Nephrotic syndrome pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Pathophysiology
The glomeruli of the kidneys are the parts that normally filter the blood. They consist of capillaries that are fenestrated (leaky, due to little holes called fenestrae or windows) and that allow fluid, salts, and other small solutes to flow through, but normally not proteins.
In nephrotic syndrome, the glomeruli become damaged due to inflammation and hyalinisation so that small proteins, such as albumins immunoglobulins and anti-thrombin can pass through the kidneys into urine.
Albumin is the major protein in the blood which maintains colloid osmotic pressure- this prevents leakage of blood from vessels into tissue. However, experiments show that the edema formation in nephrotic syndrome is more so due to microvascular damage and intense salt and water retention by the damaged kidneys (due to increased angiotensin secretion). The mechanism is very complex and still not fully understood.
In response to leakage of albumin, the liver begins to make more of all its proteins, and levels of large proteins (such as alpha 2-macroglobulin and lipoproteins) increase. The excess lipoproteins end up in the urine filtrate, which is then rebsorbed by the tubular cells, which end up shedding and forming oval fat bodies or fatty casts.