- Basis of Acid & Base Balance - General Approach for a patient with abnormal ABG - Renal tubular acidosis, Types, Diagnosis

1. Approach to
Acid-Base
Disturbances
Mohamed Ahmed Badheeb, MBBS
National Officer on Medical Education – NAMS (Yemen)

2. Basis of Acid & Base Balance
To evaluate a case of Acid-Base imbalance, you need:
(1) A basic understanding of physiology and biochemistry.
(2) An understanding of the patient’s history.
(3) Arterial blood gas and serum electrolytes drawn at the same
point in time.
(4) Common sense.
2

3. Basis
Of Acid-Base Physiology &
Biochemistry
3

4. Hydrogen
concentration
[H]= 40 nanoEqL (0.00000004)
- Log[H]= 7.4 → pH= 7.4!
That’s why increasing of hydrogen ions
results in decreasing pH.
4
pH 6.4 is 10 times lower than 7.4!
(0.0000004) = (0.0000004) x 10!

5. Hydrogen
concentration
5

6. Acid production in our body
We are producing H+ ions from different metabolic pathways
○ Volatile acids
▪ CO2 as waste product [𝐶𝑂2 + 𝐻2𝑂 ↔ 𝐻2𝐶𝑂3 → H
+
]
Eliminated by the lung (not the kidney).
○ Non-volatile acids
▪ Some amino acids breakdown
▪ Phospholipid
▪ Lactic Acid (anaerobic metabolism)
▪ Drugs (Aspirin, methanol, ethanol glycol..etc..)
6

7. Why should we worry ?
At normal pH, all enzymes
are working in very active
state, any disturbance in the
blood acidity will lead to
misfolding of the proteins in
human body and finally shut
down of all biochemical
reactions & process.
7

8. “
Be Thankful for your
LUNGS & KIDNEYS
8

9. How pH is maintained?
○ The chemical buffers takes only seconds for in the blood to make adjustments to pH.
○ The respiratory tract can adjust the blood pH upward in minutes by exhaling CO2 from
the body.
○ The renal system can also adjust blood pH through the excretion of hydrogen ions (H+)
and the conservation of bicarbonate, but this process takes hours to days to have an
effect
9

10. How pH is maintained?
o Buffer system is a solution that resists a change in pH when acids or bases are added.
o A buffer system made of a weak acid and its salt or a weak base and its salt.
- weak acid based buffer is acetic acid (CH3COOH) and sodium acetate (CH3COONa).
- weak base buffer is made of ammonia (NH3) and ammonium chloride (NH4Cl).
10

11. How pH is maintained?
Strong Acid + weak base = weak acid + salt
Strong Base + weak acid = weak base + salt
11

12. BUFFER SYSTEM
12

13. BUFFER SYSTEM
○ PROTEIN BUFFERS IN BLOOD PLASMA AND CELLS
○ HEMOGLOBIN AS A BUFFER
○ PHOSPHATE BUFFER
13

14. BUFFER SYSTEM
14

15. BUFFER SYSTEM
○ PHOSPHATE BUFFER
𝐻𝐶𝑙 + 𝑁𝑎2𝐻𝑃𝑂4 → 𝑁𝑎𝐻2𝑃𝑂4 + 𝑁𝑎𝐶𝑙
(strong acid) + (Disodium phosphate) → (Monosodium phosphate) + (salt)
𝑁𝑎𝑂𝐻 + 𝑁𝑎𝐻2𝑃𝑂4 → 𝑁𝑎2𝐻𝑃𝑂4 + 𝐻2𝑂
(Sodium hydroxide) + (Monosodium phosphate) → (Disodium phosphate) + (water)
15

16. BUFFER SYSTEM
○ BICARBONATE-CARBONIC ACID BUFFER
The bicarbonate-carbonic acid buffer works in a fashion similar to phosphate buffers. The
bicarbonate is regulated in the blood by sodium, as are the phosphate ions. When sodium
bicarbonate (NaHCO3), comes into contact with a strong acid, such as HCl, carbonic acid
(H2CO3), which is a weak acid, and NaCl are formed. When carbonic acid comes into contact
with a strong base, such as NaOH, bicarbonate and water are formed.
16

