ASN QBank Pearls - Mineral Bone Disease Flashcards
- bone composition shows LOW bone mass
- NORMAL primary mineralization
osteoporosis
- bone composition shows LOW bone mass
- HIGH secondary mineralization
adynamic bone disease
- bone composition shows NORMAL or INCREASED bone mass
- DECREASED secondary mineralization
- INCREASED osteoid volume
secondary hyperparathyroidism
- wide osteoid seams with significant DECREASE in the rate of mineralization
- absence of cell activity and endosteal fibrosis
- aluminum disease is frequently associated with
osteomalacia
the Endocrine Society guidelines recommend vitamin D insufficiency/deficiency for whom?
high-risk populations
tumor-induced osteomalacia (TIO) is typically caused by
benign mesenchymal tumors of vascular or skeletal origin
- abnormal bone mineralization
- increased alkaline phosphatase
- long term, osteomalacia and associated fractures
is caused by?
chronic hypophosphatemia
calcitriol levels in TIO are
LOW, despite hypophosphatemia
MOST common renal manifestation of sarcoidosis
hypercalciuria
topiramate inhibits which enzyme?
carbonic anhydrase
topiramate is a/w
- proximal RTA
- distal RTA
- calcium phosphate stones
is a/w urinary crystals and is the MCC of nephrolithiasis
atazanavir
triamterene is a/w
urinary crystals
orlistat is a/w
enteric hyperoxaluria and urinary calcium oxalate crystals
- hypotension
- hyperkalemia
- hypocalcemia
- heart block
- cardiac arrest
- at risk if AKI or CKD
hypermagnesemia
hypomagnesemia
- renal magnesium wasting
- HIGH urinary Ca2+
thick ascending limb of LOH
hypomagnesemia
- renal magnesium wasting
- LOW urinary Ca2+
early distal tubule
hypomagnesemia
- renal magnesium wasting
- normal urinary Ca2+
late distal tubule
patients who are at highest risk of hypocalcemia at initiation of cinacalcet
those with already low Ca2+
how soon after starting cinacalcet should you measure Ca2+ level?
1 week
PTH level in milk-alkali syndrome (aka Ca2+-alkali syndrome)
suppressed (LOW)
AD hypocalcemia (ADH) is commonly caused by
activating mutation of CaSR gene
majority of AD hypocalcemia (ADH) patients are asymptomatic and therefore are not diagnosed until
adulthood, when hypocalcemia is noted
- hypocalcemia
- seizures
- neuromuscular irritability during periods of stress, such as a febrile illness (may be mislabeled as febrile seizures)
symptomatic children with AD hypocalcemia (ADH)
- Ca2+ 6-8 mg/dL, but as low as 5 mg/dL
- normal/slightly low PTH
- high/high normal UCa2+ excretion (rather than expected low excretion)
- recurrent nephrolithiasis and nephrocalcinosis (worse during treatment with vitamin D and calcium supplementation)
- no previous normal serum Ca2+ values
- low Mg2+ (in some patients)
AD hypocalcemia (ADH)
how to confirm diagnosis of AD hypocalcemia (ADH)?
analysis for mutation in CaSR gene
systemic medial calcification of the arterioles that leads to ischemia and subcutaneous necrosis
calciphylaxis (calcific uremic arteriolopathy)
what factors are implicated in the genesis of calciphylaxis (calcific uremic arteriolopathy)?
- hyperparathyroidism
- active vitamin D administration
- hyperphosphatemia
- elevated Ca2+ x PO4- product
what medications have been implicated as significant risk factors for the development of calciphylaxis (calcific uremic arteriolopathy)?
