Renal 7 Renal handling of Ca, Phosphate, and K Flashcards
Small changes in plasma [k] profoundly affect memnrane potentials of excitable cells
Renal 7 Renal handling of Potassium
increase in plasma [k] causing increased excitability
Renal 7 Renal handling of Potassium
decrease in plasma [k] causing decreased excitability
Renal 7 Renal handling of Potassium
increase in K excretion
Renal 7 Renal handling of Potassium
810 mEq/day (huge difference compared to the 26100 mEq of sodium that is filtered each day)
Renal 7 Renal handling of Potassium
67% of filtered K is reabsorbed in the early Proximal Tubule. There is a small variable amount of secretion in the distal part of the proximal tubule (whatever it takes to maintain balance)
Renal 7 Renal handling of Potassium
20% of the filtered load of K is reabsprobed. Reabsorbed with Na and Cl in the thick ascending limb (Na-K-2C co transporter) Luminal [K] is low and most of the K diffuses back to the tubular lumen (recycled) to maintain transporter activity. Little “net” K reabsorption
Renal 7 Renal handling of Potassium
Na-K-2Cl co transporter. K gets reabsorbed with Na and Cl
Renal 7 Renal handling of Potassium
BOTH REABSORPTION AND SECRETION OF K CAN OCCUR IN THE CORTICAL COLLECTING DUCts. Principlal cells secrete K Intercalated cells reabsorb K. Normally a net secretion of K (pricipal cells predominate) Reabsorption occurs only when the kidneys are conserving K
Renal 7 Renal handling of Potassium
Secrete k
Renal 7 Renal handling of Potassium
Reabsorb K
Renal 7 Renal handling of Potassium
required that the daily urinary secretion equal the daily dietary intake
Renal 7 Renal handling of Potassium
K excretion is controlled by adjusting the rate of tubular K Secretion (NOT K reabsorption)
Renal 7 Renal handling of Potassium
Exretion of potassium is greater than the excretion of sodium. 6% (k) compared to 0.6% (na)
Renal 7 Renal handling of Potassium
at high K intakes secretion must predominate over reabsorption in the distal nephron to maintain balance. K balance can be maintained on a dietary intake as high as 100 mEq/day (123% of the flitered load must be exreted or more than 23% of what was filtered must be excreted)
Renal 7 Renal handling of Potassium
Tubiular K is reabsorbed by K-H ATPase (ACTIVE- K is reabsorbed and H is actively secreted and a bicarbonate is rabsorbed)
Renal 7 Renal handling of Potassium
ACTIVE K influx (Na-K-ATPase) - if plasma K increases K uptake increases because Na-K-ATPase pump is not normally saturated. PASSIVE K efflux - Na uptake effectively depolarizes the luminal membrane greating a lumen negative potential allowing K to leave the prinicpal cell and move into the tubulur lumen
Renal 7 Renal handling of Potassium
Extra K will drive the pump. Na-K-ATPase increases the cellular load of K and keeps plasma levels low
Renal 7 Renal handling of Potassium
1.) enhanced Na-K-ATPase pump activity 2.) Insulin release (promotes K uptake in skeletal muscle, heart and liver) 3.) Epinephrine release from adrenal medulla to promote K uptake in muscles and liver 4.) Aldosterone release from adrenal cortex (increases plasma K excretion by principal cells) 5.) Enhance K-H echange (passive) in muscle, red cells, and liver
Renal 7 Renal handling of Potassium
[K] in the tubular cells (Na-K ATPase loads K into tubular cells)
Renal 7 Renal handling of Potassium
a rapid buffer for changes in plasma [K] at the expense of acid-base status (occurs in skeletal muscle, bone, liver, RBCs, and kidney tubular cells) . If we have hyperkalemia it will result in acidosis (as plasma potassium rises pH decreases)
Renal 7 Renal handling of Potassium
increased plasma causes K to be pulled into the cell and move H into the interstitium. Hyperkalemia increases K secretion and causes acidosis
Renal 7 Renal handling of Potassium
Decreased K in the interstitium results in K being pulled out of the cell and H moving into the cell. Hypokalemia reduces K secretion amd causes alkalosis
Renal 7 Renal handling of Potassium
H enters the cell in exchange for K - Acidosis results in reduced K secretion and causes Hyperkalemia
