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B&B Renal: Acid-Base Disorders Flashcards

1
Q

Acid-Base regulation

Renal Functions

A
  1. Reabsorb / generate bicarbonate
  2. Excrete H+
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2
Q

Types of acids

Acid Excretion

A

2 types of acids produced via metabolism
1. Volatile acids
2. Non-volatile acids

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3
Q

Volatile acids

Acid Excretion

A

CO2
* Combines w/ H2O to form carbonic acid (H2CO3)
* Eliminated by lungs (respiration)

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4
Q

Non-volatile acids

Acid Excretion

A

Derived from AAs, fatty acids, nucleic acids
* Non-volatile acids are buffered by bicarbonate
* Prevents changes in blood pH due to build up of acidic metabolic products
* Bicarbonate must be replenished by the kidneys

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5
Q

Bicarbonate reabsorption

Proximal Tubule

A

All filtered bicarbonate is reabsorbed in the kidneys
2. 1. Na+/H+ exchanger in apical membrane transports Na+ into cells & H+ into urine
2. H+ & HCO3- in urine form H2CO3
3. CA converts H2CO3 to CO2 & H2O
4. CO2 & H2O diffuse into cells
5. CA converts CO2 & H2O back to H2CO3
6. H2CO3 divides into H+ & HCO3-
7. NBC in BL membrane cotransports Na+ & HCO3- into blood

80% of bicarbonate reabsorption occurs in proximal tubule

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6
Q

Bicarbonate generation

Collecting Duct

A

Bicarbonate is generated in intercalated cells of CD to replace any that was used to buffer non-volatile acids
1. CO2 & H2O are combined to form H2CO3 by CA
2. H2CO3 divides into H+ & HCO3-
3. HCO3- is transported from cell into blood
4. H+ is pumped out of cell into urine by H+-ATPase; high urine [H+} has low pH, needs to be buffered

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7
Q

Urinary Buffers

H+ Excretion

A
  1. Titratable acids
  2. Ammonia
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8
Q

Titratable Acids

Urinary Buffers

A

Phosphate
* HPO4 is filtered by glomerulus
* Becomes H2PO4 in urine w/ addition of H+
* Picks up H+ produced in HCO3- generation
* H2PO4 is excreted in urine = excretion of H+

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9
Q

Ammonia

Urinary Buffers

A
  • Limited supply of titratable acids
    • Varies with dietary intake (especially PO4)
  • Supply of ammonia is adaptable
  • Kidneys generate more NH3 when H+ increases
    • Synthesized from glutamine (Glu = 2 NH3)
  • NH3 picks up H+ produced in HCO3- generation
    • NH4+ is excreted in urine = excretion of H+
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10
Q

Renal Acid-Base

Summary

A
  • Non-volatile acids in serum are buffered by HCO3-
    • Prevents changes in blood pH
  • Low HCO3- levels stimulate:
    • PCT: HCO3- resorption
    • CD: HCO3- generation & H+ excretion
  • H+ in the urine is buffered by urinary buffers:
    • Titratable acids: phosphate (HPO4-, H2PO4)
    • Ammonia (NH3, NH4+)
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11
Q

Acid-Base Equilibrium

Acid-Base Principles

A

CO2 + H2O <–> HCO3- + H+
* H+: determines pH
* HCO3-: maintained by kidneys, metabolism
* Low HCO3- –> high H+ (low pH)
* High HCO3- –> low H+ (high pH)
* CO2: maintained by lungs
* Low CO2 –> low H+ (high pH)
* High CO2 –> high H+ (low pH)

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12
Q

Henderson-Hasselbalch Equation

Acid-Base Principles

A

pH = 6.1 + log [HCO3-] / (0.03 x pCO2)

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13
Q

Normal Values

Acid-Base Equilibrium

A
  • Normal HCO3- = 26 mEq/L
  • Normal pCO2 = 40 mm Hg
  • Normal pH = 7.4
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14
Q
  • Hyperventilation
    • Kussmaul breathing
  • Depression of myocardial contractility
    • Decreased CO
  • Cerebral vasodilation
    • Increased cerebral blood flow (CBF)
    • Increased intracranial pressure (ICP)
  • CNS depression
    • Due to high CO2 levels
  • Hyperkalemia
    • Shifts H+ into cells in exchange for K+
  • Shift in Hgb dissociation curve
    • Bohr effect
    • Low pH leads to greater O2 dissociation