17. BUFFER SYSTEM
○ BICARBONATE-CARBONIC ACID BUFFER
𝑁𝑎𝐻𝐶𝑂3 + 𝐻𝐶𝑙 → 𝐻2𝐶𝑂3 + 𝑁𝑎𝐶𝑙
(sodium bicarbonate) + (strong acid) → (Carbonic acid) + (salt)
𝐻2𝐶𝑂3 + 𝑁𝑎𝑂𝐻 → 𝐻𝐶𝑂3 − +
𝐻2𝑂
(carbonic acid) + (strong base)→(bicarbonate) + (water)
17

18. 18

19. RENAL REGULATION
19
○ Step 1: Sodium ions are reabsorbed from
the filtrate in exchange for H+ by an antiport
mechanism in the apical membranes of cells
lining the renal tubule.
○ Step 2: The cells produce bicarbonate ions
that can be shunted to peritubular
capillaries.
○ Step 3: When CO2 is available, the reaction is
driven to the formation of carbonic acid,
which dissociates to form a bicarbonate ion
and a hydrogen ion.
○ Step 4: The bicarbonate ion passes into the
peritubular capillaries and returns to the
blood. The hydrogen ion is secreted into the
filtrate, where it can become part of new
water molecules and be reabsorbed as such,
or removed in the urine.

20. 20

21. IN CONCLUSION
𝒑𝑯 ∝
𝑯𝑪𝑶𝟑
𝑪𝑶𝟐
This equation concludes
the whole process of
acid-base regulation.
Bicarbonate
Is the main to be regulated via the kidney, once it decreases the pH
decreases in a direct relation.
A decrease of blood bicarbonate can result from:
1. The inhibition of carbonic anhydrase by certain diuretics.
2. from excessive bicarbonate loss due to diarrhea.
3. Addison’s disease (chronic adrenal insufficiency), in which
aldosterone levels are reduced.
4. damage, such as chronic nephritis.
5. Elevated levels of ketones (common in unmanaged diabetes
mellitus), which bind bicarbonate in the filtrate and prevent its
conservation.
21

22. 22

23. IN CONCLUSION
𝒑𝑯 ∝
𝑯𝑪𝑶𝟑
𝑪𝑶𝟐
This equation concludes
the whole process of
acid-base regulation.
Bicarbonate
Is the main to be regulated via the kidney, once it decreases the pH
decreases in a direct relation.
A decrease of blood bicarbonate can result from:
1. The inhibition of carbonic anhydrase by certain diuretics.
2. from excessive bicarbonate loss due to diarrhea.
3. Addison’s disease (chronic adrenal insufficiency), in which
aldosterone levels are reduced.
4. damage, such as chronic nephritis.
5. Elevated levels of ketones (common in unmanaged diabetes
mellitus), which bind bicarbonate in the filtrate and prevent its
conservation.
23

24. THE RESPIRATORY
REGULATION
24
○ The respiratory system contributes to the
balance of acids and bases in the body by
regulating the blood levels of carbonic acid. CO2
in the blood readily reacts with water to form
carbonic acid, and the levels of CO2 and
carbonic acid in the blood are in equilibrium.
○ Doubling the respiratory rate for less than 1
minute, removing “extra” CO2, would increase
the blood pH by 0.2. This situation is common if
you are exercising strenuously over a period of
time.

25. SMALL
RULE
BIG
IMPACT
25
𝒑𝑯 ∝
𝑯𝑪𝑶𝟑
𝑪𝑶𝟐
This equation concludes the
whole process of acid-base
regulation.

26. Basis
Of Acid-Base Interpretation
26

27. Step 1: Is it Acidosis or Alkalosis?
27
○ (7.35-7.45)
○ Less than 7.35 is acidosis
○ More than 7.45 is alkalosis

28. Step 2: Is it Metabolic or Respiratory?
28

29. Step 3: Is there compensation?
Is there compound (mixed) disorder?
29

30. Step 3: Is there compensation?
Is there compound (mixed) disorder?
30

31. Acidosis
pH less than 7.35
31

32. Step 2: Is it Metabolic or Respiratory?
32
○ Respiratory acidosis: PaCO2 > 45 mmHg
○ Metabolic acidosis: serum HCO3 < 22 mEq/L
After deciding if there’s an Acidemia or Alkalemia ask, "What do I expect the CO2 to be - high
or low?“ If there’s a pH < 7.4, expect the CO2 to be higher than normal - that is >40. If it is, the
acidemia is caused by a respiratory acidosis. If it isn’t, the acidemia is caused by a metabolic
acidosis.
If there’s a pH >7.4, expect the CO2 to be lower than normal (loss of respiratory acid). If it is,
the alkalemia is caused by a respiratory acidosis. If it isn’t, the alkalemia is caused by a
metabolic alkalosis.

