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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
Metabolic Alkalosis Compensation | Mixed Acid-Base Disorders
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
26
Respiratory Acidosis Compensation | Mixed Disorders
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)
27
Respiratory Alkalosis Compensation | Mixed Disorders
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)
28
Compensation Timeframe | Acid-Base Disorder
* 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
29
Caused by hyperventilation * Pain * Early high altitude exposure * Early aspirin overdose | Etiology
Respiratory Alkalosis | pH > 7.4; pCO2 < 40 m Hg
30
High Altitude | Respiratory Alkalosis
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
31
Aspirin Overdose | Acid-Base Disorder
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
32
Aspirin Overdose | Presentation
* 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
33
Caused by hypoventilation * Lung disease * COPD * Pneumonia * Asthma * Narcotics * Respiratory muscle weakness * Myasthenia gravis * ALS * Guillain-Barre syndrome * Muscular dystrophy | Etiology
Respiratory Acidosis | pH < 7.4; pCO2 > 40 mm Hg
34
Hypercapnia | Respiratory Acidosis
* 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
35
* ECV contraction * Hypokalemia * Diuretics * Vomiting * Hyperaldosteronism * Antacid use | Etiology
Metabolic Alkalosis - Loss of H+ or gain of HCO3- | pH > 7.4; HCO3- > 26 mEq/L
36
Contraction Alkalosis | Respiratory Alkalosis
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
37
Hypokalemia | Metabolic Alkalosis
K+ can exchange with H+ to shift in & out of cells * Low serum K+ --> K+ shifts out --> H+ shifts in * Hypokalemia --> alkalosis (vice versa)
38
Diuretics | Metabolic Alkalosis
Loop & TZ diuretics --> metabolic alkalosis * Volume contraction * Decreased Na+/H2O resorption * Hypokalemia * Increased Na+ delivery to CD * Increased Na+ resorption, K+ & H+ secretion
39
Bartter & Gitelman Syndromes | Metabolic Alkalosis
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
40
Vomiting | Metabolic Alkalosis
* 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
Urinary Chloride | Metabolic Alkalosis
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
* Adrenal hyperplasia * Adrenal adenoma (Conn's syndrome) | Etiology
Hyperaldosteronism
43
Hyperaldosteronism | Metabolic Alkalosis
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
Aldosterone Escape | Hyperaldosteronism
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
Antacid Use | Metabolic Alkalosis
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
Metabolic Alkalosis | Treatment
IV Fluid Administration * Resolves most forms of metabolic alkalosis * "Fluid responsive" forms of metabolic alkalosis * Diuretic use * Vomiting * Contraction alkalosis * Exceptions: hyperaldosteronism, hypokalemia
47
Chem 7 | Acid-Base Disorders
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
Anion Gap | Calculation
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
Anion Gap | Metabolic Acidosis
* 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
Anion Gap | Significance
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
Secondary Respiratory Acid-Base Disorder | Metabolic Acidosis
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
Secondary Metabolic Acid-Base Disorder | Metabolic Acidosis
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
1. Diarrhea 2. Addison's disease 3. Acetazolamide use 4. Spironolactone use 5. Saline infusion 6. Hyperalimentation 7. Renal tubular acidosis (RTA) | Etiology
Non-AG Metabolic Acidosis
54
Diarrhea | Non-AG Metabolic Acidosis
HCO3- is lost in stool * Low HCO3- --> acidosis * Compensatory Cl- retention --> no AG
55
Acetazolamide | Non-AG Metabolic Acidosis
Blocks formation & resorption of HCO3- in PCT * Acetazolamide = CA inhibitor * Low HCO3- --> acidosis * Compensatory Cl- retention --> no AG
56
Addison's disease | Non-AG Metabolic Acidosis
Loss of aldosterone effects (hypoaldosteronism) * Decreased H+ secretion in CD * Increased serum H+ --> acidosis
57
Spironolactone | Non-AG Metabolic Acidosis
Loss of aldosterone effects - Spironolactone = aldosterone receptor blocker - Decreased H+ excretion in CD - Increased H+ --> acidosis
58
Saline Infusion | Non-AG Metabolic Acidosis
Suppresses RAAS activity * Decreased aldosterone --> reduced H+ secretion in CD * Increased serum H+ --> acidosis
59
Hyperalimentation | Non-AG Metabolic Acidosis
Metabolism of nutrients creates HCL * Increase serum H+ --> acidosis
60
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
AG Metabolic Acidosis | Mnemonic: MUDPILES
61
Methanol | AG Metabolic Acidosis