Symptoms

A

Acidosis

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15
Q
  • Inhibition of respiratory drive
  • Depression of myocardial contractility
  • Cerebral vasoconstriction
    • Decreased CBF
  • Hypokalemia
    • Shifts K+ into cells in exchange for H+
  • Shit in Hgb dissociation curve

Symptoms

A

Alkalosis

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16
Q

Approach to Acid-Base Problems

Acid-Base Principles

A
  1. Check the pH
  2. Check HCO3- & pCO2
  3. Determine acid-base disorder
  4. Calculate anion gap (metabolic acidosis only)
  5. Check for mixed disorders
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17
Q

Step 1: Check the pH

Approach to Acid-Base Problems

A

pH < 7.4 = acidosis

pH > 7.4 = alkalosis

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18
Q

Step 2: Check HCO3- & pCO2

Approach to Acid-Base Problems

A

HCO3-: venipuncture; normal = 26 mEq/L
CO2: ABG; normal = 40 mm Hg

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19
Q

Step 3: Determine acid-base disorder

Approach to Acid-Base Problems

A
  • Acidosis + low HCO3- = metabolic acidosis
  • Acidosis + high pCO2 = respiratory acidosis
  • Alkalosis + high HCO3- = metabolic alkalosis
  • Alkalosis + low pCO2 = respiratory alkalosis
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20
Q

Compensatory Changes

Acid-Base Disorders

A
  • Metabolic acidosis: pH < 7.4; low HCO3-
    • Compensation: decrease pCO2
  • Metabolic alkalosis: pH > 7.4; high HCO3-
    • Compensation: increase pCO2
  • Respiratory acidosis: pH < 7.4; high pCO2
    • Compensation: increase HCO3-
  • Respiratory alkalosis: pH > 7.4; low pCO2
    • Compensation: decrease HCO3-
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21
Q

Respiratory Compensation

Acid-Base Disorders

A

Changes pCO2 to compensate for metabolic disorders
- Metabolic acidosis –> Hyperventilation
- Blows off CO2 –> pCO2 decreases
- Less H+ in blood –> pH rises
- Metabolic alkalosis –> Hypoventilation
- Retains CO2 –> pCO2 increases
- More H+ in blood –> pH falls

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22
Q

Metabolic Compensation

Acid-Base Disorders

A

Changes HCO3- to compensate for respiratory disorders
* Respiratory acidosis –> HCO3- resorption
* Bicarbonate is reabsorbed
* Excess H+ is filtered / secreted into nephron
* Urinary buffers are excreted = H+ is excreted
* Respiratory alkalosis –> HCO3- secretion
* Reverse of acidosis

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23
Q

Mixed Disorders

Acid-Base Disorders

A
  • 2 concurrent acid-base disorders
    • Metabolic acidosis & respiratory alkalosis / acidosis
    • Metabolic acidosis & metabolic alkalosis
    • 2 metabolic acidoses
  • Determined expected compensatory response to assess for mixed disorders
    • Expected HCO3- for respiratory disorder
    • Expected CO2 for metabolic disorder
    • Use renal formulas to determine expected response
  • 2nd disorder is present if actual response does not equal expected response
    • Body cannot compensate to normal pH
      • If pH = 7.4 in context of acid-base disorder, mixed disorder is likely
    • If actual (A) does not equal expected (X), determine abnormality
      • CO2 > X: 2nd respiratory acidosis
      • CO2 < X: 2nd respiratory alkalosis
      • HCO3- < X: 2nd metabolic acidosis
      • HCO3- > X: 2nd metabolic alkalosis
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24
Q

Metabolic Acidosis Compensation

Mixed Acid-Base Disorders

A

Compensatory respiratory alkalosis
* Hyperventilation: decreased pCO2
* Winter’s formula: calculates expected pCO2

pCO2 = 1.5 x ([HCO3-]) + 8 =/-2
- If actual pCO2 does not equal expected, mixed disorder is present

