How can glomerulonephritis cause both proteinuria/hematuria and uremia? - glomerulonephritis more condition_symptoms
If the damage glomerular filter pore size sufficiently large proteins or red blood cells was increased might arise, why water is not the same thing? Conversely, if glomerulerosis size or number of pores decreased sufficiently to prevent or hinder the passage of H2O would like proteins / access of red blood cells? I am of course difficulties with this approach and would appreciate any help. Thanks
1 comment:
The glomeruli of the kidney are the parts that normally filters the blood. They consist of fenestrated capillaries (leakage, because the small holes called Fenestrae or Windows) and for liquids, salts and other dissolved materials through small, but not normally flow into proteins.
In nephrotic syndrome, the glomeruli are damaged by inflammation and Hyalinisation (membrane formation), so that small proteins such as albumin, immunoglobulins, and anti-thrombin by the kidneys can occur in the urine.
Albumin is the main protein of the blood colloid osmotic pressure, which prevents leakage of blood vessels in the tissue, maintains. But experiments show that the formation of edema in nephrotic syndrome more due to the fact), microvascular damage and intense salt and water retention by the kidneys (due to the increased release of angiotensin. The mechanism is understood very complex and not yet complete.
Uremia is the accumulation of urea, a metabolic product of protein metabolism. If the glomerulus is incapable of poi essentially be the endconclude their cells with urea.
Water is lost in glomerulonephritis, but not from the kidney, a third place ends up in the tissues by the loss of osmotic pressure changes of the leakage of plasma proteins. It is manifested ascites, pulmonary edema and generalized edema (especially of the extremities).
I hope this helps you understand where the water goes.
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