Nephrology JC070: Electrolyte And Acid-base Disorders

Question 1

Physiology of Kidney

Answer 1

Proximal tubule:
- Reabsorb ***NaCl, Glucose, a.a., fluids, HCO3
- Secrete drugs, poisons, H

LoH:
- Concentration gradient created for subsequent H2O reabsorption
- Thin Descending limb permeable to H2O only —> **H2O leave into interstitium by osmosis
- Thick Ascending limb permeable to NaCl only —> actively **pump Na out —> create salty interstitium —> draw H2O from Descending limb + Collecting duct

Distal tubule:
- Fine tuning of electrolyte + acid-base
- some NaCl reabsorption
- ***K, H excretion

Collecting duct:
- **NaCl, **Urea, H2O reabsorption by concentration gradient created by LoH

Question 2

Common acid-base + electrolyte problems

Answer 2

記: pH, Na, K

1. Acidosis
   - Metabolic
   - Respiratory
2. Alkalosis
   - Metabolic
   - Respiratory
3. Na
   - Hypo
   - Hyper
4. K
   - Hypo
   - Hyper

Question 3

Definition of Acid-base disorders

Answer 3

Acidaemia: [H] > normal
Alkalaemia: [H] < normal

Acidosis: a process leading to ↑ in plasma [H]
Alkalosis: a process leading to ↓ in plasma [H]

Normal pH: **7.4 (7.35-7.45) ([H]: **40 nmol/L)
- lethal: pH <7.1 / >7.7

Compensation mechanisms:
- Lungs: **immediate
- Kidneys: take **several days

When well compensated:
- no acidaemia / alkalaemia despite an underlying acidosis / alkalosis process

Question 4

Compensatory mechanisms

Answer 4

Primary metabolic acidosis (↓ HCO3):
- stimulate respiratory centre —> ↓ pCO2 —> compensatory respiratory alkalosis

Primary metabolic alkalosis (↑ HCO3):
- suppress respiratory centre —> ↑ pCO2 —> compensatory respiratory acidosis

Primary respiratory acidosis (↑ pCO2):
- kidney compensate by conserving HCO3 —> ↑ HCO3 —> compensatory metabolic alkalosis

Primary respiratory alkalosis (↓ pCO2):
- kidney compensate by excreting HCO3 —> ↓ HCO3 —> compensatory metabolic acidosis

Question 5

Metabolic acidosis

Answer 5

↓ HCO3 (***<22)
- normal [HCO3]: 22-28 mmol/L
- compensated with hyperventilation —> ↓ pCO2

Diagnosis:
1. Ensure this is Metabolic acidosis

2. Determine Serum **Anion Gap (AG): high / normal
   - Anion gap = **Na - Cl - HCO3
3. Normal Serum AG acidosis
   - determine Urine AG: [Urine Na + Urine K - Urine Cl] (advanced)
   - NaHCO3 infusion / Acid loading test: Proximal / Distal RTA (advanced)
4. Look for any **Osmolar Gap (OG): Measured osmol - Calculated osmol
   - detect **unmeasured osmotically active substances (e.g. toxic alcohols)
5. Any mixed acid/base disorder (ΔAG vs ΔHCO3)?
   - too advanced for MBBS

Question 6

Osmolar gap

Answer 6

Osmol gap = Measured osmol - Calculated osmol

***Calculated osmol: 2xNa + Urea + Glucose (cation = anion, other cations ~ bounded Na)

↑ Osmol gap: presence of unmeasured ***osmotically active substances (e.g. alcohol-related compounds ingestion)

Question 7

Anion Gap

Answer 7

Universal law: Charges must be balanced
- Total plasma cations = anions

Plasma cations: Na, K, Ca, Mg
- only Na is present in significant + may have great variations

Measured anions: Cl, HCO3

Measured cations - Measured anion = **Unmeasured anion (i.e. AG)
- Anion gap = **Na - Cl - HCO3
- Normal anion gap: ~8-14

High AG acidosis vs Normal AG acidosis:
- similar Na levels
- both have ↓ HCO3
- **↑ Cl in normal AG acidosis
- **↑ unmeasured anions in high AG acidosis