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25
Q

Metabolic Alkalosis Compensation

Mixed Acid-Base Disorders

A

Compensatory respiratory alkalosis
* Hypoventilation: increased pCO2

Change in pCO2 = 0.7 x Change in [HCO3-]
* 0.7 mm Hg increase in pCO2 per 1.0 mEq/L increase in [HCO3-]
* If actual pCO2 does not equal expected, mixed disorder is present

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26
Q

Respiratory Acidosis Compensation

Mixed Disorders

A

Acute compensation
* Occurs in minutes
* Intracellular buffers (Hgb) raise [HCO3-]
* Small pH increase
* 1 mEq/L increase in [HCO3-] per 10 mm Hg increase in pCO2
* Change in [HCO3-] = Change in pCO2 / 10

Chronic compensation
* Occurs in days
* Renal generation of [HCO3-]
* Larger pH increase
* 3.5 mEq/L increase in [HCO3-] per 10 mm Hg increase in pCO2
* Change in [HCO3-] = 3.5 x (Change in pCO2 / 10)

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27
Q

Respiratory Alkalosis Compensation

Mixed Disorders

A

Acute compensation
* 2 mEq/L decrease in [HCO3-] per 10 mm Hg decrease in pCO2
* Change in [HCO3-] = 2 x (Change in pCO2 / 10)

Chronic compensation
* 4 mEq/L decrease in [HCO3-] per 10 mm Hg decrease in pCO2
* Change in [HCO3-] = 4 x (Change in pCO2 / 10)

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28
Q

Compensation Timeframe

Acid-Base Disorder

A
  • Respiratory compensation to metabolic disorders
    • Rapid: within minutes
    • Change in respiratory rate
  • Metabolic compensation to respiratory disorders
    • Acute: cells; mild compensation in minutes
    • Chronic: kidneys; compensation in days
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29
Q

Caused by hyperventilation
* Pain
* Early high altitude exposure
* Early aspirin overdose

Etiology

A

Respiratory Alkalosis

pH > 7.4; pCO2 < 40 m Hg

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30
Q

High Altitude

Respiratory Alkalosis

A

Lower atmospheric pressure –> lower pO2
* Hypoxia –> hyperventilation
* pCO2 decreases –> pH rises
* Respiratory alkalosis
* After 24-48 hours, kidneys will excrete HCO3-
* pH will fall back toward normal
* Ventilation rate will decrease
* Acetazolamide can augment HCO3- excretion

Acetazolamide: CA inhibitor; sometimes given to those at high altitudes

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31
Q

Aspirin Overdose

Acid-Base Disorder

A

2 acid-base disorders
* Shortly after ingestion: respiratory alkalosis
* Salicylates stimulate medulla
* Respiratory control center
* Hyperventilation –> pCO2 decreases
* pH rises
* Hours after ingestion: AG metabolic acidosis
* Salicylates decreases lipolysis, uncouple oxidative phosphorylation
* Inhibits TCA cycle
* Accumulation of pyruvate, lactate, ketoacids
* pH falls

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32
Q

Aspirin Overdose

Presentation

A
  • pH: variable due to mixed disorder
    • Can be acidotic, alkalotic, or normal
    • Acidotic patient: actual pCO2 will be lower than expected compensatory pCO2
  • pCO2: low due to hyperventilation
  • HCO3-: low due to accumulation of acids
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33
Q

Caused by hypoventilation
* Lung disease
* COPD
* Pneumonia
* Asthma
* Narcotics
* Respiratory muscle weakness
* Myasthenia gravis
* ALS
* Guillain-Barre syndrome
* Muscular dystrophy

Etiology

A

Respiratory Acidosis

pH < 7.4; pCO2 > 40 mm Hg

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34
Q

Hypercapnia

Respiratory Acidosis

A
  • Hypercapnia can affect CNS system
  • Most patients with acute high pCO2 are agitated
  • Some have depressed consciousness (CO2 narcosis)
  • Altered mental status in patient with respiratory disease:
    • Consider high pCO2
    • Check ABG
    • If pCO2 is high –> ventilation
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35
Q
  • ECV contraction
  • Hypokalemia
  • Diuretics
  • Vomiting
  • Hyperaldosteronism
  • Antacid use

