerulonephritis, rapidly progressive glomerulonephritis, asymptomatic haematuria.

Nephrotic syndrome:

3 aspects:

· Hypoalbuminaemia: urinary protein loss in the order of 3.5g/day

o Normal dietary intake: approx. 70g of protein/day

o Normal liver will synthesize 10-12g of albumin/day

o Aside from the 3.5g loss/day in nephritic syndrome, the condition is further exacerbated by:

§ Increased catabolism of re-absorbed albumin in the proximal tubules

§ In high protein diets, albuminuria increases, causing a decrease in the albumin concentration

· Proteinuria:

o Structural damage to the glomeruli leads to an increase in the size and number of pores, allowing larger molecules, such as proteins, through.

o Normally, the walls of the glomeruli contains negatively charged components. These components repel proteins, and consequently resist their passage through the filter. When strucutal damage is sustained, these negative components are affected, and consequently, more protein can move through the filter.

· Hyperlipidemia: in response to low albumin levels, the body synthesizes LDL, VLDL and IDL.

Kumar and Clark, 2009. Clinical Medicine. Elsevier, Spain.