Question 8

***High AG acidosis

Answer 8

↑ AG: ↑ unmeasured anion in blood

Causes:
1. **Ketoacidosis: DKA, Alcoholic ketoacidosis
2. **Lactic acidosis
3. ***Renal failure (SO4, PO4, hippurate, others)
4. Ingestion of salicylate, formic acid (methanol), glycosylate (ethylene glycol)
5. Rhabdomyolysis (release of organic acids)
6. Altered AG in paraproteinaemia (e.g. ↓ in IgG gammopathy, ↑ in IgA gammopathy)

Question 9

***Normal AG acidosis

Answer 9

↑ [Cl]

Causes:
1. Loss of HCO3, with **compensatory ↑ Cl (via **Anion exchanger Cl/HCO3)
- GI loss: **Diarrhoea
- Renal loss: **Proximal RTA (Type 2: Fail to reabsorb HCO3), ***Carbonic anhydrase inhibitor

2. Failure to excrete H
   - **Distal RTA (Type 1: Fail to excrete H, reabsorb K —> hypoK acidosis)
   - **Type 4 RTA
3. Ingestion of excessive Cl
   - ***NH4Cl
4. Increased reabsorption of Cl
   - Ureterosigmoidostomy

Question 10

***L-Lactic acidosis

Answer 10

Overproduction of L-lactate —> ∵ **O2 deficiency (type A)
1. **Circulatory problems (e.g. hypotension, shock)
2. **Respiratory problem —> hypoxia
3. **Hb problem (e.g. CO poisoning)
4. ↑ Metabolic demand (e.g. grand mal seizure, severe exercise)

—> Rate of production can be up to 72 mmol/min with total hypoxia in type A (hypoxia)

Reduced metabolism of L-lactate **without hypoxaemia (type B)
1. **Liver problem
2. **Alcoholism
3. Thiamine deficiency
4. **Phenformin, Metformin

Diagnosis:
1. ***High AG metabolic acidosis
2. High plasma lactate level (normal <2)

Treatment:
1. Improve O2 delivery to tissue (most effective)
- correct hypotension, hypoxaemia

2. NaHCO3 therapy ineffective unless lactate production controlled
   - buy time for life saving
   - Na load limits its massive use
3. Haemodialysis with ***HCO3 dialysis

Question 11

***General management of Metabolic acidosis

Answer 11

1. Determine cause of acidosis + treat underlying cause:
   - some causes have independent threat to life e.g. methanol poisoning
   - there maybe specific treatment for certain causes e.g. methanol poisoning
2. Correction of HCO3 by NaHCO3

Risk of NaHCO3 therapy
1. ***HypoK induction
—> shifting K into cells, esp. in patients with existing HypoK / loss of K with contracted ECF resulting normokalaemia (e.g. DKA)

2. **Hypocalcaemia
   - esp. in CRF patients —> **tetany, seizure
3. Volume expansion form ***Na load
   - 200 mmol NaHCO3 given —> 200 mmol Na given —> >1L of normal saline (156)
4. ***Paradoxical cerebral acidosis
   - Too rapid correction —> too much HCO3 —> push equilibrium to make more CO2 —> diffuse into CSF from plasma (while HCO3 cannot diffuse through BBB) —> accumulation of CO2 in CSF —> ↑ H —> cerebral acidosis

Question 12

How to use Urgent IV NaHCO3 replacement appropriately

Answer 12

1. Estimation of HCO3 needed
   - HCO3 deficit = HCO3 deficit in litre x HCO3 space (= BW x 0.6)
   - usually only ***half the amount is given (BW x 0.3)
2. Give half of dose initially, recheck afterwards
3. Only replace [HCO3] to safe level acutely (pH ~7.1), then followed by slower correction / correction by other means
4. Beware of ***fluid overload esp. in oliguric patients

Question 13

Renal Tubular Acidosis

Answer 13

Normal AG acidosis with:
1. Hypo K
- Proximal RTA (type 2: ∵ loss of HCO3 (∵ ineffective reabsorption in proximal tubule))
- Distal RTA (type 1: ∵ failure of H excretion)
- Mixed (type 3)

2. Hyper K
   - Type 4 RTA (aldosterone deficiency)

Question 14

Proximal RTA (Type 2)

Answer 14

Normally HCO3 ***totally reabsorbed in proximal tubule if concentration below reabsorption threshold (~25 mmol/L)

Pathogenesis:
↓ HCO3 reabsorption threshold in proximal tubules
—> loss of HCO3 in urine —> low plasma HCO3
—> **normal AG metabolic acidosis with **compensatory HyperCl
- **alkaline urine despite acidosis, **urine pH usually >6

