- Central DI --congenital, LCH, germinoma, autoimmune hypophysitis - Congenital nephrogenic DI - Pregnancy induced DI - Hypercalcemia - Diuretic use - Glucocorticoid use - Diabetes mellitus - Primary polydipsia - HyperCa - HypoK - Fluid overload (ex post op) - Polyuric phase of renal failure or AKI/ATN - Cerebral salt wasting - UTI - Mannitol - Infiltrative renal diseases (e.g. histiocytosis) - Low sodium intake (diminished tonicity of renal medullary interstitium and NDI) - Decreased protein intake (diminished tonicity of renal medullary interstitium and NDI) - Sickle cell nephropathy - Lithium

Water Balance Flashcards by Tracey Dyer

what receptor does ADH bind in the kidneys
what kind of R
where

V2
GPCR
collecting ducts and distal tubule

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what are the ADH receptors and where are they

V1a - blood vessels: vasocronstriction

V2 - principle cells in renal collecting ducts: increased AQ2 on apical membrane

V3 (=V1b) - anterior pituitary: increases ACTH secretion

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Regulatory of ADH secretion

Osmolality&raquo_space;> Volume > Pressure
○ 1% increase in Osm = AVP release
○ 10-fold higher required for V/P
- Baroreceptors (carotid, aorta)
- atrial stretch receptors
- plasma tonicity
- Pain, nausea
○ Ex head injury

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what inhibits ADH release

GABA
Dynorphin
Somatostatin

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effect of lithium on ADH?

inhibits action of AQ2 going on cell membrane after ADH binding to R

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HyperCa effect on ADH?

inhibits action of AQ2 going on cell membrane after ADH binding to R

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Plasma osmolality - what is it and how to calc

Plasma Osmolality = Osmotically active molecules in plasma

2 x [Na+] + 2 x [K+] + Glucose

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SNS HypoNa

Seizures
Coma
Confusion/disorientation
Gait instability
Tremor
Asterixis
Myoclonus
Dysarthria
Muscle weakness
Cheyne-stokes respiration

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HypoNa -first labs to rule out

HyperBG
HyperTG
Hyperproteinemia

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HypoNa - volume status normal/high DDx

Urine Osm <200:
- Hypothyroidism
- GC def
- Nausea
- SIADH
- Carbamazepine, cyclophosphamide, vinblastine

Urine Osm >200:
- Psychogenic polydipsia
- Water intoxication

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HypoNa - hypovolemic DDx

Urine Na >30
- Diuretic
- MC def
- Kidney disease (CKD, polycystic kidney)
- CSW
- Na administration

Urine <30
- non renal loss w XS water intake
- hypovolemic dehydration
- CHF
- Nephrotic syndrome
- Cirrhosis
- PPV

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HypoNa - look at volume status and then what?

If hypovolemic -> look at urine SODIUM
– because it’s a water problem and that means you look at the Na

If eu-/hypervolemia -> look at urine OSM

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what deficiencies decrease water excretion

Hypothyroidism and adrenal insufficiency

when present may mask diabetes insipidus

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HyperNa - Ddx for hypovolemia

XS free water loss:
- Renal
– DI (C/N)
—osmotic diuresis w nonNa solute
— tubulopathy
- GI
—Diarrhea, emesis, stromal loss
- Derm
—burns
—sweating
- Premature neonates
- Pulmonary
—tachypnea
—mech vent
- AVP antagonist (captains)

Inadequate free water intake:
- inability to BF
- inadequate IVF in very sick kids
- neurologically impaired children w inability to communicate
- adipsia

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HyperNa - Ddx for N/hi volume status

Na overload (usually w impaired/immature renal fn)
- Infants concentrated formula
- Infusion hypertonic saline
- Salt poisoning (munchausen by proxy)

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Ddx polyuria

Central DI
–congenital, LCH, germinoma, autoimmune hypophysitis
Congenital nephrogenic DI
Pregnancy induced DI
Hypercalcemia
Diuretic use
Glucocorticoid use
Diabetes mellitus
Primary polydipsia
HyperCa
HypoK
Fluid overload (ex post op)
Polyuric phase of renal failure or AKI/ATN
Cerebral salt wasting
UTI
Mannitol
Infiltrative renal diseases (e.g. histiocytosis)
Low sodium intake (diminished tonicity of renal medullary interstitium and NDI)
Decreased protein intake (diminished tonicity of renal medullary interstitium and NDI)
Sickle cell nephropathy
Lithium

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what is nephrogenic SIADH
- what is it
- gene
- labs to differentiate from other SIADH

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extremely rare mutation of the V2 receptor producing chronic activation
AVP2R gene

would have low AVP/copeptin level

Meds causing SIADH

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Desmopressin
SSRI, TCA, MOA
Chemo (cisplatin, cyclophosphamide, vincristine, vinblastine)
Anti-epileptic (carbamazepine)
Ecstasy

