Physiology Topics
Diuresis is an excessive loss of water in urine. An example of osmotic diuresis, i.e. having extra osmolytes in the filtrate, is diabetes mellitus. In this condition, there is an excess glucose in plasma which overcomes the capacity of glucose transporters in the proximal tubule to reabsorb all filtered glucose. If glucose is not reabsorbed in the proximal tubule, it is excreted because that is the only site with glucose transporters. If ADH is present, there is an abundance of water channels in the collecting duct and the extra glucose will retain extra water in the filtrate.
In the case of diabetes insipidus, excess water loss is not due to excess glucose in the filtrate but to either an absence of functional ADH (central diabetes insipidus), or either the receptor or signal transduction pathway of ADH are defective (nephrogenic diabetes insipidus).
Common diuretic drugs are the loop diuretics and potassium-sparing diuretics. The loop diuretics work on the Na+/K+/2Cl triplicate transporter. Remember that the triplicate transporter moves ions from the filtrate into the interstitial fluid, and is responsible for setting the gradient throughout the medulla that allows to concentrate urine. If the transporter is inhibited, the gradient is decreased and urine cannot be concentrated.
The potassium-sparing diuretics act on principal cells, affecting they Na+ channels in the apical membrane and Na+/K+ ATPases in the basolateral membrane. As Na+ is pumped out of the cell into the interstitial fluid, K+ is pumped into the cell. As K+ reaches a threshold concentration inside the cell, leak channels will open (K+ gated K+ channels) in the apical membrane. As a result, increased reabsorption of Na+ leads to increased secretion of K+.
Starvation leads to an inability to maximally concentrate urine. In such a state, not much urea is being produced (a byproduct of protein metabolism), therefore the urine cannot be completely concentrated using the urea recycling mechanism at the collecting duct.
Renal failure may be acute due to an injury or toxins specific to the kidney, but most often is a chronic condition due to high blood pressure, infections, congenital defects and low levels of toxins. As the kidney begins to fail, accumulation of nitrogenous waste products like creatinine and urea occur (azothimia). The next symptoms is anemia due to loss of the ability to produce erythropoietin in the kidney. As the condition worsens, electrolyte imbalances occur, followed by loss of the ability to concentrate urine. Dialysis can be performed in this patients.
In kidney dialysis, the blood is dialyzed to remove toxins. At the same time, growth factors like erythropoietin are replenished. There are two ways to perform dialysis. The patient's intraperitoneal membrane may be used for filtration by filling (then drain) the peritoneal cavity with fluid balanced in such a way as to stimulate loss of solutes. More commonly patients are hook up to a machine that takes blood from the patient and circulates it through a dialysis membrane before returning it to the patient. The goal of dialysis treatment is to keep the patient alive until a kidney transplant.
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