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Renal > Hypokalemia and Hyperkalemia > Flashcards

Hypokalemia and Hyperkalemia Flashcards

1
Q

4 Mechanisms of Potassium Balance

A
  • K+ intake through the diet
  • GI losses

– GI tract secretes 5-10% of absorbed K+ daily

• Renal losses

– 90-95% is regulated by the kidney

• Transcellular K+ shift

– Overall K+ stores remain the same but redistribute between the ICF and ECF

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2
Q

Renal Handling of Potassium

A
  • K+ is freely filtered at the glomerulus
  • ~65-70% of filtered K+ reabsorbed in proximal tubule
  • Passive transport

– Paracellular route by solvent drag and diffusion

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3
Q

Renal Handling of Potassium - Ascending Loop of Henle

A
  • Reabsorbs 10-25% K+
  • Driven by luminal Na+-K+-2Cl- (NKCC2) multiporter
  • Active transport driven by Na+-K+ ATPase
  • Transporter affinity for Na+, K+ high • Max activity when TF [Na+, K+] are <5-10 meq
  • K+ recycling across luminal membrane allows for continued activation of NKCC2
  • Activity of K+ channel is inhibited by ATP allowing a link to level of Na+ reabsorption
  • As more Na+ enters cell, Na+ will be transported out of the cell into the peritubular capillary by Na+-K+ ATPase –> lowering cellular ATP level and stimulates activity of luminal K+ channel
  • Permits return of reabsorbed K+ into lumen and further Na+ absorption
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4
Q

Renal Handling of Potassium Primary Regulatory Site Of K+ Excretion: Principal Cell

A
  • K+ actively transported into cell by Na+-K+ ATPase at basolateral membrane
  • Secreted into tubular fluid (TF) down a favorable electrochemical gradient via luminal K+ channels (ROMK)
  • Governed by factors that affect passive transport
  • Concentration gradient across luminal membrane

– High intracellular [K+] and low TF [K+]

  • Electrical gradient generated by reabsorption of Na+ via luminal Na+ channels (ENaC)
  • K+ permeability of luminal membrane

– # of open K+ channels

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5
Q

K+ Regulation in the Principal Cell 4 main factors that affect K+ secretion into the tubular fluid

A
  • Aldosterone
  • Plasma K+ concentration
  • Distal Flow Rate
  • Distal Na+ delivery
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6
Q

K+ Regulation in the Principal Cell 4 main factors that affect K+ secretion into the tubular fluid: Aldosterone

A

– augments K+ secretion in principal cells

– Increase # open Na+ and K+ channels in luminal membrane

– Enhances activity of Na+-K+ ATPase pump

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7
Q

K+ Regulation in the Principal Cell 4 main factors that affect K+ secretion into the tubular fluid: Plasma K+ concentration

A

– Increase # open Na+ and K+ channels in luminal membrane

– Enhances activity of Na+-K+ ATPase pump

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8
Q

K+ Regulation in the Principal Cell 4 main factors that affect K+ secretion into the tubular fluid: Distal Flow Rate

A

– Increase in distal flow rate washes secreted K+ away and replaces with relatively K+ free fluid–> favorable [K+] gradient for secretion into TF

– When distal flow rate reduced, high luminal [K+] (due to less washout of secreted K+) and low urine flow –> reduction in absolute rate of K+ secretion (additionally voltage gated channels – Maxi K – stimulated by flow)

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9
Q

K+ Regulation in the Principal Cell 4 main factors that affect K+ secretion into the tubular fluid: Distal Na+ delivery

A

– Entry of Na+ via Na+ channel (ENaC) makes lumen electronegative

– Transport of Na+ into peritubular capillary by ATPase pumps more K+ into cell

– More K+ secreted into electronegative lumen

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10
Q

Renal Handling of Potassium Intercalated cell in the collecting duct is a site of K+ reabsorption

A
  • α-Intercalated cells reabsorb K+ via apical H+-K+ ATPase – Active process
  • Actively secretes H+ into luminal fluid in exchange for K+ reabsorption
  • Active reabsorption by H+- K+ATPase enables urinary K+ excretion to decrease to <15 mmol/d in severe K+ deficiency
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11
Q

