URINE&ELECTROLYTES&AND& OSMOLALITY& · • Disorders&of&intravascular&volume& • Hyponatremia •...
Transcript of URINE&ELECTROLYTES&AND& OSMOLALITY& · • Disorders&of&intravascular&volume& • Hyponatremia •...
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URINE ELECTROLYTES AND OSMOLALITY
Assoc. Prof. Damjan Kovač, MD, PhD University Medical Centre Ljubljana Department of Nephrology
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Urine electrolytes
• Na+
• K+
• Cl-‐
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• NH4+
• Mg2+
• Ca2+
• PO4-‐
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When are urine electrolytes indicated?
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In the following clinical circumstances: • Acute kidney injury • Disorders of intravascular volume • Hyponatremia • Hypernatremia • Polyuria • Acid – base disorders • AbnormaliYes of serum potassium concentraYon
Remember! 1. electrolyte and osmolality analysis should be done before insYtuYon of therapy 2. urine can be saved and analysed at a later Yme
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Osmolality
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Number of moles of solute per kg of solvent (water).
Urine osmolality can vary in healthy person from 80 -‐1200 mOsm/kg H2O
Most important osmols in the urine are caYons Na+, K+, NH4+ with their
corresponding anions and urea. It can be calculated:
Uosm = 2 x (Na+ + K+ + NH4+) + (urea) + (glucose)
It is measured by an osmometer.
Osmolality [mOsm/kg H2O] = depression of freezing point [mK] ÷ 1.858
1. Freezing point osmometers 2. Vapor pressure osmometers 3. Membrane osmometers
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Nonosmotic influences:
• Drugs
• ê efective arterial volume
• Nausea
• Postoperative pain
• Pregnancy
High blood osmoticity
AnYdiureYc hormone (ADH)
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ADH acYon
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ADH
H2O
H2O
H2O
urine renal interstitium
H2O
H2O
H2O
H2O H2O
H2O
Protein kinaze A
ATP
cAMP
d i s t a l t u b u l e
V2 receptor
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OSMOLALITY vs. SPECIFIC GRAVITY
• Osm: determines only number of parYcles • SG: determines number of paYcles and their weight
• Usually they change in paralel • SG of 1.020-‐1.030 à osmolality 800-‐1200 mOsm/kg H2O
• SG of 1.005 à osmolaity <100 mOsm/kg H2O • DisproporYonate increase of SG if urine contains
– glucose or proteins – radiocontrast material
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Sodium excreYon
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• Filtered in the glomerulus (25.000 mmol/day)
• 1-‐3 % of this filtreed load is excreted in the urine (FRACTIONAL EXCRETION)
• Na+ determianYon in the urine is very suitable for differenYal diagnosis of AKI
• Any acute kidney injury causes Na+ loss (é FE)
• In hypovolemia and hypoperfusion Na+ is rebasorbed to a grater extent (ê FE)
• DeterminaYon of 24-‐h Na+ excreYon is useful tool for determinaYon of salt consumpYon (17 mmol Na+ = 1 g salt)
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Impact of hypovolemia on urine Na+
Hypovolemia
é Renin
Na+ tubular reabsorbYon
é Angiotensin II
é Aldosterone
é ADH
Concentrated urine with low Na+
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Diagnosing the cause of AKI by urine Na+
Prerenal azotemia? or Acute tubular necrosis? Urine Na+ < 20 mmol/L ê prerenal azotemia (osmolality > 500 mOsm/kg) Urine Na+ > 40 mmol/L ê acute tubular necrosis (osmolality < 350 mOsm/kg)
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Diagnosing the cause of AKI by urine Na+
STATES WHEN URINE Na+ CAN BE MISLEADING • Metaboloc alkalosis with volume depleYon (vomiYng):
Urine Na+ is not maximally reduced à obligate Na+ excreYon with HCO3
-‐
Urine Cl-‐ is more accurate in such condiYons (Cl-‐ < 20 mmol/L). • Prerenal azotemia in preexisYng CKD • DiureYc use
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HCO3-‐
Na+
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FracYonal excreYon of Na+
The most accurate test to disYnguish prerenal AKI from ATN in oliguric AKI (24h urine < 400 ml) DefiniYon: % of filtered Na+ excreted in the urine FE 1 % à 99 % of filtered Na+ reabsorbed, 1 % excreted in urine
urine Na+ X serum creaYnine FENa% = x 100
urine creaYnine X serum Na+
< 1%: prerenal AKI >2 %: ATN
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Piqalls of FENa It should allways be taken with cau8on. It is validated only in persons with oliguria. FENa in healthy person is allways <1%. Low in several renal condiYons not associated with volume depleYon:
• GN • contrast AKI • pigment nephropathy • vascular diseases • vasculiYs • liver disease
Some hypovolemic paYents will not have low FENa. Value of excreted sodium is related to GFR: as GFR decreases-‐ FENa increases. Elderly pts and pts with CKD are not able to generate FENa <1%.
