Sodium, Potassium and H20 Disorders

Maria E. Ferris, MD, MPH

Case Presentation

• 14 y.o male chronic illnesses is admitted for knee surgery & 12 hr. post Sz (GTC)

• Labs: Na 128, K 4.5, Cl 98, CO2 20, Ca 9, Mg 2, glucose 130 & U.Na 35

• a) CHF, b) total body Na, c) dilutional Natremia, d) Renal Na wasting e) third spacing of fluid

Answer

• C) Dilutional Hyponatremia

• Must investigate the IVF that were hung during surgery (D5W)

Question

• Maintenance daily Na requirements for a 50 Kg, 12 y.o. boy?

• a) 150 mEq, b) 100 mEq, c) 63 mEq,

d) 50 mEq and e) 45 mEq

Answer

• c) 63 mEq/ day

Na Transport along the nephron

ANPNa Channels3%Late Distal Tubule & CCT

AldosteroneNaCl symport4 %Distal Tubule

Aldosterone1 Na-1K-2Cl symport

25 %Loop of Henle

Angiotensin II, Epinephrine, Norepinephrine & Dopamine

Na-H exchange, NA co-transport w/ a.a. & org. solutes, Na/H/Cl/anion exchange

67 %Proximal Tubule

HormonesMechanism of Na Reabsorption

Filtered load reabsorbed

Segment

ADH & ANP

Passive8-17%Late Distal Tubule & CCT

NoneNone0 %Distal Tubule

NoneDescending Thin Limb

15 %L.of Henle

NonePassive67 %Prox. Tubule

HormonesMechanism of H2O Reabsorption

Filtered load reabsorbed

Segment

H2O Transport along the nephron

Na and Cl Reabsorption

• In the Proximal Tubule, 17,000 mEq of the 25,200 mEq (67%) of NaCl filtered per day is absorbed by para-cellular and trans-cellular pathways.

• Auto regulation of the GFR, glomerular-tubular balance, load dependency by the L.of H. & the DT, maintain a constant fraction of the filtered Na load to the beginning of the collecting duct.

Hyponatremia

• In .95 of the cases it is due to impairment of H2O excretion

• Factors that affect this excretion are:– Fluid intake– Ability to deliver NaCl to diluting segment and

its reabsorption– ADH suppression

Hyponatremia

• In renal dysfunction, a 1-2 fold change in SCr will volume excretion of free H2O by 4-fold

• This in great part due to delivery

Case Presentation

• 6y.o c/o VP shunt malfunction, afebrile and lethargic

• BUN 3, SCr 0.5, NA 125,Cl 90, Urine Osmolality 300, UNa 60. Best next step?

• a) Demeclocycline b) diuretics, c) IV Normal Saline, d) Immediate VP shunt removal e) fluid restriction

Answer

• e) fluid restriction

Case Presentation

• 4 y.o. with severe DH due to NV, (-) PMHx

• Labs: Na 125, Serum Osm 315. Findings are most likely due to an increase in:

• a) Cl, b) SCr c) glucose, d) P & e) K

Answer

• c) Glucose

Hypernatremia

Case Presentation

• 2 Wk old, + PNC, nl delivery w/ GTC Sz

• Wt. 2.5 Kg (200 gm < birth wt) male, BP 70/40,P:140, R:50

• Glu: 120, BUN 50, NA 170, CO2 12, Ca 9 & Mg 1.5. The Sz is likely due to

• a) Ca, b) glycemia, c) Mg, d) intracraneal hge. e) meningitis

Answer

• d) Intracraneal hemorrhage due to hypernatremia

Case Presentation

• 2 y.o. with Cong. heart Dz 1 day Hx of resp. distress & LE’s edema

• BUN 40, SCr 1.5, NA 125, K 4, Cl 95,

CO2 20. Most appropriate next test?