Effect:
1. **Loss of Na coupling with loss of HCO3
—> Hypovolaemia
—> **Hyperaldosteronism
—> ***HypoK

2. Associated with Hyperphosphaturia, Hypercitraturia (preventing nephrocalcinosis / stones), Hyperuricuria
3. Hyperphosphaturia
   —> Rickets, Osteomalacia
4. Fanconi syndrome
   - a pan-dysfunction of proximal tubules with **amino-aciduria, **glycosuria on top of RTA, hyperphosphataemia

Summary (↓ HCO3 reabsorption):
- Alkaline urine
- Na: ↓
- K: ↓ (hyperaldosteronism)
- HCO3: ↓
- Hyperphosphaturia —> Rickets, Osteomalacia
- Hypercitraturia
- Hyperuricuria
- Amino-aciduria, Glycosuria (Fanconi syndrome)

Question 15

Distal RTA (Type 1)

Answer 15

Pathogenesis:
***Due to inability to excrete H:
1. Failure of pumping H against concentration gradient
- H/ATPase pump defect

2. H back leak
   - ↑ H permeability

Effect:
1. ***Urine pH always >6 ∵ failure to maintain a steep plasma-urine H gradient

2. ↓ H excretion
   —> ↑ K excretion for exchange of Na reabsorption in distal tubule
   —> ***HypoK
3. Acidosis
   —> ↑ Ca reabsorption from bone + ↓ Tubular Ca, PO4 reabsorption
   —> Hypercalciuria, Nephrocalcinosis / stones

Summary (Inability to excrete H):
- Alkaline urine
- K: ↓ (↑ K excretion for exchange of Na reabsorption)
- Hypercalciuria, Nephrocalcinosis / stones

Question 16

***Causes of Proximal + Distal RTA

Answer 16

Proximal RTA (type 2: HCO3 loss)
Hereditary
1. Cystinosis
2. Galactossaemia
3. ***Wilson’s disease
4. Lowe’s syndrome

Acquired
1. Dysparaproteinaemia
2. Toxins: Heavy metal poisoning
3. Drugs: **Carbonic anhydrase inhibitors
4. Renal disease: **Amyloidosis, renal transplant rejection, Sjögren’s syndrome
5. HyperPTH, HyperCa

Distal RTA (type 1: Inability to excrete H)
Hereditary
1. **Primary hypercalciuria
2. Marfan syndrome
3. **Ehlers-Danlos syndrome

Acquired
1. Autoimmune disease: **Sjogren’s, RA, SLE, PBC
2. Drugs: Amphotericin B, Lithium, Analgesic nephropathy
3. Renal disease: **CRF, urinary tract obstruction, interstitial nephritis, medullary sponge disease
4. **Paraproteinaemia, hypergammaglobulinaemia
5. **HyperPTH, hyperVit D

Question 17

Diagnosis of RTA

Answer 17

Clinical suspicion when:
1. Normal AG acidosis with **HypoK
- hint: ↑ Cl with normal Na
2. Urine pH >5.5 (*Alkaline urine) in presence of acidaemia

Confirmatory tests:
1. **Fractional excretion of HCO3 (FE HCO3): Proximal RTA
2. **Acid loading test (NH4Cl): Distal RTA

Question 18

Fractional excretion of HCO3

Answer 18

Test whether there is excessive HCO3 loss in urine

FE HCO3 = (Urine [HCO3] / Plasma [HCO3]) ÷ (Urine [Cr] / Plasma [Cr])

Proximal RTA: **>15% (i.e. HCO3 loss)
- sensitivity ↑ after **NaHCO3 infusion at 0.5-1.0 mmol/kg/hour to bring up plasma HCO3 level, urine pH >7.5

Distal RTA: normal (i.e. <5%)

Question 19

Acid loading test (NH4Cl)

Answer 19

Test whether urine can be acidified: i.e. whether a steep H gradient across plasma and urine can be maintained

***Oral NH4Cl 0.1g/kg to bring acidosis

Normal: urine pH <5.5
***Distal RTA: urine pH remains >6.0 (i.e. Inability to excrete H)
Proximal RTA: variable

Question 20

Type 4 RTA

Answer 20

Characterised by:
- Normal AG metabolic acidosis + ***HyperK (vs other RTA: HypoK)

