Potassium Acid-Base disorder
Kanin Thammavaranucupt, M.D. Nephrology division, Maharat Nakhonratchasima Hospital
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
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
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
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
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