Diagnostic Criteria

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Hyponatremia <134
Hypoosm <280
Euvolemia
High urine Na >40
inappropriate conc urine for hypoNa >100
Excluded AI
Excluded hypothyroid
Excluded diuretic use

Tx options for SIADH

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3% saline if sx’atic
fluid restrict
Loop diuretics (furosemide) - preferentially excrete free water over sodium or potassium
Sodium supplementation
Vaptans -> ADH-R antagonist

DI Criteria

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Pathlogic polyuria and polydipsia >2L/m2/day
AND
(EITHER Serum osm >300 and/or Na >145 with urine Osm <300
OR water dep w serum osm >300 and/or Na >145 with urine osm <600 and NOT rising despite plasma osm rising)

Causes of CDI

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surgery
trauma
cranio
germinoma
infiltration: LCH, sarcoid, mets
autoimmune
Idiopathic
Drugs: Ethanol; Phenytoin; Opiate antagonists; Halothane; Alpha-adrenergic agents
Congenital hypopituitarism
Familial
— AD mutation in ADH: magnocellular cell death by the accumulation of misfolded AVP precursors within the endoplasmic reticulum (“toxic gain of function”)
— AR mutation in ADH: early onset polyuria and hypernatremia
—Wolfram syndrome (DIDMOAD: CDI, DM, optic atrophy, and deafness) AR with incomplete penetrance

Causes of NDI

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Drugs
- Lithium
- Vaptans
- Orlistat
- Cisplatin
- tetracyclin Abx

Labs
- hyperCa
- HypoK

Sickle cell

Syndromes:
- Bartter
- Bardet Biedl

Genetics:
- AVPR2 mutation
- AQP2 mutation

Tests for DI

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Water dep
Hypertonic Saline infusion
Arginine copeptin stimulation test

Triple phase - phases and duration, onset

DI (12h-few days) onset day 1-2 - edema, cells "stunned" - sometimes skip this phase SIADH (up to 2 weeks)\ onset day 5-8 - ADH released as cells die SI (indefinite) onset variable, by day 14

how to test or DI in infants

○ No water deprivation ○ Administer DDAVP (1 µg SQ or IV over 20 min, max dose 0.4 µg/kg) ○ Measure urine osm at baseline and Q30min x2 hours ○ If urine osm doesn’t increase by >100 mosmol/kg over baseline, the diagnosis of nephrogenic DI is made and DNA should be obtained for mutation analysis

DI test: copeptin in water dep

- Ratio of stimulated copeptin (change in copeptin level over 8hrs during water dep) to plasma sodium (at the end of test) ≥0.02pmol/L = complete central DI <0.02pmol/L = partial central DI

DI test: Plasma copeptin stimulated by hypertonic saline infusion

≤4.9 pmol/L = complete or partial central DI >4.9 pmol/L = primary polydipsia

Advantages of using copeptin

- smaller sample volume - copeptin assay does not require extraction step or other pre-analytical procedure - copeptin is stable in plasma/serum ex vivo, handling is less complicated

how does hypertonic saline test work

administration of hypertonic saline to increase serum osmolality above 300 mOsm/kg, with subsequent measurement of serum vasopressin levels -> should see it rise

Copeptin helps differentiate what, how?

CDI:copeptin levels are low primary polydipsia: intermediate NDI: elevated

CDI tx

thirst intact - DDAVP, titrate to effect thirst not intact - DDAVP - fluid restrict to 1L/m2/d

Other than DDAVP, options to tx CDI

- High free water intake - Low solute diet - Thiazide diuretic - Chlorpropamide - Carbamazepine - NSAID

Excess extracellular volume (edema, ascites) + urine w: - low Na - high Na

- low Na: hyperaldo - high Na: SIADH

what is the post pit

not a gland but only the distal axon terminals of the hypothalamic magnocellular neurons that make up the neurohypophysis

what hormone problems decreased water excretion

Hypothyroidism and adrenal insufficiency when present may mask diabetes insipidus

Atrial Natriuretic Peptide - what does it do - where is it releases - stimuli

Inhibits Aldosterone Secretion Atria increased volume, increased Na, neurologic inputs

where are the V2 receptors

collecting duct of kidneys

what will you see with DDAVP in water dec test with nephrogenic DI vs central DI

i. Nephrotic DI – urine osm <300 mOsm/kg and does not increase by >50% after DDAVP ii. Complete central DI – urine osm increase by >50% after DDAVP

2 meds to tx NDI

HCTZ - causes natriuresis which produces some contraction of extracellular fluid volume, decrease GFR, decreased delivery of fluid to the collecting duct, and a decreased urine volume ii. Indomethacin - has antidiuretic action that especially prolongs the action of vasopressin and administered DDAVP, it also decrease urine volume

Water Balance Flashcards

(40 cards)