33. SMALL
RULE
BIG
IMPACT
33
𝒑𝑯 ∝
𝑯𝑪𝑶𝟑
𝑪𝑶𝟐
This equation concludes the
whole process of acid-base
regulation.

34. THE RESPIRATORY Acidosis
34
○ Elevated PaCO2 (more than 45 mmHg), decreased extracellular pH (CO2) production at
tissue level exceeds CO2 elimination by lungs) .
○ Causes: HypoVentilation
○ CNS depression (sedatives, CNS disease, obesity-hypoventilation syndrome); pleural
disease (large pneumothoraces and pleural effusions); lung disease (COPD, ARDS);
musculoskeletal and neuromuscular disorders (kypho-scoliosis, Guillain-Barre syndrome,
myasthenia gravis, polymyositis)

35. 35

36. THE RESPIRATORY Acidosis
36
Step 3: Is there compensation?
Is there compound (mixed) disorder?

37. Case 1
37
○ A 55-year-old male is presented with a complaint of cough for 2 days
which was associated with fever. Physical examination reveals ,
tachycardia, and diminished breathing sound bilaterally, and
increased TFV.
○ The lab. Findings include:
HCO3 = 26 meq/L
pH = 7.29
Pco2 = 55 mmHg

38. Case 1
38
○ pH: 7.26
Acidosis
○ HCO3 = 26 meq/L
?!
○ Pco2 = 55 mmHg
Respiratory
Dx :
Respiratory Acidosis
○ Compensated?
55-40= 15
15x0.1= 1.5 (acute)
15x0.3 = 4.5 (chronic)
------------------------------------------
HCO3= 24+1.5= 25.5 (acute)
HCO3= 24+4.5= 28.5 (chronic)
Dx
Acute Respiratory Acidosis

39. THE METABOLIC Acidosis
39
𝒑𝑯 ∝
𝑯𝑪𝑶𝟑
𝑪𝑶𝟐

40. THE METABOLIC Acidosis
40

41. THE METABOLIC Acidosis
41

42. THE METABOLIC Acidosis
42
○ Decreased serum HCO3 (less than 22), decreased extracellular pH
○ Causes: divide into INCREASED versus NORMAL ANION GAP causes.
✓ INCREASED AG: can divide into 4 main categories: renal failure; ketoacidosis (diabetes, EtOH); drugs or
poisons (MeOH, ASA, paraldehyde, ethylene glycol); lactic acidosis (± hypoxemia); sepsis. mnemonic
MUDPILES: Methanol, Uremia, Diabetic/alcoholic ketoacidosis, Paraldehyde, Isoniazid/Iron, Lactic
acidosis/ketoacidosis, Ethylene glycol, Salicylates
✓ NORMAL AG (hyperchloremic): GI loss of HCO3; renal tubular acidosis, carbonic anhydrase inhibitor use
(e.g., acetazolamide); renal compensation for respiratory alkalosis; drugs (cyclosporine, amphoB,
cholesyramine); VIP-producing tumors; ureteral diversions. mnemonic HARDUP: Hyperventilation, Acids
(carbonic anhydrase inhibitors, Addison’s disease, TPN), RTA, Diarrhea, Ureterosigmoidostomy (and ileal
diversions), Pancreatic fistula or drainage.

43. 43

44. 44

45. 45

46. THE METABOLIC Acidosis
46
Step 3: Is there compensation?
Is there compound (mixed) disorder?

47. Case 2
47
47 year old man with 3 day of sever diarrhea present in ER , C/O
weakness, dyspnea & dizziness. O/E his supine B.P. is 100/70 & his
supine pulse 110/min. when the patient sits up his B.P. decreases to
80 mmHg & his heart rate increases to 130.
Investigations shows
Urea➔30, creatinine ➔ 1.7,
Na➔ 130, K➔ 3.2, Cl➔100 , HCO3➔ 10,
ABG on room air reveal
PH➔7.24 , PaCO2➔23 , PO2➔ 105 & HCO3➔ 9. What is the acid-base
balance?