Hypokalemia

A
  • Transcellular
  • GI Losses
  • Renal Losses
  • poor intake
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12
Q

Hypokalemia - Transcellular Shift

A

• Insulin

– Promotes K+ entry into cell by stimulating Na+-K+ ATPase

• Β2 adrenergic agonist

– Catecholamines or drugs acting via β2 adrenergic receptors increases K+ entry into cell by increasing activity of Na+-K+ ATPase

• Alkalosis

– H+ will leave cell in order to lower extracellular pH

– K+ enters cell in order to maintain electroneutrality

• Hypokalemic periodic paralysis

– Acute attacks precipitated by sudden movement of K+ into cells

– Lowers plasma K+ to 1.5-2.5 mEq/L

– Precipitated by:

  • Rest after exercise
  • Stress
  • High carbohydrate meal

– Familial

• Autosomal dominant

– mutations in dihydropyridine calcium channel in skeletal muscle

– Acquired

• Thyrotoxicosis

– Predominantly young Asian males

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13
Q

Hypokalemia - GI Losses

A

• Vomiting and nasogastric tube output

– Associated with metabolic alkalosis due to HCl loss

– K+ loss from emesis ~ 5-10 mEq/L

– Concurrent urinary losses

  • Activation of aldosterone
  • Increase in plasma bicarbonate –> increases filtered bicarbonate above its reabsorptive threshold
  • Because Na+ must pair with bicarbonate in TF

– the increase in distal delivery of Na+ further promotes K+ loss

  • Diarrhea
  • Laxatives

– Associated with metabolic acidosis due to bicarbonate losses

– K+ loss from the stool ~ 20- 50 mEq/L

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14
Q

Hypokalemia - Renal Losses

A

•Metabolic Alkalosis

  • normohypotension
  • hypertension

•Metabolic Acidosis

  • renal tubular
  • nonreabsorbable anion

•magnesium

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15
Q

Hypokalemia Renal losses associated with metabolic alkalosis - normohypotension

A

• Conditions associated with metabolic alkalosis and normohypotension

– Diuretics

  • Loops and thiazides
  • Activate aldosterone by volume depletion
  • Increase distal delivery of Na+

– Salt wasting nephropathies

  • Bartter’s syndrome
  • Gitelman’s syndrome
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16
Q

Hypokalemia Alkalosis: Salt wasting nephropathies - Bartter’s Syndrome

A

• Bartter’s syndrome (think loop diuretic)

– Autosomal recessive presents early in life

– Defect in NaCl reabsorption in thick ascending limb of Henle

– 3 main transporters can be involved by mutations

  • Na+ 2Cl- K+ (NKCC2)
  • Luminal K+ channel
  • Basolateral Cl- channel

– Clinical presentation

  • Hypotension
  • Impaired concentrating capacity
  • Hypokalemic metabolic alkalosis
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17
Q

Hypokalemia Alkalosis: Salt wasting nephropathies - Gitelman’s Syndrome

A

• Gitelman’s syndrome (think thiazide diuretic)

– Autosomal recessive can present in later childhood or early adulthood

– Defect in gene encoding the thiazidesensitive NaCl cotransporter in the distal convoluted tubule

– Clinical presentation

  • Normo-hypotension
  • Impaired concentrating capacity
  • Hypokalemic metabolic alkalosis

– Low urinary calcium distinguishes Gitelman’s from Bartter’s syndrome Hyp

18
Q

Hypokalemia Alkalosis associated with metabolic alkalosis hypertension

A

• Mineralocorticoid excess

– Primary hyperaldosteronism

  • Adrenal tumor
  • Bilateral adrenal hyperplasia

– Glucocorticoid remedial aldosteronism

• Autosomal dominant

– ACTH dependent production of aldosterone

– Renovascular disease

• Renal artery stenosis

– Defects in 11-β-hydroxysteroid dehydrogenase type 2

  • Converts cortisol to corticosterone
  • Black licorice root
  • Syndrome of apparent mineralocorticoid excess (SAME)

– Congenital adrenal hyperplasia

-Liddle’s syndrome

  • Autosomal dominant
  • Presents during adolescence and early adulthood
  • Gain of function mutation in the epithelial Na+ channel (ENaC)
  • Excessive Na+ reabsorption
  • Triad

