Potassium Acid-Base disorder

Kanin Thammavaranucupt, M.D. Nephrology division, Maharat Nakhonratchasima Hospital

Potassium Hypokalemia

Hyperkalemia

Alkalosis

Acidosis Wide-gap

Normal-gap

Topic

Potassium transport along

nephron

ENaC

ROMK Ald

Hypokalemia

Shift Loss Poor intake (less likely)

Renal Non-renal Adrenergic

surge

Nonadrenergic surge

Shift Adrenergic surge ?

Yes No

Sepsis Sympathetic

Pheochromocytoma Beta-agonist Theophilline

Amphetamine, Caffeine, Cocaine

Thyrotoxicosis PP

Congenital [Hypokalemic PP, Andersen]

Alkalosis Anabolism

[Insulin/TPN/active leukemia]

Hypothermia Drugs: paracetamol,

chloroquine

Hypokalemia

Shift Loss Poor intake (less likely)

Renal Non-renal Adrenergic

surge

Nonadrenergic surge

Diarrhea Sweat/Exercise

Cl--losing diarrhea Laxative abuse

Remote vomiting Remote diuretic

Spot urine K > 15 24hr-urine K > 20

UK/UCr > 1.5 FEK > 5 TTKG > 2

GS/Thiazide

BS/Lasix

Alkalosis ?

Hypokalemia

Shift Loss Poor intake (less likely)

Renal Urine K >20 ?

TTKG > 4 ?

Normal BP ?

Y

Y

Y

Urine Cl >15 ?

Y

diarrhea, sweating, laxative abuse remote vomiting/ diuretic

TTKG < 3: Polyuria

1°’/2° Hyperaldosteronism Cushing AME CAH Liddle Licorice

Acidosis : DKA, AKA, RTA Variable : Hippurate,Penicillin

Adrenergic surge

Nonadrenergic surge

Recent vomiting

UCa/Ucr (molar ratio)

< 0.15 > 0.20

N

N

N

N

N HypoMg

Y

A 35-year-old man was admitted due to proximal muscle weakness accompanying palpitation and weight loss. Physical examination revealed proximal muscle weakness grade 2/5 with hyporeflexia. His electrolyte were

Sodium 138 mEq/L Potassium 2.0 mEq/L

Chloride 102 mEq/L Bicarbonate 24.0 mEq/L

Urine Na 30, K 6.0 mEq/L

Which of the following mechanism would explain this electrolyte abnormality?

A. Renal potassium loss

B. Non renal potassium loss

C. Intracellular shift

D. Low potassium intake

E. Abnormal sodium/potassium ATPase pump

Autosomal dominant

Type1 : CACNA1S (60%)– Ca channel

Prevent: Acetazolamide

Type2 : SCN4A (20%) – Na channel

Prevent: Spironolactone

Andersen’s syndrome: KCNJ2 (Kir2.1)

Precipitated by rest after exercise and/or CHO-rich meal

Treat: KCl 60-120 mEq

HypoK periodic paralysis

Thyrotoxicosis periodic paralysis

Grave’s dz or Subclinical

Increased UCa, HypoPO4/Mg

Prevent: Keep euthyroid state

Propanolol 40-120 mg/day

RAIU or Sx for prevent relapse

Treat:

KCl (1st line)

Propanolol 1 mg IV q 10 min x 3

Metabolic Alkalosis

GFR

ECF

UCl

UK

HCO3 gain Milk-alkali/Ca-alkali, CaCO3

Blood transfusion (Citrate) Ringer lactate (Lactate) Acetate solution Anion exchange resin Dialysis

Low

Low

< 20

High

> 15

Metabolic Alkalosis

GFR

ECF

UCl

UK

Aldosteronism Increase

Low

< 20

High

> 15

Metabolic Alkalosis

GFR

ECF

UCl

UK

Low

> 15

< 20

High

Post hypercapnia Contraction alkalosis Remote diuretic Cl-losing diarrhea Vomiting/NG drainage

< 15

Urine Na > 20 Recent vomiting (UpH >7) Non-absorbable anion (UpH <6.5)

Urine Na < 20: Remote vomiting (UpH < 6.0)