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Hyponatremia
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• The most aboundant electrolyte disturbance, present in 15% to 30% of hospitalized paYents
• Hyponatremia represents an excess of water rela8ve to solute in the body.
• Hyponatremia usually develops as a result of the acYon of ADH in the kidney to diminish free water excreYon.
• Most common s8muli are nonosmo8c: drugs, pain, nausea, decreased effecYve arterial volume, strenuous exercise ...
• Rarely develops as a consequence of • consuming very low quanYYes of solute or • polydipsia
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Hyponatremia and anYdiureYc hormone
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280 285 290 Serum osmolality (mOsm/kg H20)
Serum [Na+] 135 mmol/L è max. suppressed ADH
ê
urine osmolality < 100 mOsm/kg
Nonosmotic ADH production
• Drugs
• ê effective art. volume
• Nausea
• Postoperative pain
• Pregnancy
Physiological respons in
hyponatremia:
U-‐Osm < P-‐Osm
137 Na+ 145
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Urine Na+ and osmolality in hyponatremia Urine sodium (mmol/L)
Urine osmolality (mOsm/kg)
True volume depleYon < 20 >300
EfecYve circulaYng volume depleYon
< 20 >300
SIADH > 40 if consuming regular diet >100-‐150, not maximaly dilute
Volume depleYon and SIADH Variable, may be <20 unYl volume depleYon corrected
>300
Water intoxicaYon Variable, may be low due to dilute urine
<100
Low solute intake (tea and toast) May be <20 Low (less than serum osmolality)
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Adapted from: Muser WP, Korzelius CA. Hosp Med Clin 2012; 1: e338-‐e352.
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Urine chemistries in hypernatremia
Reason Urine osmolality (mOsm/kg) Urine sodium (mmol/L)
Water depleYon >600-‐800 Variable
Water and volume depleYon >600-‐800 <20
OsmoYc diuresis (hyperglicemia, manitol)
>300 Variable
Diabetes insipidus (central or nephrogenic)
<300 (<100 in complete nephrogenic DI)
Variable (depends on intake)
Salt intoxicaYon >600-‐800 >20 (very high)
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• Deficit of free water relaYve to solute.
• Inadequate free water intake because of impaired access, impaired thirst (in elderly paYents).
• Most adult paYents with hypernatremia also have concurrent volume depleYon.
Adapted from: Muser WP, Korzelius CA. Hosp Med Clin 2012; 1: e338-‐e352.
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Urine chemistry in polyuria
Urine osmolality (mOsm/kg)
Urine sodium (mmol/L)
Water diuresis < 300 Low (total daily excreYon matches intake)
Solute diuresis Usually > 300 Variable (high if sodium diuresis)
Water diuresis: polydipsia diabetes insipidus Solute (osmoYc) diuresis: i.v. NaCl
hyperalimentaYon hyperglycemia high protein intake recovery from AKI
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Adapted from: Muser WP, Korzelius CA. Hosp Med Clin 2012; 1: e338-‐e352.
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Diagnosing polyuria
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Water restricYon test: 1. At 8.00 a.m.: a) Empty bladder, record the volume, and send urine osmolality b) Take a serum osmolality c) Record the paYent's weight. 2. Then for the next 8 hours check: Urine osmolality and weight every hour
Serum osmolality every 2 hours Stop the test if the paYent's weight decreases by more than 3% of body weight (or by 4kg) or the serum osmolality rises >300 mOsm/kg/H2O. 3. If the urine osmolality at 4 p.m. remains <600mOsm/kg proceed with the desmopressin test. a) Desmopressin (DDAVP) 20 μg intranasally or 2 µg intramuscularly b) Can eat and drink freely c) Hourly urine volumes and osmolality unYl 8.30 p.m.