*Hypertension

*Metabolic alkalosis

*Hypokalemia

19
Q

Hypokalemia Associated with metabolic acidosis

A

• Renal tubular acidosis (RTA)

– Hyperchloremic, nonanion gap metabolic acidosis

• Distal hypokalemic RTA (type I)

– Impaired distal acidification

– Familial

– Autoimmune disease

– Drugs (Ifosfamide)

• Proximal RTA (type II)

– Reduction in proximal bicarbonate reabsorptive capacity

– Bicarbonate wasting in urine until plasma bicarbonate has fallen to level low enough to allow filtered bicarbonate to be reabsorbed

– Familial

– Multiple myeloma

– Drugs (tenofavir)

• Nonreabsorbable anions

– Toluene

  • Paint thinner
  • Metabolite

– hippurate

– Nonreabsorable anion

– Pairs with Na+

– Leads to increased distal Na+ delivery

– Diabetic ketoacidosis

• β-hydroxybuterate

– Nonreabsorbable anion

– Pairs with Na+

– Leads to increased distal Na+ delivery

20
Q

Hypokalemia Magnesium

A

• Magnesium

– Hypokalemia occurs in 40-60% of cases

– Often due to underlying disorders that waste both Mg and K+

  • Diarrhea, diuretics
  • Renal K+ wasting occurs independently due to increased secretion into the loop of Henle and collecting duct

– Mechanism is not well understood

• Must correct Mg deficit in order to restore K+

21
Q

Hypokalemia Clinical Manifestations: Cardiovascular

A

• Cardiac arrhythmias and ECG abnormalities

– Premature atrial and ventricular beats

– Sinus bradycardia

– AV block

– Ventricular tachycardia/fibrillation

• Decrease in amplitude of T wave and increase in amplitude of U wave

– Occurs at the end of T wave

– Seen in lateral precordial leads

22
Q

Hypokalemia Clinical Manifestations: Muscular

A

• Weakness and muscle cramps

– Low K+ (<2.5 mEq/L) can hyperpolarize skeletal muscle cell impairing contraction

– Can reduce skeletal muscle blood flow by impairing local nitric oxide release

• Predisposes to rhabdomyolysis (muscle breakdown) during vigorous exercise

– Severe K+ depletion (<2.0 mEq/L) can cause respiratory muscle weakness leading to respiratory failure and death

– GI muscle weakness can result in ileus (bowel obstruction due to decreased muscular activity)

23
Q

Hypokalemia Hormonal and Renal Manifestations

A

• Hormonal

– Impairs insulin release and end-organ sensitivity to insulin

  • Worsened glucose control in diabetic patients
  • Renal

– Tubulointerstitial and cystic changes in the parenchyma of the kidney (prolonged hypokalemia)

– Polyuria

  • Severe hypokalemia impairs concentrating ability causing mild polyuria (2-3L/d)
  • Due to both increase thirst and mild nephrogenic diabetes insipidus

– Hypertension

  • Increase in renal vascular resistance
  • Sensitizes vessels to endogenous vasoconstrictors
24
Q

Hypokalemia Diagnosis

A

• Clinical history

– Help determine source of K+ loss

* Shift, GI, renal

• Urinary K+ determination

– Distinguish urinary losses from shift or GI losses

*Urinary K+ to creatinine ratio

– assumes a 24h value of urinary K+ based on a spot sample

– most patients will excrete 1000 mg of urinary creatinine in 24h

*< 15 mEq/g of creatinine suggests appropriate conservation of K+ and extrarenal loss

* > 15 mEq/g of creatinine suggests urinary losses

25
Q

Hypokalemia Diagnosis - Acid Base Status

A

• Determination of acid base status

– Metabolic acidosis

• Low urinary K+ to creatinine ratio (< 15 mEq/g)

– Stool losses

• High urinary K+ to creatinine ratio (> 15 mEq/g)

– RTA

– Nonreabsorbable anion

– Metabolic alkalosis

• Low urinary K+ to creatinine ratio (< 15 mEq/g)

– Vomiting

• High urinary K+ to creatinine ratio (> 15 mEq/g)

