Bone mineral disorders

Thyroid

Calcitonin

Bone-kidney-P-thyroid gland axis

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Bone mineral disorders
Disorders of mineral 5. Vitamin D
and bone metabolism in 6. Bone turnover
CKD patients include; 7. Soft-tissue
calcifications
Abnormalities
1. PTH
2. Calcium
3. Phosphorus
4. The Ca × P
product

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Pathophysiology
• As the GFR <30
mL/min/1.73m2
 Excess PTH
o Hyperplasia of the
oDecrease parathyroid glands
phosphorus excretion • Decreases the sensitivity to
serum calcium levels and
and calcitriol calcitriol feedback, further
production promoting sHPT
 PTH levels to begin to Consequence
rise significantly,
secondary • Alterations in bone turnover
hyperparathyroidism and the development of renal
(sHPT) osteodystrophy (ROD)

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Pathophysiology

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Presentation and Dx.

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Treatment of BMDs
Maintain the serum Diagnosis and
level of treatment is based on;
• Calcium 1. Corrected serum
• Phosphorus calcium
• PTH levels 2. Serum Phosphorus
for all stages of CKD 3. Intact PTH levels
(iPTH)

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BMD treatment targets

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Non-pharmacologic
Hyperphosphatemia
Dietary phosphorus
restriction to 0.8 to
1g/day
• Stage 3CKD or higher
• P levels at the upper
limit of the normal range
or elevated iPTH levels.
Haemo/peritoneal
dialysis
• Can remove up to 2 to 3 g of
P per week
• Pharmacologic therapy is
necessary in addition to
dialysis treatment
sHPT and CKD-BMD
o Restriction of Al exposure
and parathyroidectomy
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Non-pharmacologic
Para-thyroidectomy • Every 4–6 hours for the
• Last resort for sHPT
• Persistently elevated
iPTH levels above 800
pg/mL and refractory to
medical therapy
Monitor
o Ionized calcium
first 48–72 hours
o Administer IV calcium (1-
2gm) initially
o ……….orally with vitamin
D 8 to 10,000 IU per week
once calcium levels
normalized
o ………..for several
weeks to months after
the procedure
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Pharmacologic
1. Calcium-based
phosphate binders
• Ca2CO3 and calcium
acetate
• Effectively decrease serum
phosphate, increase Ca+2.
• Aid in the correction of
metabolic acidosis
Avoid if;
1. Serum calcium levels are
near the upper end of the
normal range or elevated
2. Arterial calcifications
3. Patients with
dynamic bone disease
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Pharmacologic
• Daily dose <1.5g of 2. Al- and Mg-
elemental calcium
containing
• Daily total elemental
calcium < 2g phosphate-binding
agents
• Adverse effects; o Serum phosphorus levels >7 mg/dL

• Constipation • Used for a short course

• Hypercalcemia (<4wks)
o To avoid Al and Mg
accumulation

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Pharmacologic
• Aluminium 3. Sevelamer
intoxication o Do not contain calcium,
• Neurotoxicity magnesium, or
o Encephalopathy or aluminium
dementia
o Worsening of anaemia • Unabsorbed and binds to
• Use is limited by the phosphate in the GI tract
GI side effects, o Prevents absorption and
primarily diarrhoea. promotes excretion of
through the GI tract
• Magnesium binder o Reduce LDL-C by up to 30%
o Hypermagnesemia and and increasing HDL-C levels
hyperkalaemia

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Pharmacologic
• May lower FGF-23 • GI complaints
levels o Nausea
o Vit D upregulation o Constipation
• Helpful in o Diarrhoea
o Elevated Ca+2 levels or 4. Lanthanum
vascular or
• Naturally occurring trivalent rare
o Soft tissue calcifications
earth element
• Sevelamer carbonate • Binds to dietary
may aid in the phosphorus, forming an
correction of metabolic insoluble compound that is
acidosis excreted in the faeces.

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Pharmacologic
• As effective as other binders
o May improve bone
turnover, compared with
calcium-containing products.
• Side effects: nausea, peripheral
oedema, and myalgias
5. Sucroferric
oxyhydroxide and
Ferric citrate
• Insoluble form of iron
• Binds to phosphate in
the GIT effective as
other binders with a
lower pill burden
• Ferric citrate
o As effectively as other
binders and can also
increase serum ferritin and
TSAT levels
• Both are commonly
associated with
diarrhoea.
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Pharmacologic

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Pharmacologic
Vitamin D regulates; • Low calcitriol level;
1. Ca+2 and PO42- absorption o Increased serum PTH level
from GIT and kidney
2. PTH secretion
• Vitamin D compounds
o Mimic the activity of
3. Maintaining muscle
calcitriol and act directly on
4. Cardiovascular the PT gland to decrease
5. Immune and brain function PTH secretion
6. Glucose control  MOA: up-regulation of
vitamin D receptor in the PT
gland and intestine
• Decreases parathyroid
gland hyperplasia.

