CKD and Lifelong Treatment Flashcards
1
Q
What is the definition of chronic kidney disease (CKD)?
A
- Abnormalities of kidney function OR structure present for >3 months.
- All patient with eGFR <60 ml/min/1.73m2 on at least 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.
2
Q
Describe the staging of CKD based on eGFR.
A
-
I
- eGFR >90
- G1
-
II
- eGFR 60-89
- G2
- CKD1 and CKD2 are usually reported as haematuria / proteinuria / structural.
-
IIIa
- eGFR 45-59
- G3a
-
IIIb
- eGFR 30-44
- G3b
-
IV
- eGFR 15-29
- G4
-
V
- eGFR <15
- G5
3
Q
Describe the staging of CKD based on albumin:creatinine ratio.
A
- A1 - <3 mg/mmol
- A2 - 3-30 mg/mmol
- A3 - >30 mg/mmol
4
Q
What would prompt a nephrology referral in a patient with CKD?
A
- Evidence of CKD progression
- Decrease in eGFR of 25% or more and change from CKD class.
- A sustained decrease in eGFR of 15ml/min/1.73m2 per year.
- eGFR <30 (CKD4).
- UACR >70 mg/mmol (unless known treated DM).
- UACR >30 mg/mmol + haematuria.
- Uncontrolled hypertension on 4+ drugs.
- Hereditary causes of CKD.
- Suspected renal artery stenosis.
- Haematological / biochemical abnormalities.
- Diagnostic uncertainty regarding aetiology / systemic disease present.
5
Q
Describe the community management of CKD1-3.
A
- CKD is asssociated with increased risk of CV disease and death.
- CKD G3 are more likely to suffer a CV event than they are to end up on dialysis.
- Proteinuria is independently associated with increased risk of CV disease and death.
- Appropriately timed reviews.
- Lifestyle advice.
- Statins (irrespective of serum lipid levels).
- Reduce the risk of primary and secondary atherosclerotic events.
- No reduction in all cause mortality or slowing CKD.
6
Q
How do you prevent the progression of CKD?
A
- Optimise BP management
- Reduce proteinuria
- Stop smoking
- Control diabetes
- Optimise weight
7
Q
What are the BP targets for patients with CKD?
A
- <140/90mmHg in CKD without proteinuria
- <130/80mmHg in CKD with proteinuria
8
Q
What is proteinuria?
What does proteinuria cause?
A
- Reduced number of nephrons in CKD results in glomerular hyper-hyper-perfusion and hypertension.
- Increased filtration of protein:
- Xs protein in Bowman’s capsule activates inflammatory and apoptic pahthways.
- 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.
- INTERSTITIAL FIBROSIS
- Proteinuria results in increased decline in renal function.
- REIN - ramipril in non diabetics for 5 years halved rate of GFR decline.
- Possible improvement and reversal of glomerular lesions (most beneficial at higher eGFRs).
- Dual blockade considered too risky (ACE and ARB).
- But recently, study suggests beneficial in diabetic population.
- REIN - ramipril in non diabetics for 5 years halved rate of GFR decline.
9
Q
What factors precipitate lactic acidosis in patients with T2DM?
A
- Cardiac failure
- MI
- Hepatic failure
- Any hypoxic state
- Clinical dehydration
- Shock (especially septic shock)
- Severe sepsis and haemodynamic instability
- Major surgery
10
Q
What effect does obesity have on the kidneys?
A
- Obesity is a risk factor for:
- Hypertension
- CKD
- ESRD
- No substantial data associated with ‘size-reduction’ except with bariatric surgery.
11
Q
Describe how anaemia is related to kidney function.
A
- Erythropoietin is 80% produced in the kidney by fibroblastoids in the peritubular interstitium.
- Erythropoiesis is increased in hypoxia:
- Acidosis causes a right shift in the oxygen-Hb dissociation curve (improving hypoxia).
- CKD results in increased hepcidin levels - reduced clearance and increased production.
- Hepcidin binds to ferropoietin which blocks the exit of iron from cells - functionally rendering iron deficiency - less absorption and less utilisation.
- Anaemia:
- Reduced EPO
- Increased bleeding risk
- Reduced red cell life span (corrected by dialysis)
- CKD3 has NN anaemia.
12
Q
Describe how levels of calcium and phosphate are related to kidney function?
A
- PO4 and Ca are absorbed in the duodenum and jejunum - absorption increased by vitamin D.
- Calcium is freely filtered and then reabsorbed across the PCT (70%) and then 20% in the thick loop. Passive absrption occurs with Na and H2O due to increasing concentration of calcium in the lumen pulling it across.
- 5-10% absorbed across the DCT. Active mechanism. Binds to calbindin and parvalbumin which are influenced by vitamin D.
- PO4 is 55% not protein bound freely filtered but there is Tmax absorption so excess is lost in urine.
- 80% in PCT absorbed through the NaPO4 cotransporter. This is reduced by PTH.
13
Q
What is the effect of PTH?
A
- Increases calcium reabsorption across the DCT.
- Reduces PO4 reabsorption across the tubule.
14
Q
What is the effect of vitamin D on the gut?
A
- Increases calcium and PO4 reabsorption across the gut.
- Increases calcium transport across the cell and across the Aptness transporter.
15
Q
What are the bone effects of calcium and phosphate?
A
- Acidosis increases tubular loss of both calcium and PO4 therefore losing calcium from bone.
- PTH causes net reabsorption from bone therefore increase serum Ca and PO4.
17
Q
What happens to PTH, Ca and PO4 in:
- primary hyperPTH?
- secondary hyperPTH?
- tertiary hyperPTH?
A
26
Q
Describe the creatinine levels in a patient on haemodialysis as opposed to peritoneal dialysis.
A
- Haemodialysis - blue
- Peritoneal dialysis - green
27
Q
Describe pre-dialysis boods compared with post-dialysis bloods.
A
- Note - creatinine and urea do not matter in patients on dialysis