• a) Serum Osmolality b) Urine FENa, c) Urine pH, d) Urine S.G, e) venous pH

Answer

• B) FENa

Potassium Disorders

K+ Homeostasis

Diet:100 mEq/d

Int. Abs: 90 mEq/d

ECF: 65mEq/dTissue Stores

Plasma K,Aldo &

ADH

Insulin, Epi &Aldosterone

Feces: 10 mEq/d

Urine 90 mEq/d

K+ Homeostasis

• K+ is one of the most abundant cations in the body and a major determinant of the resting membrane potential, which is crucial for cell growth/division & excitability of nerve muscle.

• Homeostasis is maintained by hormones & the kidneys, which adjust K excretion to match PO intake.

• K excretion is determined by the rate of K secretion by the distal tubule & CCD

3Na+

2K+ATPase

Transcellular K+ Distribution

K+cell = 140-160 mEq/L

K+e = 4-5 mEq/L

Relationship Between [K+]serum and Total Body Potassium in 70 kg Adult

Serum[K+]mEq/L

Total Body Potassium

Normal-150 mEq +150 mEq

2

3

4

5

6

Potassium Distribution

ECF

ICF3920 mEq

80 mEq

98%

2%

Potassium Content in Fruits and Vegetables

Amount of PotassiumMilligrams mEq

Potato with skin 844 mg 20

3 Oz. Dried Fruit 796 mg 20

10 Dried Prunes 626 mg 16

1 Banana 451 mg 11

Tomato 254 mg 6.5

1 Kiwi 252 mg 6.5

8 Oz. Glass of 250 mg 6.5

Orange Juice

1Grapefruit 158 mg 4

Renal Tubular Potassium Handling

Filtered load600-700 mEq

per day

K+ Reabsorption60-70%

K+ Reabsorption20-30% K+ Secretion

Urinary Excretion90mEq/day

Urinary Potassium Excretion

• Normal kidneys have the capacity to excrete 500-600 mEq per day (average K+ excretion 40-100 mEq/day).

• The key site of renal potassium excretion regulation occurs at the cortical collecting duct.

Cortical Collecting Duct - Principle Cells

Na+

K+

3Na+

2K+

AldosteroneR-Aldo

Cl-

Peritubularcapillary

Tubular lumen

ATPase

Na+

Cortical Collecting Duct

ATPase

ATPase

ATPase

Tubular lumen PeritubularCapillary

Principle Cell

Intercalated Cell

K+

H+

OH- + CO2 HCO3-

T

Cl-

H2O

H+ 3Na+

2K+

Cl-

K+

Na+

ATPase

3Na+

2K+

R-Aldo

NH3NH3H+ +

NH4+

Na+

Aldosterone

Mechanisms Leading to Hyperkalemia

• Impaired entry into cells

• Increased release from cells

• Decreased urinary excretion

3Na+

2K+ATPase

K+

H+

GlucoseInsulinDigoxinβ-blockersCell injury

Hyperkalemia – Redistribution: ICFECF

Factors that Impair Urinary K+ Excretion

• Collecting duct lumen relatively more electropositive

Flow and sodium delivery to the CCD Aldosterone production or activity

Effect of Amiloride

Predict changes in the following:

• Relative lumen charge• Renal K+ excretion• Serum potassium• Renal H+ excretion• Arterial pH ATPase

ATPase

PeritubularCapillary

OH- + CO2 HCO3-

T

Cl-

H2O

H+ 3Na+

2K+

K+

ATPase

3Na+

2K+

R-Aldo

AmilorideNa+ Channel

Amiloride

Aldosterone

Tubular lumen

Hyperkalemia: Decreased Renal Excretion

• Volume depletion decreased flow in CCD• Decreased renin-AII-aldo production

– NSAIDS renin

– ACEI AII

– Heparin aldosterone production

– Spironolactone aldosterone activity

• Inhibition of CCD Na+ channel– Amiloride, triamterene, trimethoprim, pentamidine

ECG Changes of Hyperkalemia

Serum K+ (mEq/L) ECG

9 Sinoventricular V-fib

8 Atrial standstill Intraventricular block

7 Tall T wave. Depressed ST segment

6 Tall T wave. Shortened QT interval

ECG Changes due to Hyperkalemia

Treatment of Hyperkalemia

Therapy Mechanism of Action

Calcium Stabilization of Membrane Potential

Insulin Increased K+ entry into CellsBeta-2 AgonistsBicarbonate (if pHa<7.2 in setting of

acidosis)

