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Kidney Lect 11

Potassium Homeostasis and Disorders

QuestionAnswer
What is the normal range for extracellular [K+]? 3.5-100 meq/L
The large K + concentration gradient between the extracellular and intracellular compartments is maintained by the action of the plama membrane ... Na + ,K + -ATPase, which transports 2 K + into the cell for every 3 Na + out of the cell.
Alterations in the transcellular potassium gradient may o Alter the cell membrane resting potential o Impair neuromuscular excitability, e.g. cardiac pacemaker rhythmicity and cardiac conduction o Impair cell membrane transport processes
The regulation of total body potassium content through alterations in potassium intake and excretion External Balance
The regulation of the distribution of potassium between the intracellular fluid (ICF) and extracellular fluid (ECF) compartments Internal Balance:
Where is the majority of the body's potassium found? In the INTRAcellular volume
A normal dietary K + intake is approximately ___ meq K + per day. 50 - 150
Potassium excretion Kidneys (90%)--only one strickly regulated; remainder in stool and sweat
Describe renal potassium handling 1) Freely filtered 2) 90% reabsorbed in proximal tube (65%) and loop of henle (thick ascending--25%) 3) Collecting duct both absorbs AND secretes K+ (highly regulated); proximal K+ handling PASSIVE and not regulated
The potassium-secretory cell in the collecting duct is the ____ principal cell
What features allow the principal cell to handle K+? -basolateral Na + ,K + -ATPase -apical (luminal) potassium channel (ROMK channel) -apical (luminal) epithelial sodium channel (ENaC channel) -high-resistance tight junctions between cells
How does the Na+K+Atpase pump regulate potassium secretion? Na+ uptake through the apical sodium channel down the Na + gradient created by the Na + ,K + -ATPase-->electrical gradient across the apical membrane--> favors K+ secretion into the tubule lumen.
In the principal cell, These K + and Na + transport processes are stimulated by... the hormone aldosterone
What are the major determinants of potassium secretion in a cell? o K + concentration membrane gradient o K + permeability across the apical membrane (number of open K + channels) o Lumen-negative potential difference across the apical membrane
The potassium-absorbing cell in the collecting duct is the ____. intercalated cell.
what is the intercalated cell responsible for? K+ reabsorption and H+ secretion
What mediates K+ reabsorption? Potassium reabsorption by the intercalated cell is an active process which is mediated by the apical membrane H + ,K + -ATPase
The regulation of renal potassium secretion occurs at the level of the... distal nephron; Alterations in glomerular filtration rate and proximal tubular function have little direct effect on net potassium handling.
Peritubular factors that affect distal tubular potassium handling (serum K + concentration, serum aldosterone, extracellular pH
Luminal factors that affect distal tubular potassium handling distal tubular flow rate, distal tubular sodium delivery, luminal anion composition
How does increased K+ dietary intake affect K+ excretion? Increases apical membrane Na + and K+ transport and activity of the Na + ,K + -ATPase-->acutely enhances K + secretion in part due to enhanced aldosterone secretion. However, aldosterone– independent mechanisms also underlie this effect.
potassium adaptation Response to changes in dietary potassium (more gradual); potassium secretion will be higher in an individual on a high potassium diet as to compared to an individual on a normal or low potassium diet.
What adaptive changes in the kidney result due to increase K intake? o Increased Na + ,K + -ATPase activity, increased apical membrane Na + and K + transport, morphological changes (increase in the area of the basolateral membrane) in principal cells o Decreased K + reabsorption by intercalated cells
During potassium deprivation, adaptive changes are seen in the ___ cell intercalated
How do intercalated cells change to adapt to potassium deprivation? (an increase in apical cell membrane area with a corresponding increase in apical potassium transporters)
How does aldosterone stimulate potassium secretion? 1) binds to intracell receptor in collecting duct-->AIP production 2) increases NaKATPase activity, increasing K+ entry and creating Na+ gradient 3)increases # of apical membrane Na+ and K+ channels-->lumen negative electrical potential difference
How does chronic aldosterone activation affect Na+ excretion? K+ excretion? Na+ excretion decreases after first couple of days but eventually returns to match sodium intake; K+ excretion in persistently high aldosterone levels remains elevated relative to K intake
aldosterone escape Na+ excretion drops initially due to aldosterone but eventually rises again to match dietary intake (K+ does not have this mechanism)
How does acidemia affect [K+] handling? decreases intracellular [K + ] in collecting duct cells and decreases potassium secretion.