Villous adenoma Congen.Chloridorrhea

Metabolic Alkalosis

GFR

ECF

UCl

UK

Low

> 15

< 20

High

BS/Furosemide (recent) GS/Thiazide (recent)

HypoMg Refeeding

Tubulopathy (Alc, autoimmune) > 20

Metabolic Alkalosis

GFR

ECF

UCl

UK

Low

< 20

High

Chronic diarrhea, Laxative abuse, severe hypoK

> 15

Urine Na Urine K Urine Cl

Diarrhea/ Laxative abuse

Acetazolamide

Diuretic Recent

Remote

Bartter’s syndrome

Gitelman’s syndrome

Vomiting Recent

Remote

Non-absorbable anion

Posthypercapnia

Metabolic acidosis/alkalosis

A 16-year-old female presented with nausea, vomiting, and

diarrhea. Laboratory studies reveal the following: Na 135, K 2.0,

Cl 97, HCO3 28 mEq/L, pH 7.44, PCO2 48, glucose 140 mg/dL.

Urine electrolytes: Na 50, K 50, Cl 40 mEq/L. Urinalysis showed

trace ketone.

Which ONE of the following is the most likely cause of

hypokalemia? A. Vomiting

B. Diarrhea

C. Diuretic abuse

D. Diabetic ketoacidosis

E. Hypokalemic periodic paralysis

Urine Cl > 15 Bartter syndrome Gitelman syndrome Diuretic (recent) HypoK < 2 mEq/L HypoMg Laxative abuse

A 17-year-old man has a recent history of fatigue and weakness.

with mild ECF volume contraction. Laboratory investigations He has no history of current diuretics use and he is normotensive shows arterial pH of 7.48 with PaCO2 44 mmHg, Na 138, K 2.9, Cl 92, HCO3 30 mEq/L, and Mg 1.0 mg/dl. Urine electrolytes show Na 25, K 60, and Cl 85 mEq/L. Urine calcium is 50 100 – 300). What is the MOST likely cause?

A. Poor intake B. Furosemide C. Malabsorption syndrome D. Gitelman’s syndrome E. Bartter ’s syndrome

mg/day (normal

Urine Cl > 15 Bartter syndrome Gitelman syndrome Diuretic (recent) HypoK < 2 mEq/L HypoMg Laxative abuse

Bartter VS Gitelman syndrome

A 30-year-old man come to ER due to weakness after wake up.

He had heavy alcohol drinking before sleep. PE: BP 130/80

mmHg, HR 80/min, no exophthalmos, no tremor Heart, Lung:

clear. Neuro exam: proximal muscle weakness gr II all

extremities. LAB: BUN/Cr 10/0.9 mg/dL Na 140, K 2.0, Cl 110,

CO2 30 mEq/L, Spot urine K = 30, Na = 45, Cl = 40 mEq/L, Cr = 1.3

mg/dL. UA: pH 6.0, RBC 0, WBC 0, Pro: neg. Film KUB: no stone

or nephrocalcinosis.

What’s the most likely diagnosis?

A. Hypomagnesemia

B. Laxative abuse

C. Recent vomiting

D. Post-hypercapnic state

E. Thyrotoxicosis periodic paralysis

Urine Cl > 15 Bartter syndrome Gitelman syndrome Diuretic (recent) HypoK < 2 mEq/L HypoMg Laxative abuse

An 18-year-old actress presents with fatigue for 2 weeks. Physical examination shows a BP of 120/80mmHg, grade III of proximal muscle weakness of all extremities. Others are unremarkable.

LAB: Na 138, K 2.2, Cl 90, CO2 30 mEq/L

Urine electrolyte: Urine Na 25, K 20, Cl 3 mEq/L

The most likely diagnosis is? A. Bartter’s syndrome

B. Gitelman’s syndrome

C. Surreptitious (self-induced) vomiting

D. Recent diuretic abuse

E. Hypokalemic periodic paralysis

Urine Cl < 15 Contraction alkalosis Cl-losing diarrhea Post hypercapnia Remote diuretic Vomiting Non-absorbable anion

A 16-year-old female presented with fatigue. BP

90/60 mmHg, PR 110 bpm, dry lip, JVP 0-1 cm.