Dialysis Potassium removalCation Exchange Resin (sodium polystyrene = Kayexalate)

Differential Diagnosis of Hypokalemia

• Increased entry into cells

• Inadequate intake or GI losses

• Urinary losses

3Na+

2K+ATPase

K+

Hypokalemia: Redistribution: ECFICF

Insulinβ-2 agonistsAlkalosis

Barium poisoningHypokalemic periodic paralysis

Factors that Enhance Urinary K+ Excretion

• Lumen of CCD more electronegative

• Enhanced flow and sodium delivery to the CCD

• Increased aldosterone

Thiazide Diuretics

Loop diuretics

Na+K+2Cl--

BloodLumen

Loop diuretics

Na+Cl-

Thiazide diuretics

Sites of Action of Diuretics

Lumen Blood(Defect = Bartter’s)

(Defect = Gitelman’s)

Interpretation of Urinary K+ in the Setting of Hypokalemia

GI Losses or prior Renal K Loss or

Diuretic Therapy Current Diuretic

Use

24o Urine K < 20 mEq > 30 mEq

FeK < 6 % > 10 %

Ser

um [

HC

O3-

]U

pHU

[Cl- ]35

30

25

20

7.0

5.5

4.0503010

Generation Phase Late Maintenance Phase

Volume Depletion

Metabolic Alkalosis in Vomiting

Early Maintenance Phase

Effect of Gastric Loss of HCl, Na+/H2O (Volume)

Predict changes in the following:

1. Relative lumen charge2. Renal K+ excretion3. Serum potassium4. Renal H+ excretion5. Arterial pH

ATPaseATPase

Tubular lumenPeritubularCapillary

OH- + CO2 HCO3-

T

Cl-

H2O

H+ 3Na+

2K+

K+

Na+

ATPase

3Na+

2K+

R-Aldo Aldosterone

Na+

HCO3-

Urine Na+ and Cl- in the Differential Diagnosis of Metabolic

Alkalosis and Hypokalemia

Urine ElectrolytesNa+ Cl-

Condition (meq/L)

VomitingAlkaline urine >15 <15Acidic urine <15 <15

DiureticDrug active >15 >15Remote use <15 <15

Hyperaldosteronism >15 >15

K+ disequilibrium

• Acid-base disturbances– Acute metabolic acidosis = K

– Chronic metabolic acidosis = K– Metabolic alkalosis = K

• Exercise (+ -blockers = K)• Cell lysis (trauma, burns, tumor-lysis, G-I bleed)• Plasma osmolality ( by 10 mOsm/Kg = K)• Changes in tubular fluid flow

Case Presentation

• 10 month old with CHF on 2 mg/Kg lasix b.i.d. His most likely serum labs?

• a) pH 7.2, K 3.0, b) pH 7.2, K 3.5, c) 7.2, K 4.5, d) pH 7.5 K 3.0, e) pH 7.5, K4.5

Answer

• d) Metabolic alkalosis with hypokalemia

Case Presentation

• After gaining 150 yards and 28 carries a football player becomes disoriented, gross hematuria & LOC

• T:106.7,P160,R30,100/60, BUN54, CK Next day oliguria develops despite CR and fluid support. Most likely Dx?

• a) Heat stroke, b) HUS, c)Hgic. shock & encephalopathy, d)Reye Sx. e) viral Sx

Answer

• a) Heat stroke and Rhabdomyolysis

Chloride disorders

Answer

• a) Urinary Cl

Case presentation

• 6 Week old baby c/o emesis p. each feed X 2 wks. ‘always hungry’, emaciated, dry mucosas, ? RUQ abdominal mass. Labs?

• a) Hypochloremic metabolic acidosis, b) Hypochloremic metabolic alkalosis, c) Resp. alkalosis, d) Respiratory acidosis & metabolic compensation, e) nl. electrolytes

Answer

• b) Hypochloremic metabolic alkalosis likely 2o. To pyloric stenosis