CKD and lifelong treatment Flashcards
What is CKD?
- Abnormalities of kidney function or structure present for 3 months or more
- eGFR <60 on 2 occasions 90 days apart
- Presence of ongoing nephrological cause of haematuria
- Electrolyte abnormalities due to tubular disorders
- Renal histological abnormalities
- Renal structural abnormalities
- Kidney transplantation
What are the stages?
I >90 II 60-89 IIIa 45-59 IIIb 30-44 IV 15-29 V <15
A1 <3mg/mmol
A2 3-30
A3 >30
CKD referral
- Evidence of progression - decrease in eGFR of 25% or more and change from CKD class or a sustained decrease in eGFR of 15ml/min per year
- eGFR <30
- UACR >70 (unless known treated DM) or UACR>30 with haematuria
- Uncontrolled HTN on 4+ drugs
- Hereditary causes of CKD
- Suspected renal artery stenosis
- Haematological/biochem abnormalities
- Diagnostic uncertainty regarding aetiology/systemic disease
Community management of CKD
CKD 1-3
Associated with inc risk of CVD and death
Proteinuria independently associated with inc risk of CV disease and death
Appropriately timed reviews
Lifestyle advice
Statins - reduce risk of primary and secondary atherosclerotic events, no reduction in all cause mortality or slowing CKD
Prevention of progression
Optimise BP management Reduce proteinuria Stop smoking Control diabetes Optimise weight
Relation of Na to HTN
Lower sodium associated with greater effect on RAS blockade
High Na intake results in increased ECV, glomerular hyperfiltration therefore RAS activation, fluid overload/HTN etc
Proteinuria
Reduced no of nephrons results in glomerular hyperperfusion and hypertension
Inc filtration of protein
Inc decline in renal function
interstitial fibrosis
Xs protein (proteinuria)
Xs protein in Bowman’s capsule activates inflamm and apoptotic pathways
Xs protein through podocytes releases TGF-beta1 and resultant myofibroblast differentiation of mesangial cells
Xs protein in PCT results in localised toxicity with resultant cytokine and vasoactive mediator release
Factors precipitating lactic acidosis in T2 patients
cardiac failure hepatic failure MI Hypoxia Dehydration Shock/sepsis Major surgery
Anaemia
EPO is produced in kidney by fibroblastoids in peritubular interstitium
Erythropoeisis is increased in hypoxia
Acidosis causes a right shift in oxygen - Hb dissociation curve (improving hypoxia)
CKD results in increased hepcidin levels - reduced clearance and increased production. Hepcidin binds to ferroportin which blocks the exit of ironed from cells - functionally rendering ID - less absorption and less utilisation
Anaemia gives reduced EPO, inc bleeding risk and reduced RBC life span (corrected by dialysis)
Calcium and phosphate
Absorbed in duodenum and jejunum increased by vit D
Freely filtered and then reabsorbed across the PCT and then 20% in thick loop. Passive absorption occurs with Na and water due to increasing conc of calcium in lumen pulling it across
5-10% absorbed across the DCT - active mechanism - binds to calbindin and parvalbumin which are influenced by vit D
PO4 is 55% not PPB freely filtered but there is Tmax absorption so excess is lost in urine
80% in PCT absorbed through NaPO4 cotransporter - this is reduced by PTH
PTH effects on Ca and PO4
Increases calcium reabsorption across the tubule
Reduced PO4 reabsorption across tubule
Calcium inhibits PTH secretion
Vit D effects
Increases Ca and PO4 reabsorption across gut
Increases Ca transport across cell and across the aptness transporter
Bone effects
Acidosis increases tubular loss of both Ca and PO4 therefore losing Ca from bone
PTH causes net reabsorption from bone therefore increases serum Ca and PO4
Vit D
Colecalciferol from skin and gut converted in liver then kidney to active form
Increases effect of PTH on bone so increases Ca and PO4 reabsorption from bone
Inhibits PTH secretion
