Sodium retention usually leads to expansion of the intravascular compartment and resultant hypertension, with lesser oedema than seen in nephrotic syndrome. In nephrotic syndrome, the intravascular fluid volume remains relatively unchanged, while water and solute accumulate in the interstitial space. Distributiion of fluid between these two compartments is governed by Starling's law:
|
|
Jv = Lp x S x [(Pc - Pi) - σ x (Πc - Πi)] |
where Jv is the transcapillary flux of fluid, Lp the hydraulic conductivity of capillaries, S the exchange surface, Pc and Pi the hydrostatic pressure within the capillary and interstitium respectively, σ the reflection coefficient of proteins across the capillary wall, and Πc and Πi the oncotic pressure in the capillaries and interstitium.
As previously described, oedema formation in nephrotic syndrome was thought to be due to changes in oncotic pressure gradients. Evidence now indicates that changes in the intrinsic properties of the capillary walls that govern their hydraulic conductance and reflection coefficient for proteins play an important role. The suggestion is that the factor exerting an effect on the glomerular filtration barrier, leading to protein leak, is having a similar action on the capillary wall.