48. Case 1
48
○ pH: 7.24
Acidosis
○ HCO3 = 9 meq/L
Metabolic
○ AG= Na-Cl-HCO3
130-100-9= 21
○ Pco2 = 23 mmHg
?!
Dx :
AG Metabolic Acidosis
○ Compensated?
Winter Formula
1.5 [HCO3] + 8 +/-2
[1.5 x 9] + 8 +/- 2 = [19.5-23.5]
------------------------------------------
Dx
High AG Metabolic Acidosis

49. Remember
49
Winter Formula Interpretation
- Predicted PaCO2 = Estimated PaCo2: Pure Metabolic Acidosis
- Predicted PaCO2 > Estimated PaCo2: Concurrent Respiratory Alkalosis
- Predicted PaCO2 < Estimated PaCo2: Concurrent Respiratory Acidosis

50. THE METABOLIC Acidosis
50
Additional Step: Is there other
metabolic compensation/disturbance?
Delta gap
It is used in a case of metabolic acidosis to check metabolic
compensation
𝐶𝑎𝑙𝑐𝑢𝑙𝑎𝑡𝑒𝑑 𝐴𝐺 − 𝑁𝑜𝑟𝑚𝑎𝑙 𝐴𝐺
𝑁𝑜𝑟𝑚𝑎𝑙 𝐻𝐶𝑂3 − 𝑀𝑒𝑎𝑠𝑢𝑟𝑒𝑑 𝐻𝐶𝑂
The ratio gives one of four results:
1. < 0.4 due to a pure NAGMA
2. 0.4 – 0.8 due to a mixed NAGMA + HAGMA
3. 0.8 – 2.0 due to a pure HAGMA
4. >2.0 due to a mixed HAGMA + metabolic alkalosis

51. Alkalosis
pH more than 7.45
51

52. THE RESPIRATORY Alkalosis
52
○ Elevated PaCO2 (less than 35), decreased extracellular pH (CO2) production at tissue level
exceeds CO2 elimination by lungs) .
○ Causes: Hyperventilation
catastrophic CNS disorder (ICH); drugs (salicylates, progesterone); pregnancy (generally during
3rd trimester); decreased lung compliance (such as interstitial fibrosis) leading to
hyperventilation and respiratory alkalosis even in the absence of hypoxemia; anxiety;
cirrhosis; sepsis.

53. SMALL
RULE
BIG
IMPACT
53
𝒑𝑯 ∝
𝑯𝑪𝑶𝟑
𝑪𝑶𝟐
This equation concludes the
whole process of acid-base
regulation.

54. THE RESPIRATORY Alkalosis
54
Step 3: Is there compensation?
Is there compound (mixed) disorder?

55. Case 1
55
○ A 56-year-old male is presented with a complaint of dyspnea for 10
days which was increased recently, he is known case of hepatitis B
virus for 5 years for which he receives therapy. On examination, the
patient was dyspneic, jaundice on sclera, abdominal distention with
positive fluid thrill.
○ The lab. Findings include:
HCO3 = 17 meq/L
pH = 7.55
Pco2 = 25 mmHg

56. Case 1
56
○ pH: 7.55
Alkalosis
○ HCO3 = 17 meq/L
?!
○ Pco2 = 25 mmHg
Respiratory
Dx :
Respiratory Alkalosis
○ Compensated?
25-40= 15
15x0.2= 3 (acute)
15x0.4 = 6 (chronic)
------------------------------------------
HCO3= 24-3= 21 (acute)
HCO3= 24-6= 18 (chronic)
Dx
Chronic Respiratory Alkalosis

57. THE METABOLIC Alkalosis
57
○ Increased serum HCO3 (more than 26), increased extracellular pH (may see mild increase
in PaCO2 as compensation)
○ Causes: generally either volume contraction (volume loss: GI tract, kidneys, skin,
respiratory system, third-spaced fluid, bleeding) or hypokalemia. Also, excessive
glucocorticoids or mineralocorticoids, Bartter’s syndrome, exogenous alkalai ingestion.
Two types: Chloride responsive and Chloride resistant.
Chloride responsive: vomiting, diuretics, NG suction, diarrhea, villous adenoma. Spot urine Cl
should be less than 10 (except with diuretic use) since the kidney should be conserving Cl.
Treatment with 0.9NS should fix the disturbance.
Chloride resistant: distal exchange site stimulation by aldosterone resulting in increased H+
and K+ excretion in exchange for resorption of Na+ as NaHCO3.