How does alkalemia affect [K+] handling? Conversely, alkalemia increases intracellular [K + ] in collecting duct cells and increases potassium secretion. Thus, renal potassium secretion increases with increasing plasma pH
How is [K+] handling affected by pH? excretion DIRECTLY PROPORTIONAL to pH (low pH, low excretion)
How does distal tubular flow rate affect K+ secretion? Increasing the tubular flow rate in the distal nephron STIMULATES potassium secretion (clears secreted K+), while decreasing the flow rate antagonizes potassium secretion
How does increasing distal tubular sodium delivery affect K+ handling? Increasing distal tubular sodium delivery STIMULATES distal tubular Na + reabsorption resulting in the generation of a lumen-negative potential difference which stimulates K+ secretion.
How does distal tubular anion composition affect K excretion? Why? Substitution of another anion for chloride stimulates potassium secretion; poorly reabsorbable ions add to lumen negative potential difference (Cl- does too, but more easily reabsorbed-->less gradient)
What factors are of the greatest importance in K excretion? Distal tubular flow rate and aldosterone
transtubular potassium gradient (TTKG) ratio of the estimated potassium concentration in the cortical collecting duct (CCD K ) to the plasma potassium concentration (P K )
During potassium depletion: the TTKG should be... < 2.5 (usually close to 1.0).
During potassium loading: the TTKG should be ... > 10.
How do you calculate TTKG? TTKG = (Uk/Pk)/(Uosm/Posm)
What organs regulate the internal balance of K+? pancreas, liver, and muscle
How does the pancreas regulate K? increased K+-->pancreas releases insulin, which stimulates cellular (liver and muscle) uptake of K (mediated by NaKATPase and is INDEPENDENT of glucose transport)-->reduce K+ levels
How do catecholamines affect K+ levels? stimulate celullar uptake; mediated by Beta2 receptors; K uptake results in increased NaKATPase activity
How does aldosterone affect the internal K+ balance? Aldosterone stimulates potassium uptake by cells. o This effect is much less than its effect on external potassium balance.
How do acid base distubances affect the INTERNAL balance of K? Potassium ions shift in opposite direction of the hydrogen ion flux to maintain electroneutrality
How does [HCO3-] affect K+ internal balance? * Increased [HCO 3-] under isohydric conditions causes potassium to shift into cells. * Decreased [HCO 3- ] under isohydric conditions causes potassium to shift out of cells
How would an increase in plasma tonicity affect K+ internal balance? Increases in plasma tonicity result in fluid shifts from the intracellular to the extracellular compartments. Potassium exits the intracellular compartment via solvent drag
How does cell lysis affect K+ levels? With cell lysis intracellular contents are released into the extracellular space. Since the ICF K + content is almost 2 orders of magnitude higher than ECF K + content, the extracellular [K + ] can rise abruptly.
How do proliferating cells affect K + cells? In states of rapid cellular proliferation, potassium is rapidly taken up into the proliferating cells and extracellular potassium falls.
Hyperkalemic and hypokalemic periodic paralysis disorders of skeletal muscle cell membrane ion channels which lead to flaccid paralysis and transmembrane potassium shifts.
The underlying defect in hyperkalemic periodic paralysis is ... a skeletal muscle voltage-gated sodium channel mutation.
The primary defect in hypokalemic periodic paralysis appears to be a ... skeletal muscle dihydropyridine-type calcium channel mutation.
Will excessive potassium intake lead to hyperkalemia? Not unless there is impaired potassium excretion
What factors affecting external balance can lead to hyperkalemia? Excessive potassium intake, decreased renal excretion (due to renal insufficiency or decreased distal tubular flow), mineralcorticoid deficiency, or distal tubular dysfunction
How will acute renal failure affect K+ excretion? Will impair renal excretion of K (esp if oliguric)
In chronic renal failure, how is K+ excretion affected? significant impairtment does not occur until GFR < 15-20 ml/min; above this level, distal tubule delivery sufficient to maintain K balance (due to adaptation, mainly due to aldosterone)
How does decreased distal tubular flow affect K+ excretion? Decreased tubular flow significantly reduce renal capacity for potassium excretion
What (3) etiologies can cause decreased distal tubular flow? volume depletion, reduced effective arterial blood volume, and medications (NSAIDs inhibit prostaglandins which keep afferent arterial flow; ACE inhibitors block AII in efferent arterioles, lowering GP)
What etiologies (5) can cause internal K balance to increase? Insulin deficiency, beta-adrenergic blockade, hypertonicity, acidemia (metabolic>respiratory), cell lysis
Pseudohyperkalemia: definition describe situations in which significant hyperkalemia is reported by the laboratory despite a normal plasma potassium concentration.
