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