Pathogenesis:
- ***Aldosterone deficiency / resistance

Aldosterone promotes distal K + H secretion, Na reabsorption
- Retention of K —> HyperK
- ↓ H excretion —> Acidosis (usually mild)
- Urine pH variable

Causes:
1. Drugs
- **ACEI, ARB
- **K sparing diuretics (spironolactone, amiloride, triamterene)
- Cyclosporin A, Tacrolimus

2. ***Hyporeninism
   - DM nephropathy
3. ***Renal failure
4. ***Mineralocorticoid deficiency
5. Kidney transplant rejection - tubulitis

Question 21

Management of RTA

Answer 21

Type 1 and 2 RTA:
1. **Oral NaHCO3 to correct acidosis
- **very high dose is required in proximal RTA ∵ loss of HCO3 in urine
- **K citrate is a better alternative for Distal RTA (citrate —> HCO3 by liver)
2. **K supplement for HypoK
3. ***Steroid for Distal RTA due to Sjogren

Type 4 RTA:
1. Stop / ↓ inciting drugs
2. ***Loop diuretics + Low K diet for HyperK

Question 22

Metabolic alkalosis

Answer 22

Causes:
1. Loss of H
- GI loss: **vomiting, nasogastric drainage
- Renal loss
—> **Diuretics (Loop, Thiazide), **HypoK
—> **Mineralocorticoid excess: primary / secondary
—> Bartter’s / Gitelman’s syndrome

2. Retention of HCO3
   - Intake of NaHCO3
   - Milk-alkali syndrome

Treatment:
1. If ECF contracted, **expand with saline —> HCO3 will ↓ with expansion
2. Correct HypoK
3. If ECF expanded, correct alkalosis with **IV HCl / ***oral NH4Cl

Question 23

Na homeostasis

Answer 23

[Na] does **NOT reflect absolute content of Na in body but **amount of solvent: H2O
- primarily an ***extra-cellular cation

In the absence of Na loss / retention:
- HypoNa —> H2O retention
- HyperNa —> H2O depletion

Situation will be complicated when concomitant Na loss / retention

Na in kidney:
- ***67% reabsorbed in PCT
- 25% reabsorbed in Ascending LoH
- 5% reabsorbed in DCT
- 3% reabsorbed in Collecting duct

Question 24

Pseudohyponatraemia

Answer 24

↓ Serum [Na] but normal osmolality
- ∵ occupation of large amount of non-water (e.g. Fat, Paraprotein) in plasma
—> ↑ plasma volume while actual plasma water Na is normal
—> [Na] appears to be low

Causes:
1. **Hyperglycaemia
2. **↑↑ TG
3. ***Paraproteinaemia
4. ↑↑ WCC

Clue:
- Check serum osmolality —> normal

Confirmation:
- Check plasma water [Na]

Question 25

***Approach to HypoNa

Answer 25

睇3樣野: Serum osmolarity (判定係咪True HypoNa)
—> Volume status + Urine Na (3x2表)

1. ***Serum Osmolarity
   - low —> true HypoNa
2. ***Volume status
3. Urine osmolarity (>100 = ADH is working, appropriate?)
4. ***Urine Na level (>20 = inappropriate i.e. SIADH)

HypoNa
—> Serum osmolarity (+ RFT, TFT, cortisol, Urine osmolarity, Urine Na)
—> ↓ Serum osmolarity —> True hyponatraemia
—> Volume status

1. Hypovolaemia (***Na depletion)
   —> ↓ Na intake
   —> Renal (Urine Na ↑)
   —> Extra-renal loss (Urine Na ↓)
2. Hypervolaemia (Dilutional)
   —> Urine Na ↓ + Urine osmolarity ↑ —> CHF, cirrhosis, nephrotic syndrome
   —> Urine osmolarity ↓ —> Primary polydipsia
3. Euvolaemia
   —> SIADH

Question 26

Causes of SIADH

Answer 26

CL Lai: 記any CNS + respiratory diseases

1. CNS
   - **Meningitis, Encephalitis, Brain abscess
   - **Head trauma, SAH, CVA, ↑ ICP
2. Respiratory
   - **CA lung
   - **Chest infection
   - Positive pressure breathing
3. Drugs
   - ***SSRI
   - Ecstasy
4. ***Hypothyroidism

