Progressive Chronic Kidney Disease (ppt) 2mb
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  • Kidney Check Australia Taskforce CARI – caring for australians with renal impairment

Progressive Chronic Kidney Disease (ppt) 2mb Progressive Chronic Kidney Disease (ppt) 2mb Presentation Transcript

  • Progressive Chronic Kidney Disease
    • Cherelle Fitzclarence
    • August 2009
  • Overview
    • Case studies
    • Discussion
    • Take home messages
  • Case 1
    • 50 yo diabetic – 5 yr hx
    • Initial poor control but good last 3 years with combo of insulin and oral hypoglycaemics
    • Monitors own sugars
    • Post prandial BSL’s <10mmol/L
    • HbA1c – 5-7%
    • No peripheral neuropathy
    • No retinopathy
    • Albuminuria
    • Hypertension
  • Case 1 cont.
    • In large epidemiological surveys for diabetes and chronic kidney disease, which of the following are correct?
      • About 1 in 20 people have abnormalities on urinalysis
      • About 8% of the general population have evidence of diabetes mellitus
      • About 1 in 10 type 2 diabetics have evidence of diabetic nephropathy
      • Those with diabetes are at risk of end stage kidney disease
  • Case 1 cont.
    • Question 1
    • In large epidemiological surveys for diabetes and chronic kidney disease, which of the following are correct?
      • About 1 in 20 people have abnormalities on urinalysis
      • About 8% of the general population have evidence of diabetes mellitus
      • About 1 in 10 type 2 diabetics have evidence of diabetic nephropathy
      • Those with diabetes are at risk of end stage kidney disease
  • Discussion Case 1
    • AusDiab 1 in 7 pts in Australia have diabetes. This can be as high as 1 in 3 in indigenous Australians
    • CKD was defined by presence of blood or protein on urinalysis and/or serum creatinine >150
    • 8% of the surveyed group had diabetes and half of them were unaware of Dx
    • 30% of those surveyed had hypertension with half being unaware of Dx
    • 1 in 3 type 2 diabetics will develop nephropathy
  • Take home message
    • Type 2 Diabetes is now worldwide, the most common cause of end stage kidney disease
    • Indigenous populations have much higher rates of end stage kidney disease (ESKD)
    • Risk factors for ESKD
      • Hypertension
      • Diabetes
      • Family history
      • Ethnicity
      • Smoking
      • Obesity
  • Case 1
    • Question 2
    • Which of the following is the most appropriate investigation when screening for CKD?
      • 24 hr urinary protein
      • 24 hr urinary albumin excretion
      • Urinary prot/creat ratio on a spot urine
      • Urinary alb/creat ratio on a spot urine
      • MSU with dipstick, spot ACR, microscopy and culture
  • Case 1
    • Question 2
    • Which of the following is the most appropriate investigation when screening for CKD?
      • 24 hr urinary protein
      • 24 hr urinary albumin excretion
      • Urinary prot/creat ratio on a spot urine
      • Urinary alb/creat ratio on a spot urine
      • MSU with dipstick, spot ACR, microscopy and culture
  • Discussion
    • CARI/KCAT reviewed evidence
    • Combo screening the best –
      • U/A
      • MSU - m,c,s
      • ACR
      • BP
      • Serum creatinine (GFR)
    • This should be done yearly in high risk groups – eg diabetics, ATSI
    • Further discussion
  • Take home message
    • Single urine dipstick for protein – limitations false positives, false negatives
    • Kidney function should be measured at least yearly in those at increased risk CKD
    • Screening should include measurement of BP, serum creatinine (GFR), MSU
    • Protein creatinine ratio or albumin creatinine ration
  • Case 1
    • Question 3
    • Which of the following is/are true statements concerning tests for assessing CKD?
      • Serum creatinine is an accurate measure of renal function and if <120 excludes nephropathy
      • GFR estimated from a formula is an accurate measure of renal function
      • A deterioration in eGFR or more than 15% over a period of months is sign of acute renal failure
      • An eGFR of >20mls/min excludes clinically relevant renal disease
  • Case 1
    • Question 3
    • Which of the following is/are true statements concerning tests for assessing CKD?
