Renal - CKD Flashcards
What is CKD?
Reduced kidney function or kidney disease of any form that has been present for some time.
Increased prevalence - obesity and type 2 DM
Increases risk of IHD, progresses causing complications requiring renal replacement therapy, affects with drugs
Cause of death in CKD
IHD MCC of death in CKD patients on or off dialysis/ renal replacement
Changes in renal function with age
Kidney function declines with age in all people - product of age and lifestyle (obesity, type 2 DM) so many older people have low GFR but will not have specific kidney disease
- aggressive investigation of renal function in the elderly is only useful if it is outside the normal range for their age
Renal impairment (not necessarily disease) has drug consequences
- drugs normally excreted will accumulate
- NSAIDs reduce GFR in patients with already reduced renal function
Why is serum creatinine not always an accurate representation of renal function?
Creatinine does not rise above normal limits until there is a large (50%) reduction in GFR, so may not be accurate for early CKD. Is used in late CKD because GFR changes very little as creatinine rises.
GFR most commonly reported as eGFR using MDRD formula - uses “CAGE” variables:
- serum creatinine
- age
- gender
- ethnicity
Factors which affect result of eGFR
Pregnancy
Muscle mass
Eating red meat 12 hours prior to the sample being taken
eGFR is much less accurate with relatively good renal function; interpret with caution when eGFR is predicted to be >60ml/min
CKD stages
5 stages based on eGFR
Stage 1 - greater than 90ml/min, with some sign of kidney damage on other tests
Stage 2 - 60-90ml + signs of kidney disease
Stage 3a - 45-59ml/min
Stage 3b - 30-44ml/min
Stage 4 - 15-29ml/min
Stage 5 - less than 15ml/min, established kidney failure - dialysis or kidney transplant needed
Investigating CKD
Most patients asymptomatic - usually identified on blood tests for other reasons
2 goals of assessment:
i) determine whether there is a specific cause of CKD
ii) assess severity - determines what general measures are needed (e.g. BP control)
History and examination:
- large bladder - urinary obstruction
- BP
- Urinalysis for protein and blood (low levels of proteinuria, albumin: creatinine ratio (ACR) useful, urine protein: creatinine ratio (PCR) can be used*
- USS may be useful to check anatomy and exclude obstruction
*Differs for non diabetics and diabetics - ACR of >30mg/mmol in non diabetics significant; ACR > 2.5mg/mmol in men, or >3.5mg/mmol in women is significant
End stage renal disease
Occurs when patients require renal replacement therapy with dialysis or transplantation
- number of functioning nephrons declines, surviving nephrons compensate which damages remaining nephrons and accelerates loss
What is the uraemic syndrome?
Refers to complications of chronic renal failure such as anaemia, confusion, coma, asterexis, seizures, pericardial effusions, itch and bone disease. Renal replacement therapy improves these problems, but patients with end stage renal disease have higher morbidity and mortality than rest of the population
Distinguishing between AKI and CKD
Severe acute and chronic kidney disease both raise plasma potassium, urea and creatinine and cause metabolic acidosis
Severe CKD usually evidence of chronic complications - e.g. anaemia caused by reduced EPO, bone disease (low serum Ca++, high PTH and high phosphate)
Plasma Ca++ is characteristically low in CKD unless tertiary hyperparathyroidism is present
Small kidneys on USS - key feature (atrophy and fibrosis)
Acute problems in CKD
Acute problems can occur in both acute and chronic renal failure
- emergency dialysis or haemofiltration - hyperkalaemia, severe acidosis, pulmonary oedema, and uraemic symptoms
Sudden deterioration in patients with renal impairment not on dialysis - hypertension, infection or nephrotoxic drugs (NSAIDs and ACEi cause renal deterioration by affecting renal blood flow)
Clinical features of renal bone disease
Bone pain - lower back, hips, and legs; associated with proximal myopathy and soft tissue calcification
Bone ALP usually raised
Types of renal bone disease
2 types distinguished on biopsy:
1) High bone turnover disease - excess PTH
- PTH stimulates bone resorption
- new bone has disordered collagen
- radiographs: subperiosteal resorption in phalanges, erosion of phalangeal tufts, and erosion of clavicle heads
2) Low bone turnover disease - low PTH
- low bone turnover, osteomalacia + poorly mineralised bone
- calcium intake and plasma calcium levels high enough to suppress PTH secretion below level required for normal bone turnover
- vit D levels may be low
- radiographs: multiple fractures or pseudofractures (radiolucent cortical zones perpendicular to bone surface)
Causes of high turnover renal bone disease
Main cause - renal phosphate retention and inadequate renal vitamin D production
Vit D deficiency - reduces gut calcium and phosphate absorption
- loss of 1,25 hydroxylation in CKD due to nephron loss
Kidneys retain phosphate –> net rise in phosphate and loss of calcium
Rise in phosphate further lowers calcium by causing calcium phosphate deposition in tissues
Hypocalcaemia –> PTH stimulation –> secondary hyperparathyroidism
- PTH secretion can become autonomous even when serum Ca++ returned to normal = Tertiary hyperparathyroidism
Other factors:
- high phosphate level directly stimulates PTH secretion and directly inhibits renal vit D production, normally vit D inhibits PTH (negative feedback), so deficiency causes excess PTH secretion
- acidosis stimulates bone resorption
Treating high turnover bone disease
Phosphate
- dialysis removes some
- low phosphate intake recommended
- phosphate binding compounds taken with food (compounds containing calcium or lanthanum or synthetic resins)
Vit D
- supplementation with calcitriol (1,25 didhydroxycholecalciferol) - inhibits PTH secretion and bone turnover; raises plasma Ca++ by increasing dietary calcium absorption
- helps bone pain and proximal myopathy
PTH levels should fall without causing low turnover bone disease. If PTH does not fall when Ca++ levels rise and vitamin D administrated, calcimimetic drugs (e.g. cinacalcet) which reduces PTH levels or surgical removal of PTH glands are required