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Flashcards in CKD and Lifelong Treatment Deck (28)
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What is the definition of chronic kidney disease (CKD)?

  • 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.


Describe the staging of CKD based on eGFR.

  • 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


Describe the staging of CKD based on albumin:creatinine ratio.

  • A1 - <3 mg/mmol
  • A2 - 3-30 mg/mmol
  • A3 - >30 mg/mmol


What would prompt a nephrology referral in a patient with CKD?

  • 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. 


Describe the community management of CKD1-3.

  • 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.


How do you prevent the progression of CKD?

  • Optimise BP management 
  • Reduce proteinuria
  • Stop smoking
  • Control diabetes
  • Optimise weight


What are the BP targets for patients with CKD?

  • <140/90mmHg in CKD without proteinuria
  • <130/80mmHg in CKD with proteinuria


What is proteinuria?

What does proteinuria cause?

  • 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. 
    • 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.


What factors precipitate lactic acidosis in patients with T2DM?

  • Cardiac failure
  • MI
  • Hepatic failure
  • Any hypoxic state
  • Clinical dehydration
  • Shock (especially septic shock)
  • Severe sepsis and haemodynamic instability
  • Major surgery


What effect does obesity have on the kidneys?

  • Obesity is a risk factor for:
    • Hypertension
    • CKD
    • ESRD
  • No substantial data associated with 'size-reduction' except with bariatric surgery. 


Describe how anaemia is related to kidney function.

  • 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.


Describe how levels of calcium and phosphate are related to kidney function?

  • 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.


What is the effect of PTH?

  • Increases calcium reabsorption across the DCT. 
  • Reduces PO4 reabsorption across the tubule. 


What is the effect of vitamin D on the gut?

  • Increases calcium and PO4 reabsorption across the gut. 
  • Increases calcium transport across the cell and across the Aptness transporter.


What are the bone effects of calcium and phosphate?

  • 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.


What happens to vitamin D in the event of acidosis?

  • Cholecalcidferol 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. 
  • Calcium inhibits PTH secretion.


What happens to PTH, Ca and PO4 in:

  • primary hyperPTH?
  • secondary hyperPTH?
  • tertiary hyperPTH?


What are the drug choices in hyperPTH?

  • Vitamin D analogues: Alfacalcidol.
  • Phosphate binders: calciuim acetate, secelamer, lanthanum CO3.
  • Calcimimetics: cinacalcet


Describe the characteristics of bone in high bone turnover.

  • High PTH
  • New bone is mainly collagen
  • Increased risk of fractures


Describe adynamic bone.

  • Low PTH
  • Reduced mineralisation
  • Increased risk of hypercalcaemia
  • Over suppression with vitamin D
  • Previous PTHectomy
  • Associated with DM


What are the effects of acidosis on the bone.

What is the clinical picture?

  • CaCO3 leak out from bone to act as a buffer for the H+ ions causing bone loss. 
  • Acidosis independently increases osteoclast activity and reduces osteoblast activity. 
  • Clinically:
    • Bone pain
    • Tendon rupture
    • Pruritus
    • Ocular calcification
    • Vascular calcification


What are the treatment goals in patients with CKD G4 and G5?

  • Usually seen by nephrologist
  • Aim is to slow progression of CKD
  • Identify and treat complications of CKS
  • Reduce incidence of CV disease
  • Allow timely and informed decision making for management of ESRF (end-stage renal failure)


At what stage of renal compromise is acidosis common?

What are the complications?

  • eGFR <25ml/min/1.732
  • Complications include:
    • Exacerbation of bone disease
    • Increased muscle degradation
    • Reduced albumin synthesis
    • Increased inflammation
  • Also increases risk of therapy:
    • Increased ECF volume expansion
    • Hypertension
    • Decompensation of heart failure


At what eGFR is dialysis started?

  • In UK, average eGFR at time of starting dialysis is 7ml/min/1.732.
  • This is doctor-lead if high K+ / acidosis / fluid overload / weight loss. 
  • Patient led if lethargy / loss of concentration.
  • Ideal = pre-emptive transplantation.


Describe the preparation of a patient for dialysis (any kind).

  • When eGFR falls below 20 consistently and is on a downward trajectory. 
  • Education
  • Options:
    • Peritoneal dialysis - not suitable if previous abdominal surgery. 
    • Haemodialysis - need an AV fistula created. 
    • Transplantation - not all patients suitable. 
    • Conservative care - patient choice or too comorbid to dialyse. 


Describe the creatinine levels in a patient on haemodialysis as opposed to peritoneal dialysis.

  • Haemodialysis - blue
  • Peritoneal dialysis - green


Describe pre-dialysis boods compared with post-dialysis bloods.

  • Note - creatinine and urea do not matter in patients on dialysis


What are the arguments for transplant vs. no transplant in a patient with renal failure?

  • Factors for:
  • Patient factors
    • No dialysis
    • Better QoL
    • Better survival
  • Economic factors
    • Dialysis = £30,800 / year
    • Tx = £17,000 / year
  • Factors against:
  • 'Optional extra'
    • Cardiac disease
    • Respiratory disease
    • Malignancy
    • Severe PVD
    • BMI >35
    • Age?