– Check blood pressure and volume status

» Low to normal BP/volume depleted (diuretics, salt wasting nephropathies, ongoing vomiting with sustained metabolic alkalosis)

» High BP/volume overload (mineralocorticoid excess, Liddle’s)

– Always check Magnesium

• Hypokalemia due to low Mg cannot be corrected until Mg is corrected

26
Q

Hypokalemia Treatment

A
  • Underlying disorder needs to be corrected
  • K+ < 2.5 mEq/L carries risk of dangerous cardiac arrhythmias and needs replacement – Oral replacement
  • Mild hypokalemia

– Parenteral replacement

  • Severe hypokalemia or patients who cannot tolerate oral intake
  • Maximum KCl concentration is 20 mEq/100ml

– Administered at a maximum rate of 10 mEq/h

27
Q

Hyperkalemia

A
  • Transcellular Shift
  • Pseudohyperkalemia
  • Renal: decreased urinary secretion
28
Q

Hyperkalemia Pseudohyperkalemia

A

– Elevation in measured serum K+ is due to K+ movement out of cells during or after a blood specimen has been drawn

  • Hemolysis (destruction of red blood cells) due to technique during blood draw – Clenching, prolonged tourniquet, venipuncture trauma
  • Thrombocytosis (increased platelets)
  • Leukocytosis (acute leukemia)
29
Q

Hyperkalemia: Transcellular Shift

A

• Metabolic acidosis

– H+ will enter cell in order to buffer the extracellular pH

– K+ will leave the cell in order to maintain electroneutrality

  • Applies to inorganic acids (not organic acidosis –i.e. diabetic ketoacids)
  • Overall small effect
  • Hyperglycemia and hyperosmolarity

– Elevation in serum osmolality results in H20 movement from the ICF to ECF

  • Results in increased [K+] in the cell
  • K+ will move out of cell down concentration gradient
  • Solvent drag from water movement out of cell
30
Q

Hyperkalemia: Transcellular Shift

A

• Nonselective β-antagonists

– Interfere with K+ uptake into cell by β-adrenergic receptors

• Exercise

– K+ released by muscle cells

  • Causes local vasodilation for increased blood flow
  • Tissue breakdown

– Rhabdomyolysis (muscle breakdown)

– Lysis of large tumor burden after chemotherapy

– Burns

• Digitalis (Digoxin®) toxicity

– Inhibits Na+-K+ ATPase pump

• Hyperkalemic familial periodic paralysis

– Autosomal dominant

– point mutation in skeletal muscle Na+ channel

– Precipitated by cold, rest after fasting, K+ ingestion

31
Q

Hyperkalemia: Renal: Decreased urinary excretion

A

• Renal failure

– Able to maintain near normal levels of K+ as long as distal flow rate and aldosterone secretion is maintained

– Hyperkalemia occurs in patients who are oliguric (decreased distal flow rate) who have an additional problem

  • Excess K+ load
  • Aldosterone blockade (ACE inhibitors, angiotensin receptor blockers, and aldosterone blockers)
  • Volume depletion with decreased distal Na+ delivery

– Hypovolemia

– Effective arterial volume depletion with extracellular volume excess

  • Heart failure
  • Cirrhosis of the liver
32
Q

Hyperkalemia: Renal: Decreased urinary excretion

A

• Functional hypoaldosteronism (either low aldosteronism state or resistance to the effect of aldosterone)

– Mineralocorticoid deficiency

  • Primary adrenal insufficiency (adrenal gland does not generate aldosterone in response to renin)
  • Hyporeninemic hypoaldosteronism

– Diabetic

– type IV RTA

– Low plasma renin levels and aldosterone levels

– Tubulointerstitial disease

• Sickle cell disease and urinary tract obstruction

– Distal hyperkalemic RTA

– Impaired Na+ reabsorption in the principal cell reducing K+ and H+ secretion

33
Q

Hyperkalemia: Renal: Decreased urinary excretion- Drugs

A

• Drugs

– Block conversion to aldosterone or binding to aldosterone receptor

• ACE inhibitors, angiotensin receptor blockers, aldosterone antagonists (spironolactone, eplerenone)

– Decreased renin release

• Nonsteroidal anti-inflammatory drugs (NSAIDS), betablockers, renin inhibitors (Tekturna®)

