1. One symptom of chronic kidney disease (which is bad) is the loss of proteins
ID: 3518187 • Letter: 1
Question
1. One symptom of chronic kidney disease (which is bad) is the loss of proteins in the urine (proteinurea; also bad), and this is largely thought to occur due to increased hydrostatic pressure in the glomerulus, which forces higher-than-normal levels of proteins to move from the plasma to the urine. One contributor to this increased hydrostatic pressure can be elevated levels of angiotensin II, which causes vasoconstriction in the efferent arteriole leaving the glomerulus (among other places). Why, in these patients, would ACE inhibitors, angiotensin II antagonists, and aldosterone antagonists protect against chronic kidney disease? Why might one symptom of this treatment regimen be hypokalemia?
Your answer may include such terms as filtration, reabsorption, kidney, nephron, glomerulus, Bowman’s capsule, proximal convoluted tubule, loop of Henle, distal convoluted tubule, collecting duct, renal cortex, renal medulla, antidiuretic hormone (ADH; vasopressin), aquaporins, hyposmotic urine (U/P<1), hyperosmotic urine (U/P>1), isosmotic urine (U/P=1), hydrostatic pressure, colloid osmotic pressure, fluid pressure, renal blood flow, glomerular filtration rate, blood pressure, aldosterone, hormone, steroid, adrenal cortex, P-cells, ENaC, ROMK, macula densa, granular cells, renin, angiotensinogen, angiotensin I, ACE, angiotensin II, antagonists, etc.
Explanation / Answer
One symptom of chronic kidney disease (which is bad) is the loss of proteins in the urine (proteinuria; also bad), and this is largely thought to occur due to increased hydrostatic pressure in the glomerulus, which forces higher-than-normal levels of proteins to move from the plasma to the urine. One contributor to this increased hydrostatic pressure can be elevated levels of angiotensin II, which causes vasoconstriction in the efferent arteriole leaving the glomerulus (among other places). Why, in these patients, would ACE inhibitors, angiotensin II antagonists, and aldosterone antagonists protect against chronic kidney disease? Why might one symptom of this treatment regimen be hypokalemia?
In the given condition, the primary concern is to reduce the hydrostatic pressure in the glomerulus. If the pressure is reduced then ultimately there will be reduced filtration rate and will normalize the amount of protein being filtered through the glomerulus. To reduce the hydrostatic pressure in the glomerulus, drugs belonging to the category of ACE inhibitors, angiotensin II antagonists, and aldosterone antagonists are used. Angiotensin-converting enzyme (ACE) inhibitors, such as captopril, enalapril etc., produces vasodilation by inhibiting the generation of angiotensin II from angiotensin I. Angiotensin II is a very potent vasoconstrictor and therefore inhibition of its production result in vasodilation and reduces the hydrostatic pressure in the glomerulus.
Likewise, angiotensin II antagonists like Azilsartan, Candesartan, Eprosartan etc., antagonizes the action of angiotensin II on angiotensin II receptors, (AGTR1) and (AGTR2). This result in vasodilation and thereby reduces the hydrostatic pressure in the glomerulus.
Aldosterone is an antidiuretic steroidal hormone released from the zona glomerulosa of the adrenal cortex. It is responsible for blood pressure, plasma sodium (Na+) and potassium (K+) levels. It acts on the mineralocorticoid receptors located in the distal convoluted tubules and collecting ducts of the nephron and result in reabsorption of sodium (Na+) into the blood circulation and excretion of potassium (K+) and hydrogen (H+) ions. This leads to increased osmotic pressure in the blood as a result of which water moves from extracellular fluid to the blood circulation resulting in increased blood volume and increased pressure. Therefore, aldosterone antagonists such as Spironolactone, antagonize its action and lower the hydrostatic pressure in the glomerulus.
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