Etiology

A

Metabolic Alkalosis
- Loss of H+ or gain of HCO3-

pH > 7.4; HCO3- > 26 mEq/L

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36
Q

Contraction Alkalosis

Respiratory Alkalosis

A

Low ECV –> RAAS activation
* Ang II stimulates Na+/H+ exchanger in PCT
* Increases Na+ resorption
* Increases H+ secretion
* H+ secretion increases HCO3- resorption in PCT
* Aldosterone increased H+ secretion in CD

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37
Q

Hypokalemia

Metabolic Alkalosis

A

K+ can exchange with H+ to shift in & out of cells
* Low serum K+ –> K+ shifts out –> H+ shifts in
* Hypokalemia –> alkalosis (vice versa)

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38
Q

Diuretics

Metabolic Alkalosis

A

Loop & TZ diuretics –> metabolic alkalosis
* Volume contraction
* Decreased Na+/H2O resorption
* Hypokalemia
* Increased Na+ delivery to CD
* Increased Na+ resorption, K+ & H+ secretion

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39
Q

Bartter & Gitelman Syndromes

Metabolic Alkalosis

A

Congenital disorders
* Bartter syndrome
* Defective NKCC in TAL of Loop of Henle
* Similar to loop diuretic: non-functional NKCC
* Gitelman syndrome
* Defective NCC in distal tubule
* Similar to TZ diuretic: non-functional NCC
* Both cause hypokalemia & alkalosis
* Defective NKCC: no Na+ resorption in TAL
* Defective NCC: no Na+ resorption in DT
* Both increase Na+ delivery to CD
* Increase Na+ resorption, K+ & H+ secretion

NKCC: Na-K-Cl channel; NCC: Na/Cl cotransporter

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40
Q

Vomiting

Metabolic Alkalosis

A
  • Loss of ECV –> contraction alkalosis
  • Loss of HCl
    • Results in increased HCl production
    • HCO3- is generated during HCl production
  • Loss of K+
  • Low urine [Cl]
41
Q

Urinary Chloride

Metabolic Alkalosis

A

Useful measurement in alkalosis of unknown cause
* Low (< 10-20) in vomiting
* Loss of Cl in gastric secretions
* High (>20) in many other causes of alkalosis

42
Q
  • Adrenal hyperplasia
  • Adrenal adenoma (Conn’s syndrome)

Etiology

A

Hyperaldosteronism

43
Q

Hyperaldosteronism

Metabolic Alkalosis

A

Aldosterone increases Na+ reabsorption, K+ & H+ secretion in CD
* Excess H+ & K+ secretion
* Results in alkalosis & hypokalemia
* Excess Na+ & H2O resorption
* Results in resistant HTN

Patient with resistant HTN & hypokalemia –> consider hyperaldosteronism

44
Q

Aldosterone Escape

Hyperaldosteronism

A

Pts with hyperaldosteronism often do not have edema
* Excess Na+ & H2O –> HTN
* Compensatory mechanisms are activated
* ANP secretion
* Increased Na+ & free H2O excretion
* Result: diuresis –> normal volume status
* Urinary chloride will be elevated

45
Q

Antacid Use

Metabolic Alkalosis

A

Milk-Alkali syndrome
* Excessive intake of:
* Calcium
* Alkali (base)
* Usually calcium carbonate and/or milk
* Often taken for dyspepsia
* Hypercalcemia –> results in volume contraction
* Inhibition of NKCC in TAL
* Blocks ADH-dependent H2O resorption in CD
* Volume contraction + alkali intake = alkalosis

46
Q

Metabolic Alkalosis

Treatment

A

IV Fluid Administration
* Resolves most forms of metabolic alkalosis
* “Fluid responsive” forms of metabolic alkalosis
* Diuretic use
* Vomiting
* Contraction alkalosis
* Exceptions: hyperaldosteronism, hypokalemia

