Renal acid-base disorders

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Author:
yuiness
ID:
39331
Filename:
Renal acid-base disorders
Updated:
2010-10-11 15:08:17
Tags:
renal
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Description:
Acid-base disorders of renal origin
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  1. Define uremic acidosis
    Renal tubular acidosis + failure to filter food-derived acids (phosphate, sulfate)
  2. T/F: Renal tubular acidoses (RTAs) result in increased anion gap
    F – for every bicarb you lose, you pick up a chloride
  3. Fanconi’s Syndrome can result in what type of RTA?
    Proximal RTA
  4. What is the general defect in proximal RTAs?
    Defective bicarb reclamation
  5. Obstruction leading to urine reflux into the collecting duct can result in what type of RTA?
    Distal RTA
  6. T/F: Defective bicarb generation can occur in the absence of a distal tubular defect
    T – could be a problem with ammoniagenesis
  7. How does defective ammoniagenesis result in a RTA?
    Ammonia acts as a H+ trap in the collecting duct; without it, H+ cannot be secreted and therefore HCO3- cannot be generated/reabsorbed
  8. How does hypoaldosteronism result in a RTA?
    Decreased aldosterone → decreased ammonia production and bicarb generation by the collecting duct
  9. The luminal (urine) pH must be below [#] in order for the CD H+ pump to work
    4.5-5
  10. T/F: RTAs are always associated with decreased renal function
    F – they can be associated with normal renal function (GFR > 50 mL/min.)
  11. T/F: Uremic acidosis is always associated with decreased renal function
    T – GFR is usually less than 20 mL/min.
  12. 3 causes of proximal RTA (pRTA)
    • Fanconi’s (generalized reabsorption defect) | • Defective basolateral Na+/HCO3- transporter | • Acetazolamide-induced defect in brush-border carbonic anhydrase
  13. T/F: Patients with pRTA can still generate new bicarb
    T – collecting duct function is intact
  14. Why are pRTAs associated with mild hypokalmia?
    • Decreased paracellular K+ reabsorption in PCT | • Increased Na+ reabsorption in CD → increased K+ secretion
  15. Which RTA affects bones, and how?
    pRTA → demineralizing bone disease (rickets, osteomalacia) | size • Enhanced H+/Ca2+ exchange on bone surfaces | • Decreased Vit. D production by PCT size
  16. Pharmacological therapy for pRTAs
    Potassium citrate (citrate can be metabolized to bicarb, so it increases both K+ and bicarb)
  17. dRTAs could be caused by genetic defects in which transporters?
    • Basolateral HCO3-/Cl- exchanger | • Apical H+ ATPase or H+/K+ ATPase
  18. Classical dRTA: | • Urine pH | • Potassium status | • Rare or common? | • Urine NH4+
    • High (> 6) | • Chronic hypokalemia | • Rare | • Low
  19. Which RTA is a risk factor for kidney stones, and why?
    dRTA → kidney stones (CaHPO4) | size • Acidosis stimulates citrate reabsorption for PCT bicarb generation → increase in free urine Ca2+ because it isn’t solvated by citrate | • Increased urine pH favors crystal formation size
  20. Pharmacological therapy for dRTAs
    Replenish bicarb and K+ | • Replace daily H+ generation (50-100 mEq)
  21. What is the cause of Type 4 dRTA?
    Reduced Na+ transport by the CD principal cells
  22. What could cause reduced principal cell Na+ transport (in Type 4 dRTA)?
    • Aldosterone deficiency | • Drastically decreased distal Na+ delivery to the collecting duct
  23. What could cause decreased Na+ delivery to the collecting duct (in Type 4 RTA)?
    • Diabetes mellitus – poor JGA function | • ACE inhibition | • Angiotensin II receptor blockade
  24. Type 4 dRTA: | • Rare or common | • Potassium status | • Urine pH | • Urine NH4+ | • Treatment
    • Common | • Hyperkalemia | • Low (< 5.5) | • Low | • Loop diuretics
  25. Why does hyperkalemia develop in Type 4 dRTA and sick collecting duct syndrome?
    Decreased Na+ presentation to the principal cell → decreased Na+ ENaC reabsorption → decreased K+ ROMK1 secretion
  26. Sick collecting duct syndrome (dRTA): | • Rare or common | • Potassium status | • Urine pH | • Urine NH4+ | • Treatment
    • Common | • Hyperkalemia | • Variable | • Low | • Bicarb
  27. How do chronic RTAs affect calcium status?
    • Osteomalacia/rickets | • Nephrolithiasis (renal stones) | • Hypercalciuria | • Muscle weakness from decreased intracellular Ca2+ stores in skeletal muscle
  28. In uremic acidosis, the anion gap is [increased, decreased, or normal]
    increased
  29. Increased anion gap in uremic acidosis results from poor filtration of [?] and [?]
    sulfate and phosphate
  30. Uremic acidosis is associated with [high, low, or normal] bicarb
    low
  31. Patients with a non-anion gap acidosis normally have [high, low, or normal] chloride
    high
  32. T/F: Patients can have a combined uremic acidosis and RTA (hyperchloremic)
    T – this is very common
  33. Uremic acidosis + RTA: | • Chloride level | • Anion gap
    • High | • Increased
  34. Normal [Cl-]
    105 mEq/L
  35. Normal [Na+]
    140 mEq/L
  36. Normal BUN
    15 mg/dL
  37. Normal anion gap
    10 mEq/L

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