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Management of Stage 3 Chronic Kidney Disease (CKD) in General Practice Dr. Valli Manickam Renal Physician.

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Presentation on theme: "Management of Stage 3 Chronic Kidney Disease (CKD) in General Practice Dr. Valli Manickam Renal Physician."— Presentation transcript:

1 Management of Stage 3 Chronic Kidney Disease (CKD) in General Practice Dr. Valli Manickam Renal Physician

2 Objectives: Statistical data about CKD Target values in ESKD When to Refer patients

3 400 500 600 700 800 900 1000 ESKD services ($millions) Steady state Linear growth Steady state 559.9640.1688.0724.5754.5782.3811.3 Linear growth 559.9652.5712.9763.8808.6852.5899.1 2004567892010 Cass et al Kidney Health Australia Report 2006 Projected annual ESKD costs Why worry about CKD & ESKD?

4 ESKD has a life expectancy between that of Colon Cancer & Lung Cancer USRDS 2001

5 ESKD and Cardiovascular Mortality Foley et al AJKD 1996

6 ) Creatinine Clearance (ml/min ) Residual Renal Function Timely Start ? 25 30 20 10 15 5 0 Late Referral Early Referral Why be interested? – Slowing progression

7 StageDescription GFR (ml/min/1.73 m 2 ) 1 Kidney Damage with Normal or  GFR >90 (with proteinuria) 2 Kidney Damage with Mild  GFR 60-89 3 Moderate  GFR 30-59 4 Severe  GFR 15-29 5 Kidney Failure <15 or (or dialysis) CKD Definitions Adapted from Am J Kidney Dis 2002; 39 (2, Suppl. 1): S17-S31 and using AusDiab data

8 Stage 5 – kidney failure Stage 1-3 Stage 4 – GFR <30 1.7 MILLION 30,000 4.5+ MILLION AT RISK Hypertension or diabetes 16,000 Kidney Disease in Australia The titanic/iceberg model AusDiab data, 2005 Adults over 25 years of age

9 CKD and the risk of death,CV events and hospitalisation Go et al N Engl J Med 2004; 351:1296-1305 N = 1,120,295 Kaiser Permanente Renal Registry All cause mortalityCardiovascular mortality

10 Outcomes in patients with CKD Kaiser Permanente Longitudinal Study Keith et al Arch Int Med 2004 n = 27988, FU = 66 mo Patients with CKD are 20 times more likely to die from cardiovascular events than survive to reach dialysis

11 GFR and Ageing Prevalence of eGFR < 60 ml/min in popn NHANES III Estimated GFR (MDRD) Median and interquartile range GFR declines by 5-8mL/min/1.73m 2 each decade

12 With CKD

13 Mr Bruce Battamsseen 02/08 –74 yo, retired –Smoker – 20 / day, alcohol - 30 g/day –Hypertension – 20 years –DM2 – 5 years  Oral hypoglycaemics –Diverticular disease –Infra-renal AAA – 4 cm  Incidental finding on CT for abdo pain –Stress echo - no inducible ischaemia –Medications: amlodipine, pravastatin, gliclazide, aspirin (low- dose) Bruce the Battler

14 BP 190 / 84 mmHg Peripheral pulses present Murmur Aortic Sclerosis eGFR mL/min/1.73m 2 Creatinine 160 umol/L37 [on 02/08] 115 umol/L57[on 09/07] Chol - 6.7 mmol/L: TG -4.05 mmol/L FBC normal UAtrace protein, no RBC, no WBC Bruce the Battler

15 a.The absence of significant proteinuria makes diabetic kidney disease extremely unlikely b.Quantitation of proteinuria will give important prognostic information c.He should not be started on an RAS inhibitor* to slow progression of kidney disease as he has worsening kidney function d.His smoking will worsen his kidney function e.Lipid lowering therapy has been proven to slow progression of kidney disease *ACE/ARB Question 1: Answer True or False

16 a.The absence of significant proteinuria makes diabetic kidney disease extremely unlikely FALSE –20-30% of diabetic patients may have chronic kidney disease without evidence of proteinuria  Mechanism not well understood –Likely to progress with time Minerva Endocrinol. 2005 Sep;30(3):161-77 Question 1