- warfarin
- calcium-based binders
- vitamin D analogs
- systemic glucocorticoids
how can calciphylaxis (calcific uremic arteriolopathy) develop in the setting of warfarin use?
inhibition of vitamin K-dependent carboxylation of matrix GLA protein (MGP)
what does matrix GLA protein (MGP) normally do?
it’s a mineral-binding extracellular matrix protein that actively inhibits calcification of arteries
potential side effect of sodium thiosulfate
HAGMA
mechanism for HAGMA d/t sodium thiosulfate
unknown
key regulator of phosphate homeostasis
FGF-23
FGF-23 is produced by
bone osteocytes
FGF-23 is stimulated by rises in serum
phosphorus (in CKD)
FGF-23 acts on numerous downstream targets in an attempt to normalize serum phosphorus levels; these targets include what?
- increases PTH secretion
- decreases Na+-dependent phosphate reabsorption by the proximal tubule
- decreases 1-α hydroxylase activity
FGF-23 excess has been a/w an increased risk for
cardiovascular mortality
the use of calcium-containing phosphate binders have been shown to increase mortality in treatment of hyperphosphatemia compared to the use of?
non-calcium-containing phosphate binders
what are the physiologic processes that predispose to metastatic calcification?
- chronic metabolic acidosis leaching calcium and phosphate from bones
- severe SHPT
- intermittent metabolic alkalosis during HD that predisposing to soft tissue precipitation of calcium salt
- elevated calcium-phosphate product
treatment for calciphylaxis (calcific uremic arteriolopathy)
- sodium thiosulfate IV
- non-calcium-containing phosphate binders
- daily dialysis with low calcium dialysate
- aggressive wound care
- adequate pain control
- stop vitamin D analogs
- lower PTH < 300 with cinacalcet or parathyroidectomy
- stop IV iron
which medications for SHPT have not been shown to improve patient survival?
cinacalcet and paricalcitol
what procedure for SHPT has been shown to improve patient survival?
parathyroidectomy
should patients with CKD stages 3-5 and evidence of CKD-MBD undergo BMD testing?
NO
why shouldn’t patients with CKD stages 3-5 and evidence of CKD-MBD undergo BMD testing?
- does not predict fracture risk as it does in general population
- does not predict type of renal osteodystrophy
based on KDIGO guidelines, when should patients with CKD stages 3-5 undergo bone biopsy?
- unexplained fractures
- persistent bone pain
- unexplained hypercalcemia
- unexplained hypophosphatemia
- possible aluminum toxicity
- before giving bisphosphonates to patients with CKD-MBD
what is MOST likely to occur during the first year after a patient has a parathyroidectomy?
increase in all-cause hospitalizations; mostly d/t hypocalcemia
cinacalcet decreases PTH concentration by an average of what percentage even in patients with SHPT?
47%
what are some of the symptoms of SHPT?
- bone pain
- myopathy
- pruritus
calcimimetics such as cinacalcet work by
increase sensitivity of CaSR for calcium which upregulates the calcium-sensing and vitamin D receptors in the parathyroid gland
- short fourth and fifth metacarpals
- rounded facies
- ?AD inheritance
- a/w TSH resistance
- high PTH
- low calcitriol
- low Ca++
- high phosphate
pseudohypoparathyroidism type 1A
condition with phenotypic appearance of pseudohypoparathyroidism type 1A, but biochemically NORMAL
pseudoPSEUDOhypoparathyroidism
MCC of increased urinary Ca++ excretion w/o an apparent underlying etiology
idiopathic hypercalciuria
patients with colon resection and ileostomy can have bicarbonate loss in the ileostomy effluent which leads to formation of an acidic urine, and in addition to low urine volume puts them at risk for
uric acid stones
- bone complication from overproduction of PTH
- increased PTH can be result of parathyroid adenoma, MEN type 1, MEN type 2A, parathyroid Ca, and renal osteodystrophy from ESRD
osteitis fibrosa cystica (OFC)
what are the indications for parathyroidectomy in primary hyperparathyroidism?
- Ca++ > 1 mg/dl about ULN
- CrCl < 60 ml/min
- bone density > 2.5 SD and/or previous fragility fracture
- < 50 yoa