Laboratory studies: Na 135, K 3.0, Cl 90, HCO3 34

mEq/L, BUN/Cr 30/1 mg/dL, pH 7.44, PCO2 48,

glucose 90 mg/dL. Urine electrolytes: Na 30, K 35, Cl

10 mEq/L. UA: pH 7.4, Sp gr 1.020, No WBC/RBC

Which one of the following is the most likely cause of

hypokalemia? A. Laxative abuse

B. Active vomiting

C. Bartter’s syndrome

D. Gitelman’s syndrome

E. Non-absorbable anion

Urine Cl < 15 Contraction alkalosis Cl-losing diarrhea Post hypercapnia Remote diuretic Vomiting Non-absorbable anion UpH < 6.5

UpH > 7

Potassium

Hypokalemia

Alkalosis

Acidosis

Wide-gap

Normal-gap

Topic

A 60-year-old man presented with unconsciousness

for 1 hour. Physical examination revealed an alcohol

smell breath odor upon breathing. Lab revealed Na

135, K 4.1, Cl 102, CO2 12 mEq/L, negative serum

ketone, glucose 394 mg/dL, BUN/Cr 23/4 mg/dL,

and measured plasma osmolality 344 mOsm/L.

What is the most likely diagnosis?

A. Salicylate poisoning

B. Alcoholic ketoacidosis

C. Methanol poisoning

D. Diabetic ketoacidosis

E. Ethanol overdose

AG = 21 Wide-gap MA

1. pH: 7.4 2. pH, PCO2 same direction?

pH PCO2 Primary Respiratory acidosis 3. Resp: 1 ,2 ,4, 5 & Acute-Acute-Chronic-Chronic & a/b/a/b 4. Metabolic

i. Expected PaCO2

MA : PaCO2 = (1.5 x HCO3) + 8 ± 2 (absolute: HCO3 < 15) = 15 + HCO3 MB : ∆ PaCO2 = 0.6 x ∆ HCO3 (absolute: HCO3 > 45) = 15 + HCO3

ii. AG: Corrected AG = AG + 2.5 x (4.5 - Alb) >>> Normal 10 ± 2 iii. ∆AG/∆HCO3 (= AG-10/25-HCO3)

< 1 : Wide + Normal gap MA 1-2 : Pure wide gap MA > 2 : Wide MA + MB

Step approach to acid-base disturbance

Wide Gap Metabolic acidosis

Ketoacidosis L-lactate

Lactic acidosis Normal

Osmolar gap

GFR < 20 Advance renal

failure

<10 >10

Wide Gap Metabolic acidosis

Ketoacidosis L-lactate

Lactic acidosis Normal

Osmolar gap

GFR < 20 Advance renal

failure

<10 >10

DKA

AKA

SKA

• Hx of chronic ethanol abuse, decreased food intake, and often a Hx of nausea and vomiting

• Glucose levels usually low but may be slightly elevated

Pathogenesis

Alcohol withdrawal + Vol depletion + Starvation ↑ Catecholamines, Cortisol, Glucagon, GH ↑ Fatty acid oxidation Ketosis

Ethanol metabolism ↑NADH:NAD Ketosis, lactic acidosis

Alcoholic ketoacidosis

Comprehensive Clinical Nephrology, 5thEd. 2015

Treatment Thiamine supplement (After IV glucose WKS)

IV Glucose in NSS for ↑ Insulin Inhibit ketosis

Correct HypoPO4, HypoK, HypoMg (HypoPO4 with in 12-18 hr after correct)

No insulin requirement

Alcoholic ketoacidosis

Brenner & Rector’s The Kidney, 10th Ed

Starvation for 24-48 hrs ↓ Insulin Ketosis Mild AG metabolic acidosis

Relative Insulin def and glucagon excess

Serum HCO3- is rarely < 18 mmol/L and Serum

ketone not above 10 mmol/L due to

• Ketone stimulate pancreatic islets to release insulin inhibit lipolysis

Treatment: IV glucose in NSS

Starvation ketoacidosis

Brenner & Rector’s The Kidney, 10th Ed Comprehensive Clinical Nephrology, 5thEd. 2015

