complications of CKD Flashcards
stages of CKD
definition of CKD mineral and bone disorder
A systemic disorder of mineral and bone metabolism due to CKD
manifested by either one or a combination of the following:
• Abnormalities of calcium, phosphorus, PTH or vitamin D
metabolism
• Abnormalities in bone turnover, mineralization, volume,
linear growth or strength
• Vascular or other soft tissue calcification
physiology of vitamin D
what hjappens in CKD
treatment of hyperparathyroidism
- Control of hyperphosphatemia with phosphate binders/diet
- Correction of hypocalcaemia
- Administration of Vitamin D
- Calcimimetic therapy
- Parathyroidectomy
- Control of hyperphosphatemia with phosphate binders/diet
- Calcium binders
- Non calcium – Sevelamer / Lanthanum
- Correction of hypocalcaemia
- Oral calcium
- Administration of Vitamin D
- Oral (cheap) or IV (expensive/ESRD)
- Potential beneficial ‘off target’ effects
- Calcimimetic therapy
- Cinacalcet
- Parathyroidectomy
- Surgical operation with ass morbidity/ mortality
- Last resort in pts with tertiary hyperparathyroidism
phosphate binders
• Hyperphosphatemia clearly linked to increased mortality
• Required by most patients as GFR declines as dietary modification arduous
• First line therapy controversial
• Calcium containing binders used most often as cheaper and will increase
serum calcium levels, however concern remains regarding calcium load and
its effects on vascular calcification
• Non calcium containing binders more expensive and despite being heavily
marketed may not be superior
• All phosphate binders need to be taken with or before meals, considerable
tablet burden likely to reduce compliance
• Whilst effective in ‘normalizing’ biochemical parameters none have been
shown to have any effect on mortality or morbidity ass with CKD - MBD
calcimimetic therapy
- Cinacalcet
- Oral administration
- Works directly on the calcium receptor in the PTH gland
- ‘Tricks’ the PTH gland into believing that serum calcium is normal
- Directly inhibits PTH secretion
- Role unclear at present
- Licensed for treatment of tertiary hyperparathyroidism
- ? Role at earlier stages
- Expensive
renal osteodystrophy
• An alteration of bone morphology in patients with CKD
• It is one measure of the skeletal component of the systemic
disorder of CKD – MBD that is quantifiable by bone biopsy
• Most forms attributable to variations in PTH, therefore PTH
commonly used as surrogate marker for bone turnover in
addition to serum calcium, phosphate and alkaline
phosphatase
• Spectrum of disorders of bone turnover
• Osteitis fibrosa cystica – high PTH/ high turnover
• Osteomalacia
• Adynamic bone disease – low turnover/ low PTH
• As well as contributing to overall disordered biochemical
picture it can lead to bone pain and increased risk of fractures
valscular calcification
• Large, medium and small arteries anywhere in vascular tree
• Predictor of mortality in dialysis and pre-dialysis patients
• Associated with cardiac events – MI and sudden death
• Pts with highest degrees of calcification at higher risk (up to 2.5 fold
increased risk of death)
• Mechanisms poorly understood at present but may involve smooth
muscle cell transformation into osteoblast like cells
• Current treatments center on the control of hyperparathyroidism
and in particular hyperphosphatemia which has been shown to be
strongly linked to its progression
vascular calcification pathway
death and gfr
• Not only is GFR an risk
factor for mortality, but
the presence of
albuminuria is also
independently and
inversely associated with
death
• Increased risk seen early
at GFR < 60ml/min
Patients with GFR <
60 at increased risk of
cerebrovascular
disease
• Overall Risk Ratio
1.43 for CVA in
pts with eGFR <
60
cardio facts
• Cardiovascular morbidity and mortality are inversely and independently
associated with kidney function and albuminuria
• Rate and severity of coronary artery disease (CAD) increases with GFR
decline
• Rate of cerebrovascular disease increased with CKD
• Rates of congestive cardiac failure/ arrhythmias/ sudden death increased
with CKD
• Risk particularly increased at GFR < 15ml/min but present at higher levels
• Prognosis after CV event poorer in those with low GFR
• Traditional risk factors only partly account for excess mortality seen
interplay of CKD and CVD
treatment
Identify and treat modifiable risk factors
• Blood Pressure (? RAS blockade superior)
• Lipid lowering therapy (conflicting results from several trials)
• Glycemic control
• Lifestyle modification
• Smoking cessation
• ? Treatment of hyperparathyroidism/ hyperphosphatemia
vascular calcification
ckd and anaemia
• Renal anemia is common in patients with CKD (10-25% of
pts with CKD stage 3 or higher)
• More common in elderly/ those with co-morbidities
• Higher in African Americans than Caucasians
• Associated with higher rates of hospitalization, mortality
and progression to ESRD
• Associated with reduced quality of life
