Renal acid-base disorders
Card Set Information
Renal acid-base disorders
Acid-base disorders of renal origin
Define uremic acidosis
Renal tubular acidosis + failure to filter food-derived acids (phosphate, sulfate)
T/F: Renal tubular acidoses (RTAs) result in increased anion gap
F – for every bicarb you lose, you pick up a chloride
Fanconi’s Syndrome can result in what type of RTA?
What is the general defect in proximal RTAs?
Defective bicarb reclamation
Obstruction leading to urine reflux into the collecting duct can result in what type of RTA?
T/F: Defective bicarb generation can occur in the absence of a distal tubular defect
T – could be a problem with ammoniagenesis
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 HCO
cannot be generated/reabsorbed
How does hypoaldosteronism result in a RTA?
Decreased aldosterone → decreased ammonia production and bicarb generation by the collecting duct
The luminal (urine) pH must be below [#] in order for the CD H
pump to work
T/F: RTAs are always associated with decreased renal function
F – they can be associated with normal renal function (GFR > 50 mL/min.)
T/F: Uremic acidosis is always associated with decreased renal function
T – GFR is usually less than 20 mL/min.
3 causes of proximal RTA (pRTA)
• Fanconi’s (generalized reabsorption defect) | • Defective basolateral Na
transporter | • Acetazolamide-induced defect in brush-border carbonic anhydrase
T/F: Patients with pRTA can still generate new bicarb
T – collecting duct function is intact
Why are pRTAs associated with mild hypokalmia?
• Decreased paracellular K
reabsorption in PCT | • Increased Na
reabsorption in CD → increased K
Which RTA affects bones, and how?
pRTA → demineralizing bone disease (rickets, osteomalacia) | size • Enhanced H
exchange on bone surfaces | • Decreased Vit. D production by PCT size
Pharmacological therapy for pRTAs
Potassium citrate (citrate can be metabolized to bicarb, so it increases both K
dRTAs could be caused by genetic defects in which transporters?
• Basolateral HCO
exchanger | • Apical H
ATPase or H
Classical dRTA: | • Urine pH | • Potassium status | • Rare or common? | • Urine NH
• High (> 6) | • Chronic hypokalemia | • Rare | • Low
Which RTA is a risk factor for kidney stones, and why?
dRTA → kidney stones (CaHPO
) | size • Acidosis stimulates citrate reabsorption for PCT bicarb generation → increase in free urine Ca
because it isn’t solvated by citrate | • Increased urine pH favors crystal formation size
Pharmacological therapy for dRTAs
Replenish bicarb and K
| • Replace daily H
generation (50-100 mEq)
What is the cause of Type 4 dRTA?
transport by the CD principal cells
What could cause reduced principal cell Na
transport (in Type 4 dRTA)?
• Aldosterone deficiency | • Drastically decreased distal Na
delivery to the collecting duct
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
Type 4 dRTA: | • Rare or common | • Potassium status | • Urine pH | • Urine NH
| • Treatment
• Common | • Hyperkalemia | • Low (< 5.5) | • Low | • Loop diuretics
Why does hyperkalemia develop in Type 4 dRTA and sick collecting duct syndrome?
presentation to the principal cell → decreased Na
ENaC reabsorption → decreased K
Sick collecting duct syndrome (dRTA): | • Rare or common | • Potassium status | • Urine pH | • Urine NH
| • Treatment
• Common | • Hyperkalemia | • Variable | • Low | • Bicarb
How do chronic RTAs affect calcium status?
• Osteomalacia/rickets | • Nephrolithiasis (renal stones) | • Hypercalciuria | • Muscle weakness from decreased intracellular Ca
stores in skeletal muscle
In uremic acidosis, the anion gap is [increased, decreased, or normal]
Increased anion gap in uremic acidosis results from poor filtration of [?] and [?]
sulfate and phosphate
Uremic acidosis is associated with [high, low, or normal] bicarb
Patients with a non-anion gap acidosis normally have [high, low, or normal] chloride
T/F: Patients can have a combined uremic acidosis and RTA (hyperchloremic)
T – this is very common
Uremic acidosis + RTA: | • Chloride level | • Anion gap
• High | • Increased
Normal anion gap