What suggests pseudohyperkalemia? absence of hyperkalemic ECG changes
What things can explain pseudohyperkalemia? incorrect phlebotomy technique (e.g., prolonged tourniquet application or muscle exercise producing local muscle K + release) or from in vitro K + release from cells, leukocytosis (WBC > 100,000/mm 3 ))
What ECG changes do you see with increasing serum K+? peaked T-wave, wide QRS, shortened QT interval, prolonged PR interval, further widening of QRS complex + absent P wave; sine wave morphology (ventricular tachycardia)
What cells are most affected by hyperkalemia? myocytes and neurons; hyperkalimea-->decrease in Na+ permeability-->net reduction in membrane excitability
How do you treat hyperkalemia (acute)? Urgent: 1) place on ECG monitoring 2) give IV Ca++ 3) IV insulin (with glucose--NO bolus) 4) beta adrenergic agonists 5) IV sodium bicarbonate 6) diuretics, IV saline 7) GI resins 8) dyalisis (if needed)
How does IV calcium help hyperkalemia? MEMBRANE STABILIZATION; raises threshold potential-->decreases cardiotoxic effects of hyperkalemia without affecting plasma K concentration
How does IV insulin help in hyperkalemia? increases redistribution into cells
How do beta-adrenergic agonists help hyperkalemia? β-agonists stimulate the cellular uptake of potassium due to increased Na+K+ATPase activity; albuterol works (inhaled)
How do you treat chronic hyperkalemia? 1) treat underlying process 2) restrict K intake 3) stop offending drugs 4) enhance distal tubular sodium delivery and flow (liberal Na+ intake, diuretics), 5) mineralcorticoid replacement (rarely needed)
What mineralcorticoid replacement might help patients with hyperkalemia (chronic)? fludrocortisone
What factors affect K+ external balance? total body K deficiency may be due to inadequate K intake, from increased extrarenal K+ losesses, or increased renal K+ losses
What clinical settings contribute to inadequate intake of K+? alcoholism and malnutrition
What etiologies result in increased external potassium loses? GI losses (diarrhea, laxative abuse, vomiting, nasogastric suction/drainage); cutaneous losses (profuse sweating + burns)
How does gastric fluid loss lead to K+ wasting? *Although potassium is lost directly in the gastric fluid during protracted vomiting or nasogastric drainage, majority of the L losses in this setting results from renal potassium wasting due to metabolic alkalosis and secondary hyperaldosteroni
What etiologies are responsible for increased renal potassium losses? Can be linked to hypertension (due to mineralocorticoid excess); normotensive disorders may be caused by increased distal tubular flow rate, presence of poorly reabsobed anions, primary tubular dysfunction, an secondary hyperaldosteronism
What etiologies are associated with hypertensive hypokalemic disorders? hyperreninemia (renal artery stenosis or renin secreting tumor); primary hyperaldosteronism (Conn's syndrome); Cushing's syndrome (exogenous steroid therapy, cortisol hypersecretion); congenital adrenal hyperplasia
What etiologies are associated with normotensive hypokalemic disorders? diuretic therapy, osmotic diuresis, renal tubular acidosis, prolonged vomiting or nasogastric drainage, ureteral diversion
How does prolonged vomiting or nasogastric drainage lead to normotensive hypokalemic disorders? Prolonged loss of gastric secretions results in a severe metabolic alkalosis. Renal potassium wasting results from increased delivery of bicarbonate (poorly reabsorbable anion) to the distal nephron and secondary hyperaldosteronism.
What factors affecting internal balance may contribute to hypokalemia? insulin excess, catecholamine excess, alkalemia, cell proliferationhyperpolarization
Initially, hypokalemia results in membrane ___ due to the decrease in the extracellular:intracellular potassium concentration ratio. hyperpolarization
More severe hypokalemia results in a secondary increase in sodium .... conductance that results in membrane depolarization.
What changes are seen in ECG during hypokalemia? flat t-wave, prominent U-wave, depressed ST segment
What renal manifestations are seen in patients with hypokalemia? increased renal generation of ammonia and nephrogenic diabetes insipidus
Why does renal generation of ammonia increase in hypokalemia? With hypokalemia intracellular K + shifts to the extracellular fluid compartment and hydrogen ion moves intracellularly to maintain electroneutrality. Increased intracellular H + ion concentration directly stimulates renal ammoniagenesis.
How does hypokalemia contribute to nephrogenic diabetes insipidus? Nephrogenic diabetes insipidus results from a diminished responsiveness of the cortical collecting tubule to ADH.
How is hypokalemia treated? consists of correction of the underlying disorder (if possible) and potassium replacement; K+ sparing diuretics
How can potassium be repleted? oral route preferred; IV (caution), with max rate at 10 meq/hr; K+ requires finite time to enter cells; too rapid infusion may result in transient hyperkalemia (!)
What diuretics should you use in patients with hypoklaemia and: primary renal potassium wasting? hyperaldosteronism? amiloride and triamterene; spironalctone
Created by: karkis77