47
Q

Chem 7

Acid-Base Disorders

A
  1. Na+: 140 mEq/L
  2. K+: 4.5 mEq/L
  3. Cl-: 100 mEq/L
  4. HCO3-: 24 mEq/L
  5. BUN: 15 mg/dL
  6. Creatinine: 1.2 mg/dL
  7. Glucose: 100 mg/dL
48
Q

Anion Gap

Calculation

A

Anion Gap = Cations (+) - Anions (-)
* Cations (+): Na
* Anions (-): Cl & HCO3
* Cl- is often indicative of AG vs. non-AG metabolic acidosis
* High Cl- –> non-AG metabolic acidosis
* Normal / Low Cl –> AG metabolic acidosis
* Anion Gap: Na - (Cl + HCO3)
* Normal: < 12 (+/- 4)
140 - (100 + 26) = 13

49
Q

Anion Gap

Metabolic Acidosis

A
  • Results from unmeasured ions
    • Cations: Ca2+, Mg2+, other minerals
    • Anions: proteins (albumin), phosphates, sulfates
  • Low anion gap
    • Can be caused by hypoalbuminemia
      • Negative albumin is primarily responsible for AG
    • Also caused by multiple myeloma
      • IgG is cationic (+)
        • Repels other cations (e.g., Na+) out of plasma
        • Draws anions (e.g,. Cl-) into plasma
      • Lowers measured (+) ions / raises measured (-) ions
        • Decreases anion gap
50
Q

Anion Gap

Significance

A

Anion gap divides metabolic acidosis causes into 2 groups
* Acidosis from primary loss of HCO3-
* Body compensates with retention of Cl-
* AG = Na - (Cl + HCO3)
* Low HCO3-
* High Cl-
* Normal anion gap
* Acidosis from primary retention of acid (i.e., ketoacids, lactic acids)
* HCO3- is consumed as buffer for non-volatile acids
* HCO3- falls without compensatory rise in Cl-
* Rise in unmeasured acids to compensate for fall in HCO3-
* AG = Na - (Cl + HCO3)
* Low HCO3-
* Normal Cl-
* Increased anion gap

51
Q

Secondary Respiratory Acid-Base Disorder

Metabolic Acidosis

A

Winter’s Formula
pCO2 = 1.5 x [HCO3-] + (8 +/- 2)
* Acidosis –> compensatory respiratory alkalosis
* Hyperventilation –> decreased pCO2
* WF calculates expected compensatory pCO2
* 2nd respiratory disorder if actual is not equal to expected
* Check WF for all metabolic acidoses

52
Q

Secondary Metabolic Acid-Base Disorder

Metabolic Acidosis

A

Delta Ratio (DD)
* Used to evaluate potential 2nd metabolic acid-base disorder
* Applies only to AG metabolic acidoses
* Increase in AG should be consistent w/ decrease in HCO3-
* Change in AG: AG - 12
* Change in HCO3-: 24 - [HCO3-]
* DD = Change in AG / Change in HCO3-
* DD 1-2 = normal
* DD <1 = secondary non-AG metabolic acidosis
* HCO3- is too low
* DD >2 = secondary or preexisting metabolic alkalosis
* HCO3- is too high

53
Q
  1. Diarrhea
  2. Addison’s disease
  3. Acetazolamide use
  4. Spironolactone use
  5. Saline infusion
  6. Hyperalimentation
  7. Renal tubular acidosis (RTA)

Etiology

A

Non-AG Metabolic Acidosis

54
Q

Diarrhea

Non-AG Metabolic Acidosis

A

HCO3- is lost in stool
* Low HCO3- –> acidosis
* Compensatory Cl- retention –> no AG

55
Q

Acetazolamide

Non-AG Metabolic Acidosis

A

Blocks formation & resorption of HCO3- in PCT
* Acetazolamide = CA inhibitor
* Low HCO3- –> acidosis
* Compensatory Cl- retention –> no AG

56
Q

Addison’s disease

Non-AG Metabolic Acidosis

A

Loss of aldosterone effects (hypoaldosteronism)
* Decreased H+ secretion in CD
* Increased serum H+ –> acidosis

