Step I primary hyperPTH

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goljan RR pg. 505

I dont understand the lab findings of primary hyperparathyroidism. There is normal anion gap metabolic acidosis due to decreased proximal tubule reclamation of bicarbonate and type II renal tubular acidosis.

Why does primary hyperparathyroidism (increased PTH, increased calcium, decreased phosphorus) result in decreased reclamation of bicarb?

i don't get it. PLEASE explain!
 
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If you reason it out:

PTH promotes phospate excretion. With phospate excretion, H+ is excreted too in the form of H2PO4. So the H+ decreases, meaning more alkalosis occurs. How does the body compensate? By excreting more HCO3-.
 
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