10-6-08 Calcium & Phosphorous Metabolism
Calcium Balance
 Intake/Absorb – consume ~1000mg of Ca++ each day, ~150mg absorbed
 ECF – most Ca++ is here, half bound (proteins, complexes), half free ions (biologically active)
 Bone Dynamics – 500mg deposited, 500mg reabsorbed each day
 Kidney Filtration – about 9000mg filtered each day, ~150mg excreted
Phosphate Balance
 Intake/Absorb – consume ~1200mg of Ca++ each day, ~800mg absorbed
 ECF/ICF – most PO4 is ECF, some ICF
 Bone Dynamics – 250mg deposited, 250mg reabsorbed each day
 Kidney Filtration – about 6000mg filtered each day, ~800mg excreted
PTH
 Parathyroid Hormone (PTH) – secreted by parathyroids (4), regulated by:
o Calcium – low serum [Ca++] stimulates PTH, (opposite inhibits)
o Calcitriol (Vit. D) – low serum [Calcitriol] stimulates PTH, (opposite inhibits)
o PO4 – high serum [PO4] stimulates PTH
 PTH Actions – more Ca++ , less PO4:
o Increased Serum [Ca++] – mobilizes from bone, kidneys reabsorb, absorb from GI
o Increased Serum [Calcitriol] – promotes synthesis in kidneys
o Decreased Serum [PO4] – stops kidney reabsorption, stops GI absorption
 Calcitriol Actions – increases both [Ca++] and [PO4]
o Activation – 7-DHC converted to cholecalciferol in skin liver 25-chole  kidney 1,25 vit D (calcitriol)
o Reabsorption from bone/GI of Ca++ and PO4
Hypercalcemia Differential Dx
 S/Sx – kidney stones, bone pain and fractures, HTN, constipation, asthenia
 Primary Hyperparathyroidism – increases serum [Ca++], increased [Calcitriol]
o Symptoms – hypercalcemia, kidney stones, bone pain/fractures, HTN
o Treatment – if serum [Ca++] < 11, monitor; if > 11, remove adenoma
 Malignancy – tumor of parathyroids, paraneoplastic syndrome, etc.
 Sarcoidosis – granulomas produce vitamin D  hypercalcemia
 Thiazide Diuretics – limit Ca++ excretion  don’t give to hypercalcemia patient (DM!)
Kidney Stones
 Calcium Oxalate – complex which can form crystals  kidney stones
 Kidney Stone Complications – pain (renal colic), hematuria, infection, obstruction, RF
 Kidney Stone Diet – you are more likely to have kidney stones if you have lower Ca++ intake!
o High Ca++ intake  keeps oxalate bound in gut, doesn’t form crystals easily here/excreted
o Low Ca++ intake  unbound oxalate is excreted by kidneys  complex w/ Ca++ in urine  stone
 Differential – idiopathic hypercalciuria, primary hyperPTH, hyperuricosuria, distal renal tubular acidosis
 Idiopathic Hypercalciuria – high levels of Ca++ in urine but not blood, no disease (1o HPTH, sarcoid)
o Kidney Stones – more likely to have them if you have idiopathic hypercalciuria
o Vitamin D – synthesized in excess, possible origin of idiopathic hypercalciuria
o Genetics – seems to be autosomal dominant disorder
o Treatment – give thiazide diuretics (increase Ca++ retention in blood), restrict Na+ intake
 Along with Na+ excretion is Ca++ excretion, thus limit Na+ excretion  limit Ca++
 Thiazides – don’t operate by this mechanism; instead Na+ excretion, Ca++ retention
o Calcium restriction? No good for Tx  will increase chances of kidney stones (oxalate)
Renal Failure & Ca/P – Renal Osterodystrophy
 Renal Failure – unable to make vitamin D, thus low [calcitriol]  low serum [Ca++], high [PO4]
 2o Hyperparathyroidism – a high [PTH] tries to correct low serum [Ca++] and high [PO4], but to no avail
o Short Run – adaptive, raises calcium, lowers PO4 in serum
o Long Run – maladaptive, bone breakdown, other toxic effects
 Acidosis – low serum Ca++  low charge? whatever?  H+ replaces in serum  acidosis
 Treatment – decrease PTH (surgery), increase Vit. D (supplement), correct [Ca] & [PO 4], no aluminum
Aluminum
 Renal Bone Disease – leads to aluminum accumulation, especially if on Al-PO4 supplements (now in disuse)
 Osteomalacia – low bone turnover, due to aluminum overload
 Osteitis Fibrosa Cystica – high bone turnover, disease instead from 1 o/2o hyper-PTH
 Clincial manisfestations – bone pain, fractures, myopathies, growth retardation, deformities, arthritis, perarticular/vascular
calcification, calciphylaxis, tendon rupture, anemia, neuropathy, impotence, asthenia, HTN
Treatment
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Goals – decrease serum PTH, increase serum calcitriol, decrease serum phosphorus, increase serum calcium, decrease
aluminum
Dietary phosphorus reduction
Phosphate binders – aluminum (not used), calcium, sevelamer (polymer binding)
Vitamin D
Parathyroidectomy
Aluminum chelation – if all else fails