      • Serum creatinine is an accurate measure of renal function and if <120 excludes nephropathy
      • GFR estimated from a formula is an accurate measure of renal function
      • A deterioration in eGFR or more than 15% over a period of months is sign of acute renal failure
      • An eGFR of >20mls/min excludes clinically relevant renal disease
  • Discussion
    • Serum creatinine can stay in the normal range until more than 50% of GFR is lost
    • Serum creatinine is dependent on age, weight, gender and muscle mass
    • Small people with low muscle mass, elderly, female may have significant renal impairment despite a ‘normal’ creatinine
    • GFR falls over hours, days or weeks in acute renal failure
    • GFR falls over months, years in chronic renal failure
    • eGFR is used to stage kidney disease
  • Discussion Stage GFR mL/min/1.73 Expected CM’s 1 >90 None or the primary disease process 2 60-89 None, hyperparathyroidism, increased risk CVD 3 30-59 Nocturia, anaemia, increased creat, decreased vit D, dyslipidaemia, abN extracellular volume 4 15-29 Uraemic symptoms, abnomalities electrolytes 5 <15 Severe uraemic symptoms, dialysis
  • Take home message
    • eGFR is useful as a screening tool for CKD
    • Should be used in conjunction with BP, U/A, ACR
    • eGFR can be used to stage CKD
  • Case 1 continues
    • Over next 12 months, renal disease progresses
    • Creat 312
    • Risk factors for cardiovascular disease poorly controlled
      • BP >150 with 4 drug therapy on board
        • ACEI, CCB, BB, Frusemide
      • Hyperlipidaemia despite statin therapy
      • ACR increasing despite ACEI
  • Case 1
    • Question 4
    • In slowing the progression of renal disease and avoiding the development of malnutrition in CKD patients with an eGFR 15-30 mls/min, which of the following statements is/are correct?
      • Nephrotic patients need a high protein diet
      • Reducing proteinuria to <1g/24 hours is associated with a reduction in rate of decline off renal function
      • Proteinuria is a good measure of renal dysfunction
      • Heavy proteinuria (>3g/24hrs) predicts the response to ACEI
  • Case 1
    • Question 4
    • In slowing the progression of renal disease and avoiding the development of malnutrition in CKD patients with an eGFR 15-30 mls/min, which of the following statements is/are correct?
      • Nephrotic patients need a high protein diet
      • Reducing proteinuria to <1g/24 hours is associated with a reduction in rate of decline off renal function
      • Proteinuria is a good measure of renal dysfunction
      • Heavy proteinuria (>3g/24hrs) predicts the response to ACEI
  • Discussion
    • CARI guidelines advise against excessive protein restriction for slowing renal function decline
    • High protein diets do little to correct the malnourished state
    • Control of BP can signifcantly reduce proteinuria esp ACEI, AR2B, aldosterone antagonists
  • Take home message
    • Low protein diets may slow progression CKD but only a small impact and may increase risk of malnutrition
    • High protein diets are not effective in treating malnutrition and may accelerate CKD
    • Lowering BP decreases proteinuria
    • Degree of preservation of renal function achieved with AHA directly proportional to decrease in proteinuria
    • ACEI/AR2B’s slow progression CKD more than explained just be AHA
  • Case 1
    • Question 5
    • When a pt with T2DM is assessed for diabetic nephropathy, which of the following is correct?
      • The absence of proteinuria excludes diabetic nephropathy
      • Hypertension usually indicates the presence of concomitant macrovascular disease
      • The severity of diabetic nephropathy is related to the severity of hypertension
      • The absence of diabetic retinopathy excludes diabetic nephropathy
      • Kimmelstiel-Wilson lesions must be present to diagnose diabetic nephropathy
  • Case 1
    • Question 5
    • When a pt with T2DM is assessed for diabetic nephropathy, which of the following is correct?