58. THE METABOLIC Alkalosis
58
Vomiting Diarrhea Diuretics

59. THE METABOLIC Alkalosis
59

60. “
Practice make PERFECT!
Some cases to apply the
60

61. Just to Remember!
61

62. Just to Remember!
62
Step 1: Is it Acidosis or Alkalosis?
Step 2: Is it Metabolic or Respiratory?
Step 2.1: if metabolic Is it high AG or not?
Step 2.2: if respiratory Is it acute or chronic?
Step 3: Is there compensation or
mixed?

63. Case 1
63
○ A 55-year-old woman is admitted with a complaint of severe
vomiting for 5 days. Physical examination reveals postural
hypotension, tachycardia, and diminished skin turgor.
○ The lab. Findings include:
Plasma [Na+] = 140 meq/L [K+] = 3.4meq/L
[Cl-] = 77 meq/L HCO3 = 9 meq/L
pH = 7.23 Pco2 = 22 mmHg

64. Case 1
64
○ pH 7.23 acidemia
○ HCO3 9 metabolic acidosis
○ Pco2 22 appropriate comp.
○ Ag = 140 – (77 + 9 ) = 54
○ D/D
● Ag 54 – 12 = 42
● HCO3 24 – 9 = 15 d/d = 42 - 15 = 27
metabolic alkalosis
Metabolic Acidosis + Metabolic Alkalosis

65. Case 2
65
○ A 58-year-old man with a history of chronic bronchitis
developed severe diarrhea caused by pseudo-membranous
colitis.
○ Lab results
[Na+] = 138 meq/L [K+] = 3.8
[Cl-] = 117 meq/L HCO3 = 9 meq/L
pH = 6.97 Pco2 = 40 mmHg

66. Case 2
66
Non-AG metabolic acidosis
+
Respiratory acidosis

67. Case 3
67
○ A 45 year-old man with liver cirrhosis and ascites admitted with
acute GI bleeding due to ruptured esophageal varices, taken to
the surgery for portocaval shunt and given 19 units of blood.
○ Lab. Tests post-op
pH = 7.53 Pco2 = 50 mmHg
HCO3 = 40 meq/L Na+ = 140 meq/L
Cl- = 86

68. Case 3
68
Metabolic Alkalosis

69. Case 4
69
○ A 54 year-old man with a history of COPD has a 2-day history
of increasing shortness of breath and sputum production, CXR
showed Lt. LL pneumonia.
○ Labs
pH = 7.25 Pco2 = 70 mmHg
Po2= 30 mmHg HCO3 30 meq/L
Na = 135 meq/L Cl = 93 meq/L

70. Case 1
70
○ pH: 7.25
Acidosis
○ HCO3 = 30 meq/L
?!
○ Pco2 = 70 mmHg
Respiratory
Dx :
Respiratory Acidosis
○ Compensated?
70-40= 30
30x0.1= 3 (acute)
30x0.3 = 9 (chronic)
------------------------------------------
HCO3= 24+3= 27 (acute)
HCO3= 24-9= 33 (chronic)
Dx
Acute on top of Chronic
Respiratory Acidosis

71. THANKS!
Any questions?
You can find me at Badheeb2009@gmail.com
71

72. RTA
Renal Tubular Acidosis
72
Mohamed Ahmed Badheeb, MBBS

73. Renal Tubular Acidosis
73
❖ General Concepts
○ Renal tubular acidosis (RTA) involves defects isolated to the renal tubules only
○ GFR may be normal or only minimally affected
○ Primary problem is defective renal acid-base regulation due to impaired ability to acidify the urine
and excrete acid
○ Results in net acid retention and hyperchloremic normal anion gap metabolic acidosis (NAGMA)
○ May be incomplete and only develop in the presence of an acid load
○ Occurs despite a normal or only mildly reduced glomerular filtration rate (GFR)
○ Causes are numerous
○ Poorly understood by many physicians
○ RTA is often detected incidentally through an abnormal blood workup, but some patients present with
clinical features such as poor growth, dehydration, or altered mental state