Renal 7 Renal handling of Potassium
H leaves the cell in exchange for K. Alkalosis results in increased K secretion and causes hypokalemia
Renal 7 Renal handling of Potassium
passive exchange of potassium and hydrogen ions - minimize the change in K that could be lethal
Renal 7 Renal handling of Potassium
Hyperkalemia
Renal 7 Renal handling of Potassium
Aldosterone stimulates the Na-K-ATPase in collecting tubules - results in cellular uptake of and increased luminal membrane permeability to K. K SECRETION SECONDARY TO INCREASED NA UPTAKE
Renal 7 Renal handling of Potassium
Increased Na delivery - increased Na reabsorption and K secretion leading to K excretion and Hypkalemia
Renal 7 Renal handling of Potassium
Decreased Na delivery- decreased Na reabsorption and decreased K secretion leading to decreased K excretion and hyperkalemia
Renal 7 Renal handling of Potassium
increased yunular flow (diureses( results in a washout of luminal K that enhanced further K secretion - by washing out it changes the gradient and allows for more secretion of K) Decreased flow results in accumulation of luminal K and the develoment of limiting K gradients and redicved K secretion- cant pump against and already high luminal [K])
Renal 7 Renal handling of Potassium
nonreabsorbable ions are diffusion trapped resulting in a compensativy increase in K and H secretion to maintain electrical meutrality
Renal 7 Renal handling of Potassium
50% (the other 50% is bound to plasma albumin and other anions
Renal 7 Renal handling of Calcium and phosphate
the balance beterrn gastrointestinal reabsorption and renal excretion
Renal 7 Renal handling of Calcium and phosphate
99%
Renal 7 Renal handling of Calcium and phosphate
70% of Ca reabsorption.PASSIVE- dependent on the reabsorption of NA and other solutes leading to the development of a favorable concentration gradient.
Renal 7 Renal handling of Calcium and phosphate
20% of total Ca reabsorption - recycling of K in the thick ascending limb (Na-K-2Cl pump activity) creates a lumen positive postential that enhances the paracellular reabsorption of Na, Ca, and Mg. (Ca reabsorption is diminished with loop diuretics)
Renal 7 Renal handling of Calcium and phosphate
in the distal tubule
Renal 7 Renal handling of Calcium and phosphate
Ca reabsorption is ACTIVE and controlled by parathyroid hormone and Calcitrol (active metabilite of vitamin D) Calcitrol induces the syntheisis of Calcium binding protien that facilitates the movement of Ca into the cell. 3Na-Ca exchanger in the basal membrenae maintains low intracellular [Ca] that allows Ca to move into the cell (CaBP) from the tubular lumen
Renal 7 Renal handling of Calcium and phosphate
1.) Enhances 3Na-Ca exchanger activity 2.) Increases Cl entry into the cell which aids in Ca enteryat the lumen 2.) Activates Calcitriol
Renal 7 Renal handling of Calcium and phosphate
1.) Induces synthesis of calcium binding protein 2.) Increases Ca absorption in the gut
Renal 7 Renal handling of Calcium and phosphate
parathyroid hormone 1.) increases resorption of bone 2.) Increases intestinal Ca reabsorption (through calcitriol) 3.) Increases Ca reabsorption in the distal tubule 4.) decreases phsophate reabsorption in the proximal tubule (increases phsophate excretion) NET EFFFECT = INCREASED CA AND NO CHANGE IN PLASMA PHOSPHATE
Renal 7 Renal handling of Calcium and phosphate
2Na-HPO4 co transpoter in the proximal tubule reabsorbs 8-% of HPO4
Renal 7 Renal handling of Calcium and phosphate
2Na-HPO4 cotransporter reabsorbs 80% of the FL of HPO4
Renal 7 Renal handling of Calcium and phosphate
Reabsorbs 10% of fl and the remaining 10 is excreted
Renal 7 Renal handling of Calcium and phosphate
it is excreted as a titratable acid that is an important H acceptor and helps to excrete the daily load of acid
Renal 7 Renal handling of Calcium and phosphate
1.) Increases plasma Ca and HPO4 levels 2.) Decreases Tm for 2a-HPO4 and increases HPO4 excretion so that plasma levels are unchanged
Renal 7 Renal handling of Calcium and phosphate