      • The absence of proteinuria excludes diabetic nephropathy
      • Hypertension usually indicates the presence of concomitant macrovascular disease
      • The severity of diabetic nephropathy is related to the severity of hypertension
      • The absence of diabetic retinopathy excludes diabetic nephropathy
      • Kimmelstiel-Wilson lesions must be present to diagnose diabetic nephropathy
  • Discussion
    • NHANES 3 study – T2DM with creat > 150 -1/3 rd had no evidence of proteinuria
    • Due to more of a Vasculopathy (particularly microvascular) than by classic histological changes of glomerular basement membrane thickening and mesangial expansion
    • Vasculopathy is associated with hypertension and may not be associated with proteinuria
    • Vasculopathy leads to progressive CKD, accelerated by diabetic control, hypertension, proteinuria
  • Take home message
    • Not all T2DM with CKD have proteinuria
    • Hypertension is common and is associated with progressive CKD
    • If hypertension is resistant, think RAS
    • Diabetic retinopathy and nephropathy are commonly but not always bound together
  • Case 1
    • Question 6
    • Which of the following is true regarding treatment aimed at slowing the progression of CKD and at preventing cardiovascular events such as AMI and CVA?
      • The target BP is <140/90
      • Only ACEI and AR2B slow progression CKD
      • In large studies, ACEi have been shown to improve overall survival in diabetics with large and small vessel vasculopathy
      • The presence of renovascular diesease is a contraindication to the use of ACEI or AR2B
  • Case 1
    • Question 6
    • Which of the following is true regarding treatment aimed at slowing the progression of CKD and at preventing cardiovascular events such as AMI and CVA?
      • The target BP is <140/90
      • Only ACEI and AR2B slow progression CKD
      • In large studies, ACEi have been shown to improve overall survival in diabetics with large and small vessel vasculopathy
      • The presence of renovascular diesease is a contraindication to the use of ACEI or AR2B
  • Discussion
    • Target BP should be <130/80
    • If diabetic with protenuria <1g/24 hours target should be <120/75
    • BP decrease alone contributes to slowing CKD
    • All antihypertensives good for this but AR2B and ACEI have greatest efficacy
    • HOPE and PROGRESS show ACEI in high risk populations decrease cardiovascular events
    • Atherosclerotic renovascular disease with evidence of RAS is not an absolute contraindication to the use of ACEI or AR2B but you need to be very careful
  • Take home message
    • Target BP
      • Proteinuria <1g/24hours 130/80
      • Proteinuria >1g/24hours 120/75
    • For diabetic CKD target BP <120/75
    • AR2B and ACEI preferred but any agent ok as long as BP controlled
    • Atherosclerotic renovascular disease not absolute contraindication to ACEi
  • Case 1
    • Question 7
    • In general, which of the following results in 50yo indicate need for referral to Nephrologist?
      • Diabetic with eGFR <60 and poorly controlled hypertension
      • A non diabetic with an eGFR 30-60mls, proteinuria <0.5g/day, controlled BP
      • Proteinuria >1g/day with normal eGFR
      • Unexplained decline in kidney function (>15% drop GFR over 3 months)
  • Case 1
    • Question 7
    • In general, which of the following results in 50yo indicate need for referral to Nephrologist?
      • Diabetic with eGFR <60 and poorly controlled hypertension
      • A non diabetic with an eGFR 30-60mls, proteinuria <0.5g/day, controlled BP
      • Proteinuria >1g/day with normal eGFR
      • Unexplained decline in kidney function (>15% drop GFR over 3 months)
  • Discussion
    • Late referral to Nephrologist associated with poorer outcomes, greater morbidity for RRT and pall care groups
    • Guidelines only and controversial – if not sure err on side of caution
    • In general, stable patients with eGFR >30 don’t require referral but a significant number can benefit from referral and progression may be able to be averted
  • Take home message
    • Indications for referral to Nephrologist
      • Proteinuria > 1g/24 hrs
      • eGFR < 30mls in non diabetics
      • eGFR < 60mls in diabetics
      • Unexplained decline in kidney function
      • Glomerular haematuria with proteinuria
      • CKD with difficult to control hypertension
      • Otherwise unexplained anaemia
  • Case 1
    • Question 8
    • Pt’s Hb dropped to 90 and treatment with epo commenced. Which of the following are true?
      • Most common cause for anaemia in CKD with GFR<60 is bleeding from the upper GIT
      • If pt on EPO, iron therapy is not required if serum ferritin is >100
      • Treating the anaemia of CKD is not required until HB<100
      • Anaemia occurs earlier in the course of CKD in diabetic than non diabetic patients
  • Case 1
    • Question 8
    • Pt’s Hb dropped to 90 and treatment with epo commenced. Which of the following are true?