Wide Gap Metabolic acidosis

Ketoacidosis L-lactate

Lactic acidosis Normal

Osmolar gap

GFR < 20 Advance renal

failure

<10 >10 B|B1, B2, B3

A |Shock

B1 Liver disease Malig, B1 def

B2 MFM, NRTI

B3 Inborn error

metabolism

•Risk factor for MALA Hx of MALA****

Renal failure

CHF

Sepsis

Liver disease

Elderly

Alcohol use

Contrast media exposure

•Indication for HD Lactate level > 20 mmol/L

ABG pH ≤ 7.0

Failed medication

MFM associated with lactic acidosis

Brenner & Rector’s The Kidney, 9th Ed 2012

Elizabeth G. Phimister, october 16, 2014, NEJM 371;16

MFM: If GFR < 60: Max 2 g, GFR < 45: Not start (Max 1 g), GFR < 30: Hold

Male 40 year-old complained of sudden abdominal pain. CT: Bowel gangrene at jejunum. Small bowel resection with jejunocolonic anastomosis was done (residual small bowel 70 cm) for 2 months ago. He comes to ER with dyspnea, PE: V/S-BP 110/80, Lab: Na 132, K 3.8, Cl 90, HCO3 12 mmol/L, serum L-lactate 1.5 mmol/L, BUN/Cr 25/0.9 mg/dL, serum ketone negative What’s your definite treatment? A. Hemodialysis B. Sodium bicarbonate C. Neomycin D. Saline solution E. Search for other toxic agents

AG = 30 ΔG/ΔHCO3 = 1.7

D-lactate is not metabolized by L-LDH

Cause

1. By product of metabolism of bacteria (Lactobacillus) which overgrow in GI tract such as

Jejunoileal bypass

Short bowel syndrome

Small bowel obstruction

2. Propylene glycol metabolite

3. DKA

D-lactic acidosis

Clinical Episodic metabolic acidosis (typically after high carbohydrate

meals) with neurological S&S (confusion, slurred speech, ataxia, loss of memory)

LAB Serum D-lactate level > 3 mmol/L

Both high AG and Normal gap MA

Treatment Sodium bicarbonate

ATB (Metronidazole, Neomycin, Vancomycin)

Low carbohydrate diet

D-lactic acidosis

Brenner & Rector’s The Kidney, 9th Ed 2012 Halperin ML. Kidney Int 1996;49:1

From amine and other compound of bacterial product (Not D-Lactic)

Wide Gap Metabolic acidosis

Ketoacidosis L-lactate

Lactic acidosis Normal

Osmolar gap

GFR < 20 Advance renal

failure

<10 >10

Osmolar gap

<10 >10

D-lactate

Toluene

Pyroglutamic acid

Salicylates

Methanol, Ethanol

Ethylene glycol

Isopropanol, Acetone

Propylene glycol

Paraldehyde, Formaldehyde

Calcium Oxalate crystal Onset 4-8 hr after ingestion, found 50%

Monohydrate form: Prism/Dumbbell/Needle/Cigar-like >> Non specific (Weddelite) (Late ethylene glycol, high oxalate; Vit C, Cocoa, Garlic, Tea, Tomato, Spinach)

Dihydrate form: Octahedral/Bi-pyramidal/Enveloped >> Specific (Whewellite) (Early ethylene glycol)

Brenner & Rector’s The Kidney, 10th Ed

Salicylate LAB Ferric chloride test for urine: purple color (Non-specific: +ve in daily ASA use)

Serum salicylate level: Therapeutic level 10-30 mg/dL (Severe: >70)

Mixed respiratory alkalosis-metabolic acidosis, High AG acidosis, normal > high osmolar gap, UNC +ve (salicylate anion in urine), Hypouricemia, L- lactic acidosis, ketoacidosis, hypoglycemia

Treatment NG lavage for ingestion < 1 hour

(C/I: corrosive agent, hydrocarbon, airway compromised)

Multiple – dose activated charcoal for ingestion 1-2 hr

IV fluid with glucose (due to ↓ cerebral glucose conc)

Alkalinize urine (urine pH 7.5-8.0) >>> Alkalemia increase ionized form

• Less accumulation in CNS and increase urinary excretion

Pyroglutamic acidosis

Congenital (glutathione synthetase def)

Acquired: glutathione reduced by oxidative stress (critical illness) and overdose acetaminophen