74. Renal Tubular Acidosis
74

75. Renal Tubular Acidosis (Distal)
75
❖ General Concepts
○ Reduced secretion of H+ in
distal tubule results inability to
maximally acidify the urine
Causes
○ Hereditary (most common,
diagnosed in infants and children)
○ Autoimmune (e.g. Sjogrens, SLE,
thyroiditis)
○ Nephrocalcinosis (e.g. primary
hyperparathyroidism, vitamin D
intoxification)
○ Nephrotoxins (e.g. amphotericin
B, toluene inhalation)
○ Obstructive nephropathy
❖ Investigation
○ Urine pH remains >5.5 despite
severe acidaemia (HCO3 <
15mmol/L)
○ HCO3 loading test leads to
increased urinary HCO3
○ May require an acid load test to
see whether urinary pH remains >
5.5
○ Hyperchloraemic acidosis, alkaline
urine, and renal stone formation
○ Secondary hyperaldosteronism
results in increased K+ loss in
urine
❖ Treatment
○ NaHCO3 (corrects Na+ deficit,
ECF volume and corrects
hypokalaemia)
○ Sodium and potassium citrate
solutions can be useful if
hypokalaemia persistent
○ Citrate also binds Ca2+ in the
urine and can help to prevent
renal stones

76. Renal Tubular Acidosis (Proximal)
76
❖ General Concepts
○ Termed proximal because the main problem is impaired reabsorption
of bicarbonate in the proximal tubule
○ at normal plasma HCO3, 15% of filtered HCO3 is excreted in the urine -
> in acidosis when HCO3 levels are low the urine can become HCO3
free
○ symptoms take place when there is an increase in plasma HCO3 ->
proximal tubule cannot reabsorb the increased filtered load ->
delivered to distal tubule and is unable to be reabsorbed -> urinary
loss of HCO3
○ results in metabolic acidosis with an inappropriately high urinary pH
and hyperchloraemia (Cl- replaces HCO3 in circulation)
○ with increased distal tubular Na+ delivery, hyperaldosteronism results,
leading to K wasting
❖ Causes
○ hereditary (most common,
diagnosed in infants and children)
○ part of Fanconi syndrome
(proximal tubular defects with
impaired reabsorption of glucose,
phosphate and amino acids as
well as HCO3)
○ vitamin D deficiency
○ cystinosis
○ lead nephropathy
○ amyloidosis
○ medullary cystic disease

77. Renal Tubular Acidosis (Proximal)
77
❖ Investigation
○ metabolic acidosis (usually not as
severe as distal RTA)
○ plasma HCO3 usually > 15mmol/L
○ high urinary HCO3 (inappropriate)
○ hypokalaemia
○ during the NH4Cl loading test
urinary pH drops < 5.5
❖ Treatment
○ Treat underlying disorder
○ NaHCO3 and K+
supplementation not always
necessary (if required will
require large doses)
○ Thiazide diuretics (some
patients respond to this which
results in increased proximal
HCO3 reabsorption)

78. Renal Tubular Acidosis (Type IV)
78
❖ General Concepts
Tubular hyperkalemia
○ Associated with renal failure caused by disorders affecting the renal
interstitium and tubules
○ GFR >20mL/min (unlike uremic acidosis)
○ Always associated with hyperkalemia (unlike others)
○ Defect in cation-exchange in the distal tubule with reduced secretion of both
H+ and K+
○ Physiological reduction in proximal tubular ammonium excretion (impaired
ammoniagenesis) due to to hypoaldosteronism, results in a decrease in urine
buffering capacity
○ Associated with: Addison’s disease or post bilateral adrenalectomy
○ Acidosis not common unless there is associated renal damage affect the
distal tubule
○ The H+ pump in the tubule is not abnormal so that patients with this
disorder are able to decrease their urinary pH to < 5.5 in response to the
acidosis
❖ Causes
○ Aldosterone deficiency
(hypoaldosteronism)
● Primary
● Secondary /
hyporeninemic (including
diabetic nephropathy)
○ Aldosterone resistance
● Drugs: NSAIDs, ACE
inhibitors and ARBs,
Eplerenone,
Spironolactone,
Trimethoprim,
Pentamidine
● Pseudohypoaldosteronism

79. Renal Tubular Acidosis (Type IV)
79
❖ Investigation
○ Mild metabolic acidosis
○ Plasma HCO3 usually > 15mmol/L
○ Hyperkalaemia
❖ Treatment
○ Treat underlying disorder
○ NaHCO3 and K+
supplementation not always
necessary (if required will
require large doses)
○ Thiazide diuretics (some
patients respond to this which
results in increased proximal
HCO3 reabsorption)

80. THANKS!
Any questions?
You can find me at Badheeb2009@gmail.com
80

81. CREDITS
Special thanks to Nephrology department for this
opportunity!
81