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Pharmacologic
Calcitriol and • Serum calcium and
doxercalciferol phosphorus levels
o Within the normal range for
• Up-regulate vitamin D the stage of CKD prior to
receptors in the starting either of these
intestines therapies
o Increases Ca+2 and P
absorption
o Risk of hypercalcemia
and hyperphosphatemia

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Pharmacologic
Calcimimetics Useful
• Increases sensitivity of • Elevated PTH levels Plus
receptors on the PT gland o Increased calcium or
to serum calcium levels phosphorus levels
to reduce PTH secretion
• No effect on intestinal
absorption of calcium or
Caution
phosphorus • In seizure disorders because
low serum calcium levels
o May even lower serum can lower the seizure
calcium levels threshold.
• Eg: Cinacalcet

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Pharmacologic

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Monitoring
• At start of phosphate
binders therapy
o Monitor serum levels
every 1 to 4 weeks
o Titrate to the target and,
once target levels are
achieved,
✓ Serum Ca+2 and P levels
every 1 to 3 months
o Vitamin D therapy
✓ iPTH levels monthly, then
every 3 months once stable
o Starting or increasing
cinacalcet dose
• Serum Ca+2 and P levels
within 1 week; iPTH within
1 to 4 weeks.
• Every 3 months
✓ Once target achieved
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Renal replacement therapy
• Those who progress to
ESRD
• Modalities
1. Haemodialysis (HD)
2. Peritoneal dialysis (PD)
3. Kidney transplantation
o The preferred method owing to
improved patient survival
 Plan dialysis when
• GFR<30 mL/min/1.73m2
• Symptoms indicating
the need for dialysis
• Persistent anorexia,
nausea, vomiting,
fatigue, and pruritus.
• AEIOU
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Haemodialysis

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Haemodialysis
1. IHD
• Last 3 to 4 hours
• Blood flow rates
Ranging from 200 to 400
mL/min
• Rapid removal of volume
and solute per short period
of time
 Hypotension
• Correction of most of the
electrolyte abnormalities
2. CRRT
• Lasts much longer
• Hemodynamically unstable
patients
Recommended ultrafiltration
rate < 20 to 25-mL/kg/h
• Risks of thrombosis
Anticoagulation generally
necessary for almost all
patients
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Haemodialysis
3. Hybrid dialysis
• Hybrid extended-duration
IHD utilized in critically ill
patients
Alternative to CRRT
• Blood flow rate 150 to 200
mL/min with extended
treatment periods of 6 to 12
hours
• Risk of thrombosis
Anticoagulation
• Patients are at the state
of hypercoagulability
1. Increased level factors II
and VII
2. Redecided level of protein
C and S
• Type of membrane matters
• Regenerated cellulose >>>>
polyacrylonitrile or
polysulfone
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Haemodialysis
• No universally accepted
algorithm for
anticoagulation in dialysis
patients
• European Renal Association
• Unfractionated Hep
Load: 50IU/kg followed by
Continuous infusion of 800-
1500IU/h
Hyperkalemia, dyslipidemia,
osteoporosis and bleeding
• LMWH
Enoxaparin 100anti-Xa
IU/kg stat
Additional dose may be
needed if dialysis takes more
than 4-hour
Reduced need of blood
transfusion, low hyperkalemia
• Regional citrate
A 25% to 75% increase in ACT
at the entry to the dialyzer
Hypocalcemia, hypernatremia,
and metabolic alkalosis
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Haemodialysis

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RRT (PD)

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RRT (PD)

ISPD guideline 2021

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RRT (PD)
Peritonitis • Measures to decrease
prophylaxis
• Intranasal S.aureus
o Intranasal mupirocin
cream twice daily for 5
days each month, or
o Rifampin 300 mg orally
twice daily for 5 days,
repeated every 3 months
both S. aureus and P.
aeruginosa
o Gentamicin cream applied
twice daily and ciprofloxacin
otic solution applied daily to
the exit site
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Recommended in CKD

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