* Metabolized to formic acid * Neurotoxic: visual loss, coma * Found in antifreeze, de-icing solutions, windshield wiper fluid, solvents, cleaners, fuels, industrial products
62
* Suspected ingestion: accidental, suicide, alcoholic * Confusion (may appear inebriated) * Visual symptoms * High AG metabolic acidosis | Presentation
Methanol Toxicity
63
Methanol Toxicity | Treatment
Inhibit alcohol dehydrogenase * Blocks bioactivation of parent alcohol to toxic metabolite * Fomepizole * Ethanol
64
Ethylene Glycol | AG Metabolic Acidosis
* 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
* Suspected ingestion: accidental, suicide, alcoholic * Sx of acute renal failure: flank pain, oliguria, anorexia * High AG metabolic acidosis | Presentation
Ethylene Glycol Toxicity
66
Ethylene Glycol Toxicity | Treatment
Inhibit alcohol dehydrogenase * Blocks bioactivation of parent alcohol to toxic metabolite * Fomepizole (Antizol) * Ethanol
67
Propylene Glycol | AG Metabolic Acidosis
* 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
Uremia | AG Metabolic Acidosis
* 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
Diabetic Ketoacidosis (DKA) | AG Metabolic Acidosis
* 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
* Polyuria, polydipsia * Abdominal symptoms: pain, nausea, vomiting * Kussmaul respirations: deep, rapid breathing * High AG metabolic acidosis | Presentation
DKA | Glycosuria: increased urine [glucose] causes osmotic diuresis
71
DKA | Treatment
* Insulin --> lower serum glucose * IV fluids --> hydration * Potassium --> correct hypokalemia
72
Lactic Acidosis | AG Metabolic Acidosis
* 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
* Shock (decreased tissue perfusion) * Ischemic bowel * Metformin therapy (especially with renal failure) * Seizures * Exercise | Etiology
Lactic Acidosis | AG Metabolic Acidosis
74
Iron | AG Metabolic Acidosis
* 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
Isoniazid (INH) | AG Metabolic Acidosis
* TB antibiotic * Acute overdose causes seizures (status epilepticus) * Seizures cause lactic acidosis = AG metabolic acidosis
76
Renal Tubular Acidosis (RTA) | Non-AG Metabolic Acidosis
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
Type 1 (Distal) RTA | Non-AG Metabolic Acidosis
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
* 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
Type I (Distal) RTA | Diagnosis established if alkaline urine (pH > 5.5) w/ metabolic acidosis
79
Associated with autoimmune diseases * Sjögren's syndrome * Rheumatoid arthritis | Etiology
Type 1 (Distal) RTA
80
Associated with amphotericin B use | Etiology
Type 1 (Distal) RTA
81
* 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
Type I (Distal) RTA
82
Type I (Distal) RTA | Treatment
Sodium bicarbonate
83
Urine Anion Gap (UAG) | Non-AG Metabolic Acidosis
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
Type II RTA | UAG
UAG = (-) * Functional CD intercalated cells --> H+ secretion is intact * Acidosis --> increased excretion of NH4+ & Cl- * Urine [Cl-] increases
85
Type I RTA | UAG
UAG = (+) * Defective CD intercalated cells: impaired H+ secretion * Excretion of NH4+ & Cl- does not increase despite acidosis * Normal urine [Cl-]
86
Ammonia Challenge | RTA
Administer NH4Cl to patient * Acid load should lower pH * Distal RTA: urine pH remains >5.3
87
Type II (Proximal) RTA | Non-AG Metabolic Acidosis
Defect in proximal tubule HCO3- resorption
88
Type II (Proximal) RTA | Non-AG Metabolic Acidosis
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
* Labs * HCO3-: low to normal (12-20 mEq/L) * Symptoms * No kidney stones | Clinical Features
Type II (Proximal) RTA
90
Associated with Fanconi's syndrome | Etiology
Type II (Proximal) RTA | Fanconi's syndrome: generalized proximal tubule failure
91
* Asymptomatic: routine blood work * Mild weakness * Serum: mildly reduced [HCO3] = 10-20 mEq/L; hypokalemia * Urine: low pH < 5.5 | Presentation
Type II (Proximal) RTA
92
Type II (Proximal) RTA | Treatment
Sodium bicarbonate
93
Type IV RTA | Non-AG Metabolic Acidosis
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
Hypoaldosteronism 1. Aldosterone deficiency 2. Aldosterone resistance | Etiology
Type IV RTA
95
Hypoaldosteronism 1. Aldosterone deficiency 2. Aldosterone resistance | Etiology
Type IV RTA
96
Decreased Aldosterone | Etiology
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
Aldosterone Resistance | Etiology
1. K+-sparing diuretics: block aldosterone receptors 2. TMP / SMX (antibiotic): blocks aldosterone
98
* Diabetic patient with renal insufficiency * Unexplained hyperkalemia | Presentation
Type IV RTA
99
Type IV RTA | Treatment
Fludrocortisone | Mineralocorticoid: effects similar to aldosterone

GU / GYN & Renal (23 decks)

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