Risk factor in therapeutic dose user • woman, vigabatrin, glycine def

(sepsis, malig, preg, DMII, malnutrition, liver/renal disease), Heterozygote of glutathione synthetase (1/10,000)

Comprehensive Clinical Nephrology, 5thEd. 2015

LAB: Urine 5-Oxoproline level

Treatment: NAC Increase glutathione

Toxin & High anion gap acidosis

AG OG Ingestion Manifestation

↑ normal Acetaminophen Hepatitis

↑ normal Salicylates (Lactate, Ketone) Fever, tinnitus, Met acid + respiratory alkalosis

↑ ↑ Ethanol (Acetic acid) Alcoholic fetor, hepatitis, ∆MS, met alkalosis from vomiting

↑ ↑ Methanol (Formic acid) ∆MS, blurred vision

↑ ↑ Ethylene glycol (Glycolic

acid, Oxalic acid, Lactate)

∆MS, hypoCa, Ca oxalate, renal failure, cardiopulmonary failure

↑ ↑ Propylene glycol (Lactate) High OG alone, unexplained lactic acidosis, AKI

normal ↑ Isopropyl alcohol (Acetone) ∆MS, fruity breath, ketonuria

A 60-year-old man presented with unconsciousness

for 1 hour. Physical examination revealed an alcohol

smell breath odor upon breathing. Lab revealed Na

135, K 4.1, Cl 102, CO2 12 mEq/L, negative serum

ketone, glucose 394 mg/dL, BUN/Cr 23/4 mg/dL,

and measured plasma osmolality 344 mOsm/L.

What is the most likely diagnosis?

A. Salicylate poisoning

B. Alcoholic ketoacidosis

C. Methanol poisoning

D. Diabetic ketoacidosis

E. Ethanol overdose

AG = 21 Cal Posm = 300 Serum OG = 44

A 19-year-old man come to ER due to alteration of consciousness. He was asymptomatic 8 hours ago. He takes no medication, alcohol. PE: BP 90/60 mmHg, PR 110 bpm, RR 32 tpm. Heart/lungs: WNL. No neurological deficit. LAB: Na 142, K 3.6 Cl 108 CO2 14 mEq/L, BUN/Cr 14/1.5 mg/dL, BS 114, serum osm 290, ABG: pH 7.42, PCO2 20 PO2 94 mmHg. What is the most likely cause of this patient’s acid-base disorder? A. Alcoholic ketoacidosis

B. Ethylene glycol toxicity

C. Methanol toxicity

D. Salicylate toxicity

E. Cyanid poisoning

AG = 20 ΔG/ΔHCO3 = 1

OG = 5

Expected HCO3 = 20 ± 2

A 43-year-old hospital janitor with a history of chronic alcohol consumption was brought to ER because of having a stuporous consciousness. Lab revealed Na 140, K 4.0, Cl 106, HCO3 24 mEq/L, Cr 1 mg/dL, plasma glucose 90 mg/dL, and urine acetone 4+.

Which one of the followings is the most likely cause of his illness?

A. Alcohol ketoacidosis B. Starvation ketoacidosis C. Ethylene glycol intoxication D. Isopropyl alcohol intoxication E. D-lactic acidosis

No MA Urine ketone

Fruity smell (acetone)

No incresed AG High OG

ผู้ ป่วยชายมีประวตัิปวดหลงั กินเหล้า ต่อมามี confusion หอบเหน่ือย v/s ดี แรกรับ E’lyte: AG = 30, serum

osmolal gap = 10 ถามว่าเกิดจากอะไร? A. Methanol

B. Ethanol

C. Pyroglutamic acid

D.Isopropyl

E. Ethylene glycol

A patient with a history of Sjogren’s syndrome has the following laboratory findings: Na 139, K3, Cl 114, HCO3 15 mEq/L. Urine studies show pH 6.0, Na 15, K 10, Cl 12 mEq/L What is the most likely diagnosis? A. Type I renal tubular acidosis (RTA) B. Type II RTA C. Type III RTA D. Type IV RTA E. Chronic diarrhea

