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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

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Progressive Chronic Kidney Disease

  • Cherelle Fitzclarence

  • August 2009


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Overview

  • Case studies

  • Discussion

  • Take home messages


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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


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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


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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


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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


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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


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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


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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


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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


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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


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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


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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


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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



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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


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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


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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


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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


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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


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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


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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


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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


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Discussion

  • NHANES 3 study – T2DM with creat > 150 -1/3rd 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


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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


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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


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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


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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


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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


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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)


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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)


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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


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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


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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


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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


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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


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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


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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%


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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


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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


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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


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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


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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


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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


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Discussion

  • BENEDICT study

    • ACEi decreased albumuria in T2DM with hypertension and normal albumin excretion

    • RENAAL study

    • Similar results with AR2B


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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


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Conclusion

  • Keep your chronic disease protocols handy


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Acknowledgements

  • Information taken from chapter 11 Clinical Cases in Kidney Disease by David Harris and colleagues


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