      • Most common cause for anaemia in CKD with GFR<60 is bleeding from the upper GIT
      • If pt on EPO, iron therapy is not required if serum ferritin is >100
      • Treating the anaemia of CKD is not required until HB<100
      • Anaemia occurs earlier in the course of CKD in diabetic than non diabetic patients
  • Discussion
    • Small increased risk in GIH
    • Anaemia of CKD is due to relative erythropoietin deficiency and show up in stage 3 and is more severe in diabetics
    • Prior to epo, iron deficiency was rare due to blood transfusions
    • Now relative iron deficiency is a problem
    • EPO can only be prescribed once Hb <100
    • Aim Hb 120
    • Worse outcomes if Hb higher than this
    • Renal anaemia is often iron responsive
  • Discussion
    • Aims
    • Prior to starting epo – ferritin >100
    • Once epo started – ferritin 400-600
    • Transferrin saturation >20% prior to epo therapy
    • Transferrin saturation 30-40% post epo starting
    • Adequate iron stores required for epo to work
    • Iron deficiency is most common cause of hyporesponsiveness to epo
  • Take home message
    • Impaired absorption of oral iron and increased utilization of iron with EPO therapy have contributed to the development of iron deficiency
    • Optimize responsiveness to EPO – targets for ferritin 300-600 and saturation 30-40%
  • Case 1
    • CKD progresses and he needs dialysis. GP questions whether other therpay may have prevented such a rapid progression to ESKD
    • Question 9
      • For which of the following therapies is there level 1 evidence for efficacy in the CKD population
        • Cholesterol lowering with statins both to slow progressive decline of renal function and to reduce the increased cardiovascular risk associated with CKD
        • Uric acid reduction slows progression
        • Exercise and weight loss improve insulin resistance and slow progression
        • Aldosterone blockade can further slow progression
        • AR2B can further slow progression in pts on ACEI
  • Case 1
    • CKD progresses and he needs dialysis. GP questions whether other therpay may have prevented such a rapid progression to ESKD
    • Question 9
      • For which of the following therapies is there level 1 evidence for efficacy in the CKD population
        • Cholesterol lowering with statins both to slow progressive decline of renal function and to reduce the increased cardiovascular risk associated with CKD
        • Uric acid reduction slows progression
        • Exercise and weight loss improve insulin resistance and slow progression
        • Aldosterone blockade can further slow progression
        • AR2B can further slow progression in pts on ACEI
  • Discussion
    • Decrease uric acid, cessation of smoking, weight loss all slow progression but evidence is poor; studies small, non randomised, case studies
    • Statins thought to help but again studies not good – no RCT
    • AR2B and ACEI combo thought to help if patient proteinuric – COOPERATE study
  • Take home message
    • Allopurinol, weight loss, cessation of smoking, exercise may all slow progression of CKD but no level one evidence
    • Beneficial effect of lipid though to be present but still waiting level 1 evidence
    • AR2B and ACEi together can help delay progression in pt with proteinuria
  • Case 1
    • Question 10
    • In type 2 DM ACEi and AR2B have been shown to slow the development of progression of nephropathy in pts who are
      • Normoalbuminuric and normotensive
      • Normoalbuminuric and hpertensive
      • Microalbuminuric and hypertensive
      • Macroalbuminuric and hypertensive
  • Case 1
    • Question 10
    • In type 2 DM ACEi and AR2B have been shown to slow the development of progression of nephropathy in pts who are
      • Normoalbuminuric and normotensive
      • Normoalbuminuric and hypertensive ***
      • Microalbuminuric and hypertensive
      • Macroalbuminuric and hypertensive
  • Discussion
    • BENEDICT study
      • ACEi decreased albumuria in T2DM with hypertension and normal albumin excretion
      • RENAAL study
      • Similar results with AR2B
  • Take home message
    • ACEi and AR2B have been proven in hypertensive type 2 diabetics to slow progression of CKD, development of microalbuminuria, macroalbuminuria
    • Don’t use combination in patients who are simply hypertensive
  • Conclusion
    • Keep your chronic disease protocols handy
  • Acknowledgements
    • Information taken from chapter 11 Clinical Cases in Kidney Disease by David Harris and colleagues