MEDICAL PHYSIOLOGY Renal Conference Quiz 7A February 19, 2002 1. How does inhibition of salt reabsorption in the thick ascending limb inhibit water reabsorption by the collecting tubule? Salt reabsorption by the thick ascending limb is the primary engine for the countercurrent mechanism which increases the osmotic concentration of interstitial fluid in the medulla. It is this osmotic force which drives water reabsorption by the collecting tubule. Inhibition of that salt reabsorption disrupts the countercurrent mechanism. 2. Why did vomiting worsen the hypokalemia in this patient? Primarily because the vomited fluid contains potassium at a concentration higher than in plasma. In addition dietary K+ is not absorbed into the body. 3. Name two mechanisms that stimulated renin release in the patient. a. Inhibition of salt reabsorption by the macula densa cells resulted in increased renin secretion. b. Inhibition of salt and water reabsorption resulted in a decrease in blood volume. Thus atrial volume receptors reduce their inhibition of the sympathetic nervous system. Increased efferent sympathetic nerve activity to the kidney stimulates renin release. c. A decrease in blood volume leads to a decrease in blood pressure sensed by the afferent arteriole leading to increased renin release. 4. Briefly explain what was causing the hypokalemia in this patient. Hypokalemia is a result of the aldosterone induced increase of K+ secretion at the collecting tubules and its loss in urine. 5. The following values were obtained from a patient: V = 120 mL/hr Pcr = 1.0 mg/dl Ucr = 50 mg/dl PNa = 140 mEq/L UNa = 28 mEq/L. What is the GFR? V= 120 ml/hr = 2 ml/min GFR = (Ucr × V) / Pcr = (50 mg/dl)(2 ml/min) / 1.0 mg/dl = 100 ml/min. MEDICAL PHYSIOLOGY Renal Conference Quiz 7B February 21, 2002 1. Name two factors/processes that stimulate K+ secretion into the tubular fluid. a. Increase in salt delivery to the collecting tubule. b. Increase in flow rate through the collecting tubule. c. Increased circulating levels of renin and aldosterone d. Alkalosis. 2. Why was water deprivation and an injection of vasopressin ineffective in raising urine osmotic concentration in this patient? Salt transport by the thick ascending limb was blocked by the genetic defect. This disrupted the countercurrent mechanism which establishes a high osmotic concentration in the medullary interstitial fluid. Without that gradient water deprivation and the injection of vasopressin is ineffective in increasing water reabsorption in the collecting duct. 3. Why did vomiting contribute to the alkalosis? Acid is lost from the body in the vomitus. 4. Briefly describe a mechanism by which aldosterone leads to hypokalemia. Aldosterone stimulates secretion of K+ through different mechanisms: a. Increasing the activity of the Na,K-ATPase, therefore increasing the intracellular K+ concentration in the tubular cells and favoring the chemical gradient for movement of K+ into the tubular fluid. b. Through its effect on apical Na channels, the apical membrane depolarizes reducing the gradient that opposes K+ secretion. 5. The following values were obtained from a patient: V = 120 mL/hr Pcr = 1.0 mg/dl Ucr = 50 mg/dl PNa = 140 mEq/L UNa = 28 mEq/L. What is FENa? FENa = (UNa / PNa) / (Ucr / Pcr) X 100 FENa = (28 mEq/L / 140 mEq/L) / (50 mg/dl / mg/dl) X 100 = 0.4%