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Chapter 9. Disorders of Potassium metabolism

Nephrology Study

Hee Jung Jeon

on 18 April 2017

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Transcript of Chapter 9. Disorders of Potassium metabolism

Chapter 9. Disorders of Potassium metabolism
Thank you for your attention!
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Potassium Intake

Potassium distribution

Renal K Handling with Normal Renal Function

Renal K Handling in the Face of CKD
Clinical manifestation



Clinical manifestation



Normal physiology of
potassium metabolism
Normal physiology of potassium metabolism
Potassium intake
Potassium distribution
Renal K Handling with Normal Renal Function
Renal K Handling in the Face of CRF
Clinical manifestation/etiology/diagnosis/treatment
Clinical manifestation/etiology/diagnosis/treatment
Essential for many cellular functions

Present in most foods & excreted primarily by the kidney
typical western diet: 70~150 mmol/day
efficiently absorbed in GI tract
Potassium Intake
Sirloin steak
Clinical Manifestations
Clinical Manifestations
hypoK increases BP by 5-10 mmHg
by stimulating Na retention -> intravascular vol. expansion
by sensitizing the vasculature to endogenous vasoconstrictors
expression of the kidney-specific isoform of WNK1
NCC-mediated Na reabsorption in distal convoluted tubule
ENaC- mediated Na reabsorption in cortical collecting duct

esp. digoxin, diuretic-induced hypoK
Increases the risk of Vent. arrhythmias, V.fib, and sudden cardiac death
Clinical Manifestations
Clinical Manifestations
-> impair insulin release & induce insulin resistance
-> worsen glucose control in diabetic patients
hyperpolarizes skeletal m. cells
-> impairing m. contraction
impairs local nitric oxide release
-> reduces skeletal m. blood flow
-> predispose to rhabdomyolysis during vigorous exercise
Tubulointerstitial and Cystic Changes
K depletion
stimulates intra-renal vasocontrictors
(AT-II & endothelin)
inhibits intra-renal vasodilators
(kallikrein, NO, prostaglandins) 
renal structural change (tubulointerstitial fibrosis)
HypoK predisposes to renal cyst formation
Acid Base : metabolic alkalosis
d/t increased renal net acid excretion
severe hypoK -> resp. m. weakness -> resp. acidosis
-> impairs renal concentrating ability
-> causes mild polyuria, 2~3 liters/day
Hepatic Encephalopathy
-> increases renal ammonia production
-> 1/2 to the systemic circulation via renal veins
-> may worsen hepatic encephalopathy
(1) Pseudohypokalemia :
m/c cause : AML
large number of abnormal WBC can take up extracellular K if blood is stored for prolonged periods at room temp.
(2) Redistribution: Fig 9.3
hypokalemic periodic paralysis
genetic defect in dihydropyridine-sensitive Ca channel
(3) Extra-renal K Loss : skin, GI tract
excessive sweating or chr diarrhea, vomiting, NG suction
(4) Renal K Loss
- thiazide > loop diuretics (adjusted for natriuretic effect)
- penicillin analogues: carbenicillin
- amphotericin B : increases collecting duct K secretion
- aminoglycoside, cisplatin, toluene, licorice

Endogenous Hormone : Aldosterone, CAH
- K uptake into cells & renal K excretion

Mg depletion : inhibits renal K retention
- diuretic, aminoglycoside, cisplatin induced

Intrinsic Renal Defect
: Bartter, Gitelman’s, Liddle synd

Bicarbonaturia : increases K secretion
major intracellular cation
100~120 mmol/l in the cytosol
Total intracellular potassium content
3000~3500 mmol in healthy adults
Potassium Distribution
Only 1-2%
total body K+
Na+,K+-ATPase : active uptake
2 K+ ions into cells in exchange for extrusion of 3 Na+
 -> high intracellular K+, low Na+
Intracellular K/extracellular K ratio
major determinant of cell membrane potential
intracellular electronegativity

Serum K concentration : tightly regulated
“Feed forward” regulatory system
gut or portal potassium sensors  adjusts renal potassium excretion (independently changes in plasma potassium or aldosterone concentration)
Potassium Distribution
Cellular potassium shifts
- rate: 10 mmol/h (peri), 20 mmol/h (cent)
- 20 mmol of KCl increases the serum K by ~0.25 mmol/l

If KCl is administered in destrose-containing solutions, the resulting increase in cellular K uptake may exceed the KCl replacement rate & may worsen the hypoK

Conditions requiring urgent therapy (rare)
hypokalemic periodic paralysis
severe hypoK pts requiring urgent surgery
AMI with significant ventricular ectopy
-> IV K given 5-20 mmol during 15-20 min

Hypomagnesemia can lead to refractoriness to K replacement
=> replacement with MgSO4, periodic measure of serum Mg
Clinical Manifestations
Asymptomatic to life threatening

Alteration of cardiac conduction -> Fig 9.8

Skeletal m. weakness
"rubbery" or "spaghetti" legs
with severe hyperK, resp. failure may occur from paralysis of the diaphragm