– Binds to luminal Na+ channel (ENaC) in the principal cell

• Amiloride, triamterene, trimethoprim (Bactrim®), pentamidine

– Multiple effects

• Calcineurin inhibitors (used for organ transplant to prevent rejection)

34
Q

Hyperkalemia Clinical Manifestations

A

• Severe muscle weakness or paralysis

– Ascending weakness begins with lower extremities and progresses to trunk, upper extremities –> flaccid paralysis

• Cardiac arrhythmias and ECG abnormalities

– Bundle branch block, advanced AV block, sinus bradycardia, sinus arrest, slow idioventricular rhythm, ventricular tachycardia, fibrillation, asystole

– ECG findings

  • Early – tall peaked T waves and shortening of the QT interval
  • Late – prolongation of PR and QRS interval – May lose P wave altogether with widened QRS –> sine wave
35
Q

Hyperkalemia Diagnosis

A
  • Clinical history and physical exam
  • Measurement of plasma K+ in suspected pseudohyperkalemia
  • Plasma renin activity and aldosterone concentration

– High renin, low aldosterone

• Adrenal insufficiency

– Low renin, low aldosterone

• Type IV RTA

– diabetic nephropathy

– Normal renin, high aldosterone (aldosterone resistance)

• Tubulointerstitial disease – Sickle cell disease, urinary obstruction

36
Q

Hyperkalemia Diagnosis - Transtubular Gradient

A

• Transtubular K+ gradient (TTKG) may help distinguish functional hypoaldosteronism from other disorders (i.e. transcellular shift)

– Gradient between the tubular fluid and plasma K+ - estimates aldosterone activity by measuring the K+ concentration in the tubular fluid at the end of the cortical collecting tubule (site of K+ secretion)

– [Urine K (Urine osmolality/Plasma osmolality)] Plasma K+

– Value < 5 is suggestive of hypoaldosteronism

37
Q

Hyperkalemia Treatment

A
  • Antagonizing membrane effects of K+ with calcium
  • Driving extracellular K+ into cells
  • Removing excess K+ from the body
38
Q

Hyperkalemia treatment - Antagonizing membrane effects of K+ with calcium

A

– Reserved for patient’s with ECG changes or acute rise in serum K+

– Calcium chloride

• Mechanism

– Hyperkalemia induces depolarization of the resting membrane potential leading to inactivation of the Na+ channels and decreased membrane excitability

– Calcium antagonizes this membrane effect (mechanism is not well understood)

39
Q

Hyperkalemia Treatment - • Driving extracellular K+ into cells

A

– Insulin administered with glucose

  • Insulin will cause uptake of K+ into the cell by stimulating activity of the Na+-K+ ATPase
  • Administer with glucose to avoid hypoglycemia

– Β-2 agonist (albuterol)

• Stimulates Na+-K+ ATPase via different mechanism then insulin (cAMP) and provides synergism when used with insulin

– Can lower K+ by 1.2-1.5 mEq/L when used together

40
Q

Hyperkalemia Treatment - K+ removal

A

– Diuretics

• Loops and thiazides

–Can be used long-term in patients with chronic kidney disease

–Loops are effective in short-term when combined with saline to maintain distal delivery of Na+ and distal tubular flow

• K+ Removal

– Cation Exchange Resins

• Sodium polystyrene sulfonate (Kayexalate®)

– Takes up K+ in the gut and releases Na+

– Most preparations are prepared in sorbitol (osmotic laxative)

» Sorbitol component can lead to intestinal necrosis

» Surgical patients are highest risk

• Patiromer (Veltassa®)

– Takes up K+ in exchange for calcium in the colon

– Will likely replace sodium polystyrene sulfonate

– Dialysis

  • Warranted when the prior measures are insufficient to correct hyperkalemia
  • Or when K+ expected to increase rapidly (tissue breakdown)
  • Hemodialysis is preferred modality – can remove 25-50 mEq of K+ per hour
  • Treatment of choice in end-stage-renal-disease (ESRD) patients

-Treatment of reversible causes

  • Discontinuation of drugs that cause hyperkalemia
  • Volume expansion with saline in patients with volume depletion

Renal (26 decks)

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