57
Q

Spironolactone

Non-AG Metabolic Acidosis

A

Loss of aldosterone effects
- Spironolactone = aldosterone receptor blocker
- Decreased H+ excretion in CD
- Increased H+ –> acidosis

58
Q

Saline Infusion

Non-AG Metabolic Acidosis

A

Suppresses RAAS activity
* Decreased aldosterone –> reduced H+ secretion in CD
* Increased serum H+ –> acidosis

59
Q

Hyperalimentation

Non-AG Metabolic Acidosis

A

Metabolism of nutrients creates HCL
* Increase serum H+ –> acidosis

60
Q
  1. Methanol
  2. Uremia
  3. Diabetic ketoacidosis (DKA)
  4. Propylene glycol
  5. Iron tablets / Isoniazid (INH)
  6. Lactic acidosis
  7. Ethylene glycol
  8. Salicylates (aspirin)

Etiology

A

AG Metabolic Acidosis

Mnemonic: MUDPILES

61
Q

Methanol

AG Metabolic Acidosis

A
  • Metabolized to formic acid
  • Neurotoxic: visual loss, coma
  • Found in antifreeze, de-icing solutions, windshield wiper fluid, solvents, cleaners, fuels, industrial products
62
Q
  • Suspected ingestion: accidental, suicide, alcoholic
  • Confusion (may appear inebriated)
  • Visual symptoms
  • High AG metabolic acidosis

Presentation

A

Methanol Toxicity

63
Q

Methanol Toxicity

Treatment

A

Inhibit alcohol dehydrogenase
* Blocks bioactivation of parent alcohol to toxic metabolite
* Fomepizole
* Ethanol

64
Q

Ethylene Glycol

AG Metabolic Acidosis

A
  • Metabolized to glycolate & oxalate
  • Both are nephrotoxic (slow excretion)
    • Glycolate: toxic to renal tubules
    • Oxalate: precipitates calcium oxalate crystals in tubules
  • Found in antifreeze, solvents, cleaners, etc.
65
Q
  • Suspected ingestion: accidental, suicide, alcoholic
  • Sx of acute renal failure: flank pain, oliguria, anorexia
  • High AG metabolic acidosis

Presentation

A

Ethylene Glycol Toxicity

66
Q

Ethylene Glycol Toxicity

Treatment

A

Inhibit alcohol dehydrogenase
* Blocks bioactivation of parent alcohol to toxic metabolite
* Fomepizole (Antizol)
* Ethanol

67
Q

Propylene Glycol

AG Metabolic Acidosis

A
  • Metabolized to pyruvic acid, acetic acid, lactic acid
    • High AG metabolic acidosis from lactate
  • Many adverse effects:
    • Hemolysis
    • Seizure, coma, multisystem organ failure
  • Main clinical feature of overdose: CNS depression
    • No visual symptoms or nephrotoxicity
  • Found in antifreeze
  • Used as solvent for IV benzodiazepines
68
Q

Uremia

AG Metabolic Acidosis

A
  • Early kidney disease –> non-AG metabolic acidosis
    • Loss of tubule function: impaired Na+/H+ exchanger
      • Reduced H+ excretion
      • increased HCO3- excretion
      • Cl- retention to balance charge –> normal AG
  • Advanced kidney disease –> AG metabolic acidosis
    • Kidneys cannot excrete organic acids: phosphates, sulfates
    • Retention of non-volatile acids –> AG
69
Q

Diabetic Ketoacidosis (DKA)

AG Metabolic Acidosis

A
  • Usually occurs in type 1 diabetics
  • Insulin requirements rise but cannot be met
    * Often triggered by infection
  • Fatty acid metabolism –> production of ketone bodies
    • Beta-hydroxybutyrate, acetoacetate
    • Accumulation of ketones –> AG acidosis
70
Q
  • Polyuria, polydipsia
  • Abdominal symptoms: pain, nausea, vomiting
  • Kussmaul respirations: deep, rapid breathing
  • High AG metabolic acidosis