AG = 10 Normal gap MA

Normal gap Metabolic acidosis

U pH

Test for renal acid secretion

UAG or UNC

UOG

U NH4

Non-renal HCO3 loss

Diarrhea Ureteral diversions Biliary or pancreatic fistulas Drugs: CaCl2, MgSO4

Cholestyramine Saline infusion

Acid load

Hyperalimentation HCl NH4Cl

Pitfall of urine net charge (false positive) 1. Non-HCl (Ketosis, Salicylate, D-lactate, Hippurate) 2. Unusual salt of antibiotic

Urine net charge (UNC) = Urine anion gap = Urine Na + K – Cl

Acidosis: ไตขับกรดได้ (NH4Cl) UNC -ve ไตขับกรดไม่ได้ (NH4Cl) UNC +ve

Urine osmolal gap = measured – calculated osmolarity ไตขับกรดได้ Urine osmolal gap > 100

2(UNa + UK) + Uglu/18 + UUrea/2.8

Normal gap Metabolic acidosis

U pH > 5.5

Defect of renal acid secretion

UAG +

UOG < 100

U NH4 < 50 mmol/L

Non-renal HCO3 loss

Diarrhea Ureteral diversions Biliary or pancreatic fistulas Drugs: CaCl2, MgSO4

Cholestyramine Saline infusion

Acid load

Hyperalimentation HCl NH4Cl

YES NO

Yes No

Bicarbonate loading test

pRTA

7.5% NaHCO3 2-3 mmol/kg IV rate 1-2 mEq/kg/hr until plasma HCO3 > 20 mEq/L

FE-HCO3 > 15%

Serum K

Low K High K

U pH < 5.5

U pH > 5.5

RTA4

Voltage dependent dRTA

Bicarbonante loading test

Bicarbonante loading test

Acid loading test

Low K

Bicarbonate loading test 8.4% NaHCO3 ( 1mmol/L ) 2 ml/kg IV stat then 2 ml/min

Or NaHCO3 PO plasma HCO3

- > 30 meq/L

Until U pH > 7.8 x3 times (30-60 mins)

Urine pH < 5.5 Urine pH > 5.5

U PCO2 < 50 mmHg U-B PCO2 < 20 mmHg

U PCO2 > 70 mmHg U-B PCO2 >20 mmHg

U PCO2 < 50 mmHg U-B PCO2 < 20 mmHg

U PCO2 > 70 mmHg U-B PCO2 > 20 mmHg

Rate dependent RTA

NH3 defect Classical dRTA (H-ATPase, H/K ATPase)

Back leak dRTA (Ampho B)

Yes No

Bicarbonate loading test

pRTA

7.5% NaHCO3 2-3 mmol/kg IV rate 1-2 mEq/kg/hr until plasma HCO3 > 20 mEq/L

FE-HCO3 > 15%

Serum K

Low K High K

U pH < 5.5

U pH > 5.5

RTA 4

Voltage dependent dRTA

Bicarbonante loading test

Bicarbonante loading test

Acid loading test

RTA 4

Renin AGN, BB, COXi/CNI, DM, PHA II (Gordon’s syndrome), TID (A-B-C-D-P-T)

High K, Urine pH < 5.5

Ang I ACE-I

Ang II ARB

Adrenal gland

Heparin, Ketoconazole, Etomidate, 1°AI, 21-OH def.

MR

ACE

Ald

Voltage-dependent dRTA

Pseudohypoaldosteronism (PHA) type I, II

A Amiloride, Triamterene, Pentamidine

TID

High K, Urine pH > 5.5

B Bactrim (Trimethoprim)

C CNI (CycloA, Tacrolimus)

D alDactone

E Eplerenone, Drospirenone (Yasmin)

UTO

KT

From Angiotensinogen (liver)

JGA

Voltage dRTA

PHA type I PHA type II

Clinical Renal salt wasting, HypoNa, HyperK, MA

Salt-sensitive HT, HyperK, MA

Mechanism Decrease Na reabsorb in CCD Impaired removal of NCC in DCT, ENaC, ROMK,

TRPV5

PAC, PRA level

High PAC, High PRA Low PAC, Low PRA

Urine Ca Normal Increased Urine Ca Osteoporosis

Treatment Salt supplement, Fludrocortisone?

Thiazide

Mirror image

Liddle’s syndrome Gitelman’s syndrome

A 28-year-old woman presented with weight loss for 4 kg

and episodic fatigue and almost fainting during the past 1

month. PE: BP 100/70 mmHg, P 84/min, and JVP 0-1 cm.