Question 27

SIADH vs Addison’s disease

Answer 27

SIADH:
- Everything is low
- Low K

Addison’s disease:
- Normal / High K
- High eosinophil count (∵ cortisol promote eosinophil migration into BM)

Question 28

Treatment of SIADH (CL Lai)

Answer 28

1. Fluid restriction
2. Furosemide 20mg
3. Vaptan
4. IV Na (beware of central pontine myelinolysis)

Question 29

HypoNa

Answer 29

S/S:
- **Non-specific (e.g. malaise, lethargy, headache)
- **Confusion, convulsion, coma
- More serious with acute hypoNa

Acute:
- <48 hours
- more serious symptoms, severe symptoms at [Na] <120
- less complications if corrected rapidly

Chronic:
- >72 hours
- symptoms may not develop even [Na] <110
- ***more prone to CNS complications with rapid correction

Management:
- Rate of correction should be **slow for chronic hypoNa (>2 days) —> <0.5 mmol/L/hr or <12 mmol/L/day
- Too rapid correction —> **Central pontine myelinolysis
- Treat according to ECF volume status —> estimate amount of H2O + Na needed
- **Hypertonic saline should only be used in very experienced hands!
- **Demeclocycline / ***V2 antagonist can be considered in SIADH

Clinical features of Central pontine myelinolysis (CL Lai):
- Cranial nerve deficits
- Quadriparesis

Question 30

H2O + Na replacement in contracted ECF

Answer 30

1. Assess degree of volume depletion / excess
   - mildly dehydrated: loss of skin turgor: 5% BW loss
   - moderate: postural hypotension: 10% BW loss
   - severe: shock: 15% loss
   - mild edema: 5% in excess
2. ***Replace volume depletion with normal saline cautiously
   - initial 1/3 can be given in first 8 hours, reduce speed afterwards
   - monitor [Na] regularly

Question 31

Approach to HyperNa

Answer 31

睇3樣野: Volume status
—> Serum osmolarity, Urine osmolarity (Ratio)

Serum osmolarity, Urine osmolarity, RFT, CaPO4, Plasma renin + aldosterone, 9am cortisol

1. Hypervolaemia (Salt gain)
   —> **Primary hyperaldosteronism / **Cushing’s syndrome / ***Acute salt loading
2. Isovolaemia / Hypovolaemia
   - Urine osmolarity&raquo_space; Serum osmolarity (Serum osmolarity太低有問題)
   —> ***Extrarenal fluid loss (most common)

• Urine osmolarity < Serum osmolarity (Urine osmolarity太低)
  —> Water deprivation test / DDAVP test
  —> No change in urine osmo —> **Nephrogenic DI
  —> ↑ urine osmo —> **Cranial DI

Question 32

Management of HyperNa

Answer 32

In pure H2O loss —> calculate H2O deficit
- Water deficit = TBW x ([Na]/140 - 1)

Rate of volume replacement
- 1/3 rule:
—> 1/3 in first 8 hours
—> 1/3 in second 16 hours
—> 1/3 in third 24 hours
- Rmb to replace any ongoing H2O loss

Rate of [Na] correction
- too rapid will lead to ***cerebral edema ∵ rapidly reduced plasma osmolality —> influx of H2O into cells
- maximal ↓ of 12 mmol / 24 hours unless seriously symptomatic

Question 33

K homeostasis

Answer 33

**Intracellular cation (diffuse slowly outwards, Na-K ATPase pumps K into cells)
- Normal serum K 3.5-5 (intracellular: 150)
- Highly influenced by **acid-base status (acidosis —> K moves ***out of cells, vice versa)
- Severe HypoK + HyperK are life-threatening electrolyte disturbances —> Cardiac arrhythmia

Question 34

Approach to HypoK

Answer 34

Rule out intracellular K shift:
- **Insulin
- **Catecholamine
- **β2 agonist
- **Metabolic alkalosis
- ***Hypokalaemic periodic paralysis

HCO3 ↑ (**Metabolic alkalosis)
- TTKG <3 (trans-tubular potassium gradient) (i.e. Extra-renal loss)
—> **Vomiting

• TTKG >=3 (i.e. Renal loss)
  —> Normal BP
  —> **Diuretics, **Bartter’s syndrome, ***Gitelman’s syndrome
• TTKG >=3 (i.e. Renal loss)
  —> ↑ BP
  —> **Renal artery stenosis, **Primary aldosteronism, ***Cushing’s syndrome, Liddle’s syndrome