Presentation

A

DKA

Glycosuria: increased urine [glucose] causes osmotic diuresis

71
Q

DKA

Treatment

A
  • Insulin –> lower serum glucose
  • IV fluids –> hydration
  • Potassium –> correct hypokalemia
72
Q

Lactic Acidosis

AG Metabolic Acidosis

A
  • Low tissue oxygen delivery
  • Pyruvate converted to lactate (anaerobic respiration)
    • High serum lactate (>4.0 mmol/L) –> lactic acidosis
    • Lactate = unmeasured anion –> AG metabolic acidosis
73
Q
  • Shock (decreased tissue perfusion)
  • Ischemic bowel
  • Metformin therapy (especially with renal failure)
  • Seizures
  • Exercise

Etiology

A

Lactic Acidosis

AG Metabolic Acidosis

74
Q

Iron

AG Metabolic Acidosis

A
  • Acute iron poisioning
  • Initial GI phase:
    • Abdominal pain
    • Direct toxic effects on GI tract
  • Later (24 hours):
    • Cardiovascular toxicity: shock, tachycardia, hypotension
    • Coagulopathy: inhibition of thrombin formation / activity
    • Hepatotoxicity: worsening coagulopathy
    • Acute lung injury
  • Weeks later: bowel obstruction
    • Scarring at gastric outlet where iron accumulates
  • AG metabolic acidosis
    • From ferric irons = unmeasured anions
    • Also hypotension –> hypoperfusion –> lactic acidosis
75
Q

Isoniazid (INH)

AG Metabolic Acidosis

A
  • TB antibiotic
  • Acute overdose causes seizures (status epilepticus)
    • Seizures cause lactic acidosis = AG metabolic acidosis
76
Q

Renal Tubular Acidosis (RTA)

Non-AG Metabolic Acidosis

A

Rare disorders of nephron ion channels
* All cause non-AG metabolic acidosis
* Often present with low HCO3- or abnormal K+
* Many patients are asymptomatic

77
Q

Type 1 (Distal) RTA

Non-AG Metabolic Acidosis

A

Distal nephron cannot acidify urine
* Impaired H+ excretion -> acidosis; alkaline urine
* Alkaline urine –> precipitates kidney stones
* Urine should be acidic in metabolic acidosis as kidneys try to remove excess H+ from serum
* Bilateral kidney stones = suggestive of type 1 RTA
* Acidosis
* Stimulates Ca2+ resorption from bone
* Bone demineralization –> Rickets; growth failure
* Suppresses Ca2+ resorption in kidneys
* Results in elevated urine [Ca2+]
* Impaired K+ resorption –> hypokalemia
* Impaired H+ secretion causes buildup of negative charge
* Negative charge holds K+ in the urine
* Results in increased K+ excretion

78
Q
  • Labs
    • HCO3-: very low (< 10 mEq/L)
    • Urine pH: high (pH > 5.5)
    • Urine Ca2+: elevated
  • Symptoms
    • Adults: chronic kidney stones; Rickets
    • Children: growth failure

Clinical Features

A

Type I (Distal) RTA

Diagnosis established if alkaline urine (pH > 5.5) w/ metabolic acidosis

79
Q

Associated with autoimmune diseases
* Sjögren’s syndrome
* Rheumatoid arthritis

Etiology

A

Type 1 (Distal) RTA

80
Q

Associated with amphotericin B use

Etiology

A

Type 1 (Distal) RTA

81
Q
  • Patient with Sjögren’s disease / rheumatoid arthritis
  • Recurrent bilateral kidney stones
  • Serum: very low [HCO3-] < 10 mEq/L; hypokalemia
  • Urine: high pH > 5.5; UAG = +
    • Ammonia challenge: pH remains high

Presentation

A

Type I (Distal) RTA

82
Q

Type I (Distal) RTA

Treatment

A

Sodium bicarbonate

83
Q

Urine Anion Gap (UAG)