(1) Pseudohyperkalemia
Infectious mononucleosis
Abnormal RBC memb K permeability
prolonged tourniquet time
severe leukocytosis, marked thrombocytosis
(2) Redistribution: Fig 9.3
(3) Excess Intake
if renal K excretion impaired
ex) enteral products, Fig 9.1
(4) Impaired Renal Potassium Secretions
intrinsic renal defect - Gordon's synd.
specific medications
24-hour urine K+ excretion : type of hyperK
- renal : K+ <20 mmol/l
 => fludrocortisone :
Aldo deficiency (u-K up to >40 mmol/l)
Aldo resistance (u-K remains <20 mmol/l)
- extrarenal: K+ >40 mmol/l

Urinary K+ measurements may be difficult to interpret since K+ excretion depends on multiple factors (GFR, tubular lumen flow, diuretic use, and water reabsorption) in the distal tubule 
=> TTKG check
Distinguishing renal & nonrenal mechanisms of hyperK
Treatment of hyperK
Should not include NaHCO3 unless the pt is frankly acidotic (pH<7.2) or unless substantial endogenous renal function is present
Precautions with IV Calcium

- NaHCO3-containing solutions should not be used, d/t CaCO3 precipitation can occur
- hyperCa may occur, it may potentiate digoxin-related myocardial toxicity

Most rapid (1-3min), last for 30-60min
Dose may be repeated within 5-10 min
Consider continuous calcium infusion
- IV insulin
with or wihout glucose coadminister
continuous infusion
4~10 U/hr with D10W
- b agonist : IV, inhaled, SC
dose requir 2-8 times greater than usual nebulizer

- in severe hyperK, combined therapy with insulin &
albuterol may be more effective than either alone
♥신장내과 화이팅 ♥
Nephrology Fighting
Acidosis d/t inorganic anions (NH4Cl, HCl)  -> hyperK
Mechanism is not fully understood
Acidosis d/t organic anions (lactic acid)
Generally, do not cause transcellular K shift

Directly stimulate Na+,K+-ATPase
βb2 agonist
Intracellular cAMP↑  stimulate Na+,K+-ATPase
Opposite of bβ2 agonist
Causes of cellular potassium shifts
Aldoterone -> lower serum K
Stimulate K movement into cell (redistribution)
Increase K excretion in the Kidney > the gut

Hyperosmolality  -> hyperK
Effective plasma osmole (hyperglycemia, mannitol)
 -> water movement out of the cells
 -> cell volume↓ & intracellular K ↑
 -> Feedback inhibition of Na+,K+-ATPase
 -> Shifting K from intracellular to extracellular
Causes of cellular potassium shifts
Exercise -> hyperK
By aα-adrenergic R activation
 -> shift K out of skeletal m. cell
 -> induced arterial dilation
 -> Increased skeletal m. blood flow (adaptive mechanism)
Simultaneous βb2-adrenergic R activation
 -> Stimulate skeletal m. cellular K uptake
 -> Minimizing severity of exercise-induced hyperK

(* In patients with pre-existing K depletion, post-exercise hypokalemia may be severe and rhabdomyolysis may occur.)
Causes of cellular potassium shifts
K homeostasis is relatively well preserved, and serum K usually remains normal until the GFR is severely reduced
d/t increased K excretion per nephron & increased GI tract K excretion
Aldosterone & subclinical serum K increases may contribute to this adaptation

Pts with CKD appear to tolerate hyperK with fewer cardiac & ECG abnormalities than pts with well-preserved or normal renal function who experience AKI
=> mechanism (?)
Renal K Handling in the Face of CKD
Descending loop of Henle : K secretion
Thick ascending loop of Henle (apical membrane)
reabsorption by apical Na+-K+-2Cl- cotransporter
 -> Net K reabsorption in loop of Henle
Reverse to secretion
loop diuretics or K loading

Distal tubule & collecting duct
Major site regulate K excretion
Active secretion and absorption
Renal K Handling c Normal Renal Fx
Glomerulus : Nearly completely filtered

Prox. Tubule : reabsorbs the majority (~ 65-70%)
Very little regulated by changes in K intake
Renal K Handling c Normal Renal Fx
Principal cell(cortical collecting duct) : secretes K

Regulation factor :
luminal flow rate,
distal Na delivery,
K sparing diuretics
loop or thiazide diuretics
extracellular K & pH
Renal K Handling c Normal Renal Fx

Intercalated cell :
reabsorbs K through apical H+,K+-ATPase that actively secretes H+ into the luminal fluid in exchange for K reasorption

Metabolic acidosis can increase H+,K+-ATPase contributing to hyperkalemia
Renal K Handling c Normal Renal Fx
secretion by principal cell & reaborption by intercalated cell
-> effective regulation of renal K excretion
WNK (with no lysine) kinase
Origins of Myofibroblasts
Modified from Madeleine A et. Semin Nephrol 2010 & Liu et. Nat Rev Nephrol 2011
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