HCO3 ↓ (**Metabolic acidosis)
—> Normal AG
—> Urine AG -ve —> **Diarrhoea, **Proximal RTA
—> Urine AG +ve —> **Distal RTA

Question 35

TTKG

Answer 35

Transtubular K gradient:
- Attempt to over-ride interference from urinary concentration to determine urinary K loss

TTKG:
- Tubular [K] / Serum [K]
or
- (Urine [K] / Serum [K]) ÷ (Urine osmo / Serum osmo)
(∵ Tubular [K] = Urine [K] x Serum osmo / Urine osmo)

In presence of HypoK, TTKG >4:
- high [K] in terminal cortical collecting duct (i.e. ***renal loss)

Question 36

HypoK

Answer 36

Risk / Complications / Symptoms
1. **Muscle weakness, paralysis (proximal muscle myopathy)
2. **Cardiac arrhythmia, particularly when [K] <2.0
3. ECG changes (記)
- Large U wave
- **Loss of T wave
- **Prolonged QT interval
4. ***Ileus, constipation
5. Rhabdomyolysis
6. Polyuria

Management:
1. Oral replacement when mild

2. **IV KCl
   - oral not possible e.g. vomiting
   - moderate to severe hypoK (e.g. <=2.5)
   - **always rmb to dilute IV KCl in NS
3. Exact amount of K needed cannot be calculated ∵
   - largely intracellular
   - discrepancy between ICF and ECF [K]
   - initial distribution in ECF only - 40 mmol K will ↑ [K] 1.5 mmol/L

Question 37

Approach to HyperK

Answer 37

Exclude **PseudohyperK (e.g. **haemolysis) + **Drugs (e.g. K supplement, NSAID, **ACEI, ARB, **K-sparing diuretics, salt substitute)
1. **Renal failure
2. ***Hypoaldosteronism
3. Shift from cells

Question 38

HyperK

Answer 38

S/S
1. **Muscle weakness (usually when >8)
2. **Cardiac arrhythmia
- may occur when >6
- rate of ↑ of K important —> more tolerable with chronic HyperK
- ECG changes (記)
—> **Peak T
—> **Widening of QRS
—> ***Loss of P
(—> prolonged PR intervals, sinusoidal)

Question 39

Diagnosis of HyperK

Answer 39

1. History
   - Diet
   - ***Drug history
2. Repeat [K] if no apparent cause found (pseudohyperK? ***Haemolysis)
3. P/E: volume depleted?
4. ***Renal function test
5. TTKG <6 indicates inappropriate renal response to hyperK

Question 40

Management of HyperK

Answer 40

Emergency? (Arrhythmia, ECG changes)
記: Resonium, IV insulin, NaHCO3, Loop diuretic

1. ***IV Calcium
   - effect within several mins
   - stabilise cardiac membrane —> protects heart (↑ threshold potential) but not ↓ [K]
   - may repeat injection 5 mins later if effect not seen
2. ***NaHCO3 infusion
   - shift K into cells
   - effect within 30 mins, last for several hours
3. ***IV insulin / dextrose
   - 10 units to 30g glucose (60ml D50) —> shift K into cells (self notes: Insulin stimulate Na/K-ATPase)
   - effect within 1 hour, but effect may last for only 5-6 hours
4. Urgent haemodialysis
   - most effective in removing K
   - but takes time to to set up

Non-emergency:
1. **Cation-exchange resin - Na/Ca resin
- oral / enema
- e.g. **Resonium
2. **Loop diuretics if not oliguric
3. Remove underlying cause
- remove drugs
- volume expansion for depletion
4. **Correct metabolic acidosis (by NaHCO3)
5. Dialysis (for end stage renal disease / chronic renal failure, HD / PD)
6. Low K diet

(Resonium (web):
- Insoluble polymer cation-exchange resin
- Exchange with H in stomach —> H exchange with K from intestinal cells
1. Resonium A (Na)
- exchange H with Na
2. Resonium C (Ca)
- exchange K with Ca)

Question 41

Bartter syndrome, Gitelman’s syndrome (Self notes)

Answer 41

Bartter syndrome: Defective NKCC (~Loop diuretic)
Gitelman’s syndrome: Defective NCCT (~Thiazide)