Non-AG Metabolic Acidosis

A

Measurement used to distinguish types of RTA
* In acidosis, high [NH4] is excreted –> removes H+
* NH4+ cannot be measured directly
* UAG: Na + K - Cl –> estimates [NH4]
* NH4+ excreted in urine draws Cl- with it
* UAG becomes negative when acid is being excreted
* Increased urine H+ = increased NH4+ = increased Cl-

84
Q

Type II RTA

UAG

A

UAG = (-)
* Functional CD intercalated cells –> H+ secretion is intact
* Acidosis –> increased excretion of NH4+ & Cl-
* Urine [Cl-] increases

85
Q

Type I RTA

UAG

A

UAG = (+)
* Defective CD intercalated cells: impaired H+ secretion
* Excretion of NH4+ & Cl- does not increase despite acidosis
* Normal urine [Cl-]

86
Q

Ammonia Challenge

RTA

A

Administer NH4Cl to patient
* Acid load should lower pH
* Distal RTA: urine pH remains >5.3

87
Q

Type II (Proximal) RTA

Non-AG Metabolic Acidosis

A

Defect in proximal tubule HCO3- resorption

88
Q

Type II (Proximal) RTA

Non-AG Metabolic Acidosis

A

Defect in proximal tubule HCO3- resorption
* Urine pH < 5.5
* Initially, pH may be high due to excess HCO3- excretion
* Once acidosis develops, distal tubule secretes H+
* Increased H+ excretion –> acidic urine
* Increased NH4+ & Cl- excretion –> (-) UAG
* Hypokalemia
* Loss of HCO3- resorption –> osmotic diuresis
* Volume contraction –> RAAS activation
* Aldosterone –> increased K+ secretion in CD
* Increased K+ excretion –> hypokalemia

89
Q
  • Labs
    • HCO3-: low to normal (12-20 mEq/L)
  • Symptoms
    • No kidney stones

Clinical Features

A

Type II (Proximal) RTA

90
Q

Associated with Fanconi’s syndrome

Etiology

A

Type II (Proximal) RTA

Fanconi’s syndrome: generalized proximal tubule failure

91
Q
  • Asymptomatic: routine blood work
  • Mild weakness
  • Serum: mildly reduced [HCO3] = 10-20 mEq/L; hypokalemia
  • Urine: low pH < 5.5

Presentation

A

Type II (Proximal) RTA

92
Q

Type II (Proximal) RTA

Treatment

A

Sodium bicarbonate

93
Q

Type IV RTA

Non-AG Metabolic Acidosis

A

Loss of aldosterone effects on collecting ducts
* Impaired K+ secretion by prinicipal cells -> increased K+ retention
* Only RTA with hyperkalemia
* Impaired H+ excretion–> acidosis
* Impaired H+ secretion by intercalated cells
* Impaired NH3 secretion
* Hyperkalemia causes rise in pH of PCT cells
* K+ shifts into cells, H+ shifts out of cells
* High pH inhibits NH3 synthesis in PCT cells
* Decreased NH4 excretion = decreased H+ excretion
* Urine pH usually remains low (pH < 5.4)
* Distinguishes Type IV RTA from Type I RTA (high pH)

94
Q

Hypoaldosteronism
1. Aldosterone deficiency
2. Aldosterone resistance

Etiology

A

Type IV RTA

95
Q

Hypoaldosteronism
1. Aldosterone deficiency
2. Aldosterone resistance

Etiology

A

Type IV RTA

96
Q

Decreased Aldosterone

Etiology

A
  1. Diabetic renal disease: decreased renin release –> impaired RAAS
  2. ACEi / ARB: disrupted RAAS –> impaired aldosterone production
  3. NSAIDs: impaired aldosterone production
  4. Adrenal insufficiency: impaired aldosterone production
97
Q

Aldosterone Resistance

Etiology

A
  1. K+-sparing diuretics: block aldosterone receptors
  2. TMP / SMX (antibiotic): blocks aldosterone
98
Q
  • Diabetic patient with renal insufficiency
  • Unexplained hyperkalemia

Presentation

A

Type IV RTA

99
Q

Type IV RTA

Treatment

A

Fludrocortisone

Mineralocorticoid: effects similar to aldosterone

GU / GYN & Renal (23 decks)

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