Chronic kidney disease Flashcards
What is CKD?
- Reduced GFR and/or evidence of kidney damage
* It must be chronic (!) – CKD can’t be diagnosed from one measurement
how is GFR assessed?
• Can be measured – nuclear medicine; time-consuming and expensive
This is only done as a one off e.g. if want to donate kidney
Not done e.g. every month as monitoring
¥ Can be estimated from serum creatinine, age, sex and race
¥ Creatinine - product of muscle breakdown; muscular people produce more creatinine
⇒ MDRD4 equation: GFR = 186 x creatinine (mg/dl)-1.154 x Age-0.203
For white/Asian males – correction factor for women and for black race
When is eGFR inaccurate?
eGFR accurate for most people if <60ml/min… However
⇒ Over-estimates GFR if muscle mass is low
⇒ Under-estimates if muscle mass high
⇒ Only valid if serum creatinine is stable
⇒ Occasionally necessary to measure GFR
What are the different stages of chronic kidney disease? how are they determined?
¥ Stage 1 – GFR >90ml/min, with evidence of kidney damage*
¥ Stage 2 – GFR 60-90ml/min, with evidence of kidney damage
*Such as proteinuria, haematuria (in absence of lower urinary tract cause), or abnormal imaging
Stages 3-5 defined on GFR alone
¥ Stage 3 – GFR 30-60ml/min
(3A – 45-60ml/min; 3B – 30-44ml/min)
¥ Stage 4 – GFR 15-30ml/min
¥ Stage 5 – GFR <15ml/min, or on renal replacement therapy
What does CKD also increase the risk of?
cardiovascular risk
Progression of CKD:
-what factors influence the progression of CKD?
Some people with early CKD (stage 1-3) will progress to advanced CKD; important to identify those likely to progress
¥ Patients with proteinuria more likely to progress
¥ More proteinuria – faster progression
¥ Younger patients have longer to progress – more likely to reach stage 5
What are 7 common causes of CKD?
¥ Diabetes ¥ Hypertension ¥ Vascular disease ¥ Chronic glomerulonephritis ¥ Reflux nephropathy ¥ Polycystic kidneys ¥ Cause not always known
What symptoms are experienced in CKD? 5
¥ Symptoms due to reduced GFR don’t occur until late – GFR<20ml/min
¥ Non-specific – tiredness, poor appetite, itch, sleep disturbance
¥ Impaired urinary concentrating ability – symptoms may occur earlier - nocturia
Describe the management principles of CKD?
¥ Slow progression ¥ Reduce cardiovascular risk ¥ Identify and treat ¥ complications of CKD Prepare for renal replacement therapy
What management can be done in slowing the progression of CKD? 4
¥ Proteinuria associated with progression, and reducing proteinuria slows progression
¥ Control blood pressure
¥ ACE-inhibitors and angiotensin receptor blockers reduce BP and proteinuria (ACEI initially reduce GFR and cause hyperkalaemia)
¥ Also evidence for spironolactone
¥ Caution – initial fall in GFR; hyperkalaemia
¥ Good glycaemic control in diabetes
¥ Stop smoking
What are two main complications of CKD?
- Anaemia
- Bone disease and hyperparathyroidism
Anaemia in CKD:
- why is there anaemia in CKD?
- how is this managed?
Pathophysiology:
¥ Erythropoietin produced by the kidneys
¥ Production declines in CKD
Management:
¥ Correct deficiencies; usually intravenous iron
¥ If still anaemic – erythropoietin (Epo) may be indicated
¥ Epo – by injection; every week or fortnight
¥ Target Hb – 10.5-12.5g/dl
¥ As Epo works, iron stores depleted – need regular top-ups
This is because the iron gets used up to make Hb
Bone disease in CKD:
-why does this happen?
¥ Vitamin D hydroxylated in the kidney
¥ Impaired in CKD
¥ Leads to reduced calcium absorption, leading to secondary hyperparathyroidism – (Calcium decreases which causes PTH inscrease)
¥ In advanced CKD, serum phosphate rises – also increases PTH secretion
This is because the kidneys don’t excrete the phosphate as they fail, and PTH causes bone resorption = high phosphate
Hyperparathyroidism in CKD:
- How can secondary hyperparathyroidims in CKD lead to tertiary hyperparathyroidism?
Hyperparathyroidism=
¥ Can maintain normal serum calcium, but at the expense of the bones
(causes bone resorption as can’t get calcium from anywhere else)
¥ Hyperplasia of all glands
¥ One gland may become autonomous – PTH secretion not suppressed by calcium – tertiary hyperparathyroidism
(as the glands undergo hyperplasia one gland can become autonomous and secrete PTH no matter what the calcium conc. Is)
3o hyper-PTH can lead to hypercalcaemia
Describe the clinical features seen with bone disease in CKD?
¥ Severe bone disease (pain, radiological changes) – uncommon
¥ High phosphate and high calcium – Vascular calcification
¥ Calcified vessels – stiff
¥ Heart valves also calcified
What is the management of bone disease in hyperparathyroidism?
• Alfacalcidol – hydroxylated vitamin D – doesn’t need activation by kidneys
• Phosphate lowering treatment – advice from dietician on intake
- Phosphate binders – bind to phosphate in the gut to reduce absorption; include calcium carbonate, calcium acetate, sevelamer
When is a patient with CKD considered for dialysis? what two methods of dialysis exist?
- when GFR about 20ml/min
- resistant hyperkalaemia/unresponsive acidosis
- no better survival rate if start early
- symptom based: fatigue, itch, loss appetite, nausea, vomiting, unresponsive fluid overload
haemodialysis
peritoneal dialysis
What other management options exist for end stage CKD?
- transplantation
- conservative treatment: EPO and symptom control
Haemodialysis: what is removed and what is added to the blood?
urea, creatinine, potassium, toxins, water = out
sodium, bicarbonate, water, potassium, glucose = in
Haemodialysis: how long does this take and how many times a week?
- 4hrs
- 3X a week
How is haemodialysis given in a patient: what are the pros and cons of these?
Fistula:
pros - good blood flow, unlikely to cause infection
cons - surgery, 6 wk maturation, can block, can limit blood flow to distal arm
Tunnelled venous catheter:
pros - easy to insert, immediate use
cons - high risk infection, vein damage, blockage
Why is an infected tunnelled venous catheter infection so serious? what investigations are performed? what is the treatment?
If left untreated risk of endocarditis or discitis
Ix: blood culture, CRP, FBC, exit site swab
Treatment: vancomycin, line removal/exchange
How is haemodialysis initiated?
- gradual build up, first session 2 hours
- if too quick - disequilibrium syndrome = cerebral oedema
What are the main risks of haemodialysis?
- fluid overload
- blood leaks
- loss vascular access
- hypokalaemia and cardiac arrest
- intradialytic hypotension
What lifestyle restrictions apply when undergoing haemodialysis?
Fluid: restrict 1 litre per day
Salt: low salt diet
Potassium: low potassium diet (potatoes/bananas/choc,)
Phosphate: low phosphate diet and phosphate binders
Peritoneal dialysis: how does this work?
solute removal across peritoneal membrane
water removal as high glucose concentration in peritoneal dialysate
-can be continuous ambulatory peritoneal dialysis (CAPD) or automated
What is CAPD? risks?
4 bag exchanges per day:
Risks - membrane failure (inability to move water)
What is Automated PD?
1 bag fluid stays in all day and machine exchanges fluid overnight 9-10hours:
Risks - infection, hernias
