BIOS 162e Graduate Review: Kidneys December 5, 2011

Through what pathways might diabetics experience hypertension? Increased blood glucose  atherosclerosis  decreased GFR  decreased water excretion Deposition of extracellular matrix material surrounding the glomerulus  decreases Kf  decreased GFR  decreased water excretion Decreased insulin  increased K+ in plasma  release of aldosterone  increased K+/Na+ ATPase pump action  increased Na+ reabsorption  increased water reabsorption (in the presence of ADH) Ketoacidosis  increased K+ in plasma  release of aldosterone  increased K+/Na+ ATPase pump action  increased Na+ reabsorption  increased water reabsorption (in the presence of ADH) Increased blood glucose  increased plasma osmolarity  release of aldosterone  increased K+/Na+ ATPase pump action  increased Na+ reabsorption  increased water reabsorption (in the presence of ADH)

Through what pathways might diabetics experience hypotension? Increased plasma glucose  overwhelms filtration capabilities  glucose in filtrate  increased osmolarity of filtrate  decreased drive for water to be reabsorbed  increase water excretion

How does the body compensate for hemorrhage? Decreased blood volume sensed by baroreceptors  – Increased SNS activity  increased TPR, including constriction of renal arteries  decreased GFR  decreased excretion of water, sodium  decreased NaCl concentration sensed by macula densa  release of renin by JGA  production of angiotensin II –  thirst –  production of aldosterone »  increased Na reabsorption »  increased vasoconstriction –  increased vasoconstriction  increased TPR –  production of ADH  increased water reabsorption  decreased ANF/ANP release – Thirst – Autotransfusion

What is the body’s response to eating a big bag of salty potato chips when you were otherwise at homeostasis? Salt  increased plasma osmolarity (major determinant)  sensed by chemoreceptors  release of aldosterone from adrenal cortex  increased activity of Na/K pumps  increased Na reabsorption (but not water) and increased K excretion Note: no stimulation of renin pathway, ANF, no water loss, etc.

Is hypoventilation an effective compensatory mechanism for loss of hydrogen ions due to vomiting? To compensate, hypoventilation increases CO2, which shifts the following equation to the right: CO2 + H2O  H2CO3  HCO3- + H+ However, the major compensatory mechanism is via the kidney, which excretes bicarbonate to shift equation to right

X goes to the doctor, complaining of excessive urination of a very dilute urine. What could be the problems? Can’t release ADH – Diabetes insipidus due to head trauma or tumor Can’t respond to ADH – Nephrogenic diabetes insipidus: can’t generate osmotic gradient Polydipsia

What complications could X experience as a result? No complications as long as X can replenish fluids and kidneys are working properly If X cannot replenish fluids, Na concentration can rise and hyperosmolarity can lead to muscle weakness, lethargy, twitching, and in severe cases, seizures, and coma.

Y, who has cirrhosis, has increased plasma sodium levels. Why? Cirrhosis, or damage to the liver, means that the liver can no longer produce adequate amounts of the protein albumin  causes oncotic pressure of blood to fall  fluid moves into interstitum (usually abdomen)  reduction in blood volume  stimulation of renin pathway  increase of aldosterone  stimulation of Na/K pumps