Polydypsia Central DI Nephrogenic DI
Serum osmolality (mOsm/kg)
<295 >300 >300
Urine osmolality (mOsm/kg)
>600 (400-‐600 if chronic)
<300 ORen <200
<300
Post DDAVP urine osmolality (mOsm/kg)
No or mild response
>400-‐600 No response
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Acid-‐base disorders
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Kidney role in maintaining acid-‐base balance: -‐ resorbYon or excreYon HCO3
-‐
-‐ secreYon of H+
-‐ producYon of NH3 Most acid-‐base disorders can be diagnosed and treated without measurement of urine electrolytes. ExcepYons: 1. METABOLIC ALKALOSIS Urine Cl-‐ more useful than urine Na+ to asses volume status. HCO3
-‐ excreted in urine and followed by Na+. Urine Cl-‐ < 20 mmol/L suggests volume depleYon. 2. NON-‐ANION-‐GAP METABOLIC ACIDOSIS Urine electrolyte measurement in non-‐anion-‐gap metabolic acidosis to disYnguish between bicarbonate loss and impaired renal acid excreYon.
HCO3-‐
Na+
Metabolic alkalosis
?
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Urine anion-‐gap
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In steady state UAG is posiYve: with a mean 41 ± 9 mmol/L. NH4
+= 0.8 (Cl-‐-‐Na++K+) x Vu + 80 In severe diarrhea with metabolic acidosis urine NH3 will increase and be secreted with Cl-‐ à negaYve urine anion gap In type 4 and type 1 RTA NH3 excreYon is defecYve à posiYve urine anion gap
NH4+ NH4+
K+ K+
Na+ Na+
Cl-‐
Cl-‐
Other anions
Other anions
NegaYve anion gap
PosiYve anion gap
UAG = (urine Na+ + urine K+) -‐ (urine Cl-‐)
Diarrhea
RTA 4
NH3 + H+ à NH4+
éNH4+ à é Cl-‐
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Potassium disorders
• Daily K+ dietary load is 80-‐120 mmol, excreted mainly in the urine.
• The amount of excreted K+ arises from the tubular excreYon in the distal and collecYng tubule – effect of aldosterone.
• Daily K+ excreYon: 10 mmol -‐ 400 mmol.
• The most important indicaYon for determinaYon of urine K+ is differenYal diagnosis of hypokalemia.
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Hypokalemia, UK+ < 10 mmol/L Hypokalemia, UK+ > 30 mmol/L
Reduced potassium intake Renal potassium loss
Extrarenal potassium loss
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TRANSTUBULAR POTASSIUM GRADIENT
urine K+/serum K+ TTKG = urine osmolality/serum osmolality
High value: kidney is excreYng K+ Low values: conservaYon of K+ Urine must be isotonic or hypertonic to serum (300 mOsm/kg) Urine Na+ concentraYon must be >25 mmol/L
Potasium concentraYon in a urine spot is difficult to interpret without daily urine volume and urine concentraYon. • to assess kidneys tendency to reabsorb or excrete potassium • it is a surogate measure of aldosteron effect
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K+ K+
CollecYng duct
Distal capillary
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TTG in hypokalemia and hyperkalemia
Hypokalemia
Hyperkalemia
Transtubular potassium gradient
< 2
> 2
< 7
> 10
Cause gastrointesYnal loss
hyper-‐ aldosteronism
hypo-‐aldosteronism
Normal aldosterone effect
Example Diarrhea Conn syndrome ACEI, spironolactone
Potassium shiz, overload
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Adapted from: Muser WP, Korzelius CA. Hosp Med Clin 2012; 1: e338-‐e352.
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Magnesium excreYon
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• Mg++ concentraYon in serum does not provide accurate informaYon about the actual Mg++ content in the body.
• Renal Mg++ excreYon is suprisingly accurate at regulaYng the total Mg++ content.
• In Mg++ deficiency excreYon in the urine is reduced, therefore Mg++ excreYon can be used for diagnosing of Mg++ deficiency, even though Mg++ concentraYon is normal.
Hypomagnesemia, UMg++ < 0.5 mmol/L
Hypomagnesemia, UMg++ > 1.5 mmol/L
Extrarenal magnesium loss
Renal magnesium loss
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Conclusion
Urinary electrolytes and osmolality are useful tool in many clinical situaYons, and they have to be used more ozen, to show their full value.