Lab showed BUN/Cr 24/2.2 mg/dL, Na 120, K 5.7, Cl 100,

HCO3 15 mEq/L, osmolality 290 mOsm/kgH2O, and arterial

pH 7.33. Urinalysis showed pH 5.1, osmolality 290

mOsm/kgH2O, Na+ 60, K+ 15, and Cl- 50 mEq/L.

What is the most likely diagnosis?

A. Hyperkalemic distal RTA

B. Liddle’s syndrome

C. Adrenal insufficiency

D. Diabetic nephropathy

E. Pseudohypoaldosteronism type2 (Gordon’s syndrome)

หญิง 38 ปี Underling HT มี Strong family history of MI เดิมกินยาคุมอยู่ประจ า มาตรวจ แพทย์จึงเร่ิมมา Lisinoprilไป 1 เดือนมาตรวจซ า้มาวดั BP 152/98 mmHg ตรวจ Lab : Bun 10 Cr 0.8. Na 132

K 5.7 Cl 108. HCO3 18

ถามวา่เกิดจากอะไร? A. Liddle’s syndrome

B. Pseudohypoaldosterone type II

C. Mineralocorticoid defect from oral contraceptive pill

D. Angiotensin I defect from ACEI

E. Glucocorticoid-remediable aldosteronism

Etiology of distal RTA

Familial: AD, AR Endemic: NE in Thailand Ehlers-Danlos syndrome Hereditary elliptocytosis Sickle cell anemia Medullary cystic disease Marfan’s syndrome

Inherited

Autoimmune disease Sjogren, SLE, Thyroiditis Cryoglobulinemia PAN, PBC

Hypercalciuria with nephrocalcinosis 1oHyperPTH, Vit D intox Medullary sponge kidney Fabry’s disease, Wilson

Drug & toxins: Ampho B, toluene, Ifosfamide, Hg, Li, analgesic, foscarnet

TID: UTO, KT

Acquired

Etiology of proximal RTA

ถา้ Ifosfamide มนั MM, Medullary cystic disease จะ Wilson, Sjogren’s syndrome พา 2o HPTH with chronic hypocalcemia ครอบครวั Familial สา Cystinosis วติ Vitamine D deficiency ตร ี KT ออก Outdated tetracycline ไป Paroxysmal nocturnal hematuria (PNH) ท า Tenofovir/Topiramate/Toluene/TKI อะ Amyloidosis/Acetazolamide/Aminoglycoside ไร Lead/Mercury poisoning

CA inhibitor (No Fanconi syn) - Acetazolamide - Topiramate

RTA 1 (distal) RTA 2 (proximal) RTA 4

HypoK

Urine AG + Urine osmolal gap < 100

Renal stone (CaP) Nephrocalcinosis

- K-citrate - NaHCO3 1-2 mEq/kg/day

HypoK HyperK

Urine AG +/- Urine osmolal gap > 100

Urine AG + Urine osmolal gap < 100

Fanconi syndrome - glucosuria, hypouricemia, hypophosphatemia

- K-citrate - NaHCO3 5-15 mEq/kg/day

- Prednisolone - Fludrocortisone

U-H-U-G-A-P

A patient with a history of Sjogren’s syndrome has the following laboratory findings: Na 139, K3, Cl 114, HCO3 15 mEq/L. Urine studies show pH 6.0, Na 15, K 10, Cl 12 mEq/L What is the most likely diagnosis? A. Type I renal tubular acidosis (RTA) B. Type II RTA C. Type III RTA D. Type IV RTA E. Chronic diarrhea

AG = 10 UAG = 13

Q: Patient with the following laboratory test results

Serum electrolyte: Na 128, K 1.2, Cl 110, HCO3 10 mEq/L

Arterial blood gas: pH 7.28, pCO2 25 mmHg

Spot urine: pH 6.2, Na 74, K 20,Cl 81 mEq/L

Which condition is the most likely cause of the acid-base abnormalities?

A. Laxative abuse

B. Salicylate poisoning

C. Vomiting

D. Glue sniffer

E. Antifreeze ingestion

AG = 8 UAG = + 13

Thank you for your attention Questions are always welcome…

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