chronic kidney disease Flashcards
CKD definition
presence of kidney damage (abnormal blood, urine, x-ray findings)
or
GFR <60 that is present 3+ months
causes of CKD
diabetes htn age-related decline glomerulonephritis polycystic kidney disease medications e.g. NSAIDs, PPIs, lithium
CKD risk factors
age htn diabetes smoking use of medicines that affect kidneys
CKD presentation
pruritus loss of appetite nausea oedema muscle cramps peripheral neuropathy pallor htn
CKD investigations
eGFR
albumin:creatitine ratio (3+ is signif)
urine dipsitx - haematuria
renalUSS
Staging CKD: G score and A score
G score is based on eGFR
A score is based on albumin: creatinine ratio
staging of CKD: G1
eGFR >90
staging of CKD: G2
eGFR 60-89
staging of CKD: G3a
eGFR 45-59
staging of CKD: G3b
eGFT 30-44
staging of CKD: G4
15-29
staging of CKD: G5
eGFR<15
known as end-stage renal failure
staging of CKD: A1
<3mg/mmol
staging of CKD: A2
3-30mg/mmol
staging of CKD: A3
> 30mg/mmol
what does patient need for diagnosis of CKD
eGFR of <60 or proteinuria
CKD complications
anaemia renal bone disease CVS disease peripheral neuropathy dialysis-related problems
aims of CKD management
slow disease progression
reduce risk of CVS disease
reduce risk of complications
treat complications
CKD management: slowing progression of disease
optimise diabetic control
optimise htn control
treat glomerulonephritis
CKD management: reducing risk of complications
excersice, healthy weight, stop smoking
dietary adivce re phosphate, sodium, potassium, water intake
atorvastatin 20mg
CKD management: treating complications
metabolic acidosis: sodium bicarbonate iron supplementation vitamin D dialysis renal transplant
CKD: treating htn
ACE-I first line
must monitor serum potassium as ACEI and CKD cause hyperkalamemia
why does anaemia occur w CKD
damaged kidney cells in CKD no longer produce erythropoetin –> drop in RBC –> anaemia
how is anaemia in CKD managed
erythropoiesis stimulating agents - exogenous erythropoeitin
iron
renal bone disease is also known as
chronic kidney disease - mineral and bone disorder
CKD-MBD
features of renal bone disease
osteomalacia (softening of bone)
osteoporosis (brittle bones)
osteosclerosis (hardening of bones)
renal bone disease X-ray changes
spine shows sclerosis of both vetrerba ends (denser white) and osteomalacia in centre (less white)
classicaly known as ‘rugger jersey’ spine after stripes found on rugby shirts
pathophysiology of renal bone disease
high P due to reduced excretion. Low active vitD (kidney vital for metabolising to active form)
active VitD is needed for calcium absorption and regulates bone turnover
2ry hyperparathyroidism as parathyroid glands react to low Ca2+ and high P by inc PTH. —> inc osteoclast activity
pathophysiology of renal bone disease: osteomalacia
due to increased turnover of bones without adequate Ca suppluy
pathophysiology of renal bone disease: osteosclerosis
osteoblasts respond by inc their activity to match osteoclasts by creating new tissue in bone, however due to low Ca the new tissue is not properly mineralised
pathophysiology of renal bone disease: osteoporosis
can exist alongside renal bone disease due to other risk factors e.g. age, steroid use
management of renal bone disease
- active forms of VitD e.g. calcitriol
- low phosphate diet
- bisphosphonates for osteoporosis
htn in CKD: ACEI offered to all patients with
diabetes + ACR > 3
htn + ACR > 30
ACR >70
what needs to be monitored when giving ACEI to pt w CKD
potassium as both cause hyperkalaemia
