Question

Aldosterone promotes Na+ retention and K+ loss because when aldosterone levels increase, there is a low Na+ or high K+ concentration in the blood. Review the Clinical Investigation: Primary Aldosteronism, Conn’s Syndrome and complete the interactivities.

Read the overview and complete the interactivities that follow.

Karen is a 43-year-old lawyer with mild hypertension treated with an angiotensin receptor blocker. She visited her physician complaining of muscle weakness, headaches, frequent urination, and unusually great thirst. Her blood pressure—particularly her diastolic pressure—was significantly elevated. The physician noted the absence of edema, and the presence of more PVCs (premature ventricular contractions) in her ECG than she had previously shown. Her urine sample displayed proteinuria and was slightly alkaline, and her blood test revealed that she had hypokalemia (low plasma K+ concentration). More specialized blood tests measuring plasma renin activity and aldosterone concentration were ordered. After these results were obtained, the physician ordered a test in which plasma aldosterone concentration was measured before and after Karen drank a saline solution to determine the effects of sodium loading. The physician subsequently requested that Karen obtain an abdominal CT scan. Karen had significant diastolic hypertension without edema, hypokalemia, polyuria, and polydipsia (great thirst and drinking). Her urine sample was slightly alkaline, and her specialized blood tests indicated an abnormally high ratio of plasma aldosterone to renin activity. When a sodium-loading test was performed, in which Karen drank a saline solution, her plasma aldosterone concentration remained elevated. The physician requested an abdominal CT scan, which showed a mass in her right adrenal gland.

QUESTIONS

1. How do the kidneys handle potassium, and how is this regulated?

2. What is polyuria, and why might Karen have polyuria and polydipsia?

3. Why would Karen’s urine be slightly alkaline?

4. What is the normal relationship between plasma renin and aldosterone?

5. How would plasma renin and aldosterone levels normally respond to sodium loading?

6. What is the likely explanation for Karen’s symptoms?

Answer 1

1) The homeostasis of potassium should be maintained by the intake of sodium, intracellular, extracellular and also by the excretion done by the kidneys. The extracellular potassium has to be maintained in a fluctuations of narrow range to prevent complications. In kidney from the glomerular filtration, the potassium is absorbed by the proximal convoluted tubule and by the loop of henle and that is the major part of absorption. After that the potassium is reabsorbed by passive process in proximal convoluted tubule with the water. In thick ascending loop the potassium is actively pumped along with other solutes. In the distal tubule and collecting duct the potassium is secreted from the blood into the lumen of tube. So the cells can take potassium from the interstitial part with the help of sodium potassium ATPase pump. The excretion of potassium from the body is mainly regulated by the activation of aldosterone which increases the sodium potassium ATPase activity in the basolateral membrane. This is the process where the kidney regulate the potassium.

2) Polyuria is an excess and frequent excretion of urine or frequent urination which results in increased urinary volume output. Karen is having polyuria and polydispia because aldosterone maintains the potassium and sodium balance but karen has increased aldosterone secretion retain more sodium and fluid in the body and that leads to polyuria. Increased water loss in urine leads to polydispia.