17 b.Quantitation of proteinuria will give important prognostic information TRUE –Increasing degrees of proteinuria lead to increasing risk of ESKD  Proteinuria a stronger marker of risk of progression to ESRD than baseline GFR  But eGFR strong predictor of morbidity and mortality –Reduction of proteinuria in proteinuric disease predicts reduced mortality and reduced progression to ESKD Question 1

18 Risk of ESKD related to baseline proteinuria (dipstick) over 18 year period Iseki et al, Kidney Int 2003;63:1468-1476 N= 106,000

19 Macroalbuminuria is a better marker than GFR in predicting loss of kidney function PREVEND Study J Am Soc Nephrol 2006; 17:2582–2590. Macroalbuminuria N=8952 – F/U 4yrs General Population + RBC urine Reduced GFR – mean 45 mL/min/1.73m 2

20  Recommended Targets in CKD Proteinuria and ESRD: –20-30% of diabetic patients may have chronic kidney disease without evidence of proteinuria  Mechanism not well understood –Likely to progress with time Minerva Endocrinol. 2005 Sep;30(3):161-77

21 –Increasing degrees of proteinuria lead to increasing risk of ESKD  Proteinuria a stronger marker of risk of progression to ESRD than baseline GFR  But eGFR strong predictor of morbidity and mortality –Reduction of proteinuria predicts reduced mortality and reduced progression to ESKD

22 Albuminuria and  GFR predict mortality and morbidity (RR) NormalMacroalbuminuria  GFR Mortality (RR) CV non CV 1111 2.6 1.5 3.4 3.0 Morbidity (RR) CV 11.42.3 PREVEND Study J Am Soc Nephrol 2006;17: 2582–2590.

23 c.He should not be started on an RAS inhibitor to slow progression of kidney disease as he has worsening kidney function FALSE –RAS inhibitors beneficial in decreasing mortality in those with GFR < 60 mL/min –RAS preferred agent for BP control in CKD, particularly in those with significant proteinuria Question 1

24 Risk Stratification - BP 10 mmHg  SBP results in 10.9% increase in RR of ESRD (RENAAL STUDY)  SBP = PP < DBP in prediction of ESRD  PP > SBP > DBP in prediction of mortality -PP > 70 mmHg   risk mortality in SHEP, FHS

25 –RAS inhibitors beneficial in decreasing mortality in those with GFR < 60 mL/min –RAS preferred agent for BP control in CKD, particularly in those with significant proteinuria

26 Treatment of BP in CKD - ? which agent ACEi / ARB – independent effect over BP alone Multiple trials – DM CTS – ACEi RENAAL – ATII IDNT – ATII – Non-DM GISEN REIN Bakris Et al AJKD 2000;36:646-661

27 Target blood pressure Adults  65 years (unless there is diabetes and/or renal insufficiency and/or proteinuria  25 g/day) < 140/90 mmHg Adults <65 years and/or Adults with diabetes and/or Adults with renal insufficiency and/or Adults with proteinuria 0.25-1.0 g/day <130/80 mmHg Adults with proteinuria >1 g/day (in people with and without diabetes) < 125/75 mmHg

28 d.Smoking is associated with kidney damage in the population AusDiab Study Smoking increases proteinuria and accelerates loss of GFR Am J Med Sci 2005;330:111-119 Question 1

29 e.Lipid lowering therapy has been proven to slow progression of kidney function FALSE Question 1

30 No specific randomised trials Post hoc analysis of CVD trials  CAREPravastatin vs placebo Fall in GFR 0.6 mL/min/1.73m 2 /yr if GFR < 50 mL/min 2.7 mL/min/1.73m 2 /yr if GFR < 40 mL/min greater effect with increasing proteinuria  HPS 40 mg simvastatin vs placebo attenuation in rise of serum creatinine  GREACE atorvastatin vs placebo Atorvastatin increased CrCl 12% placebo decrease in CrCl 5 % No trials in GFR <40 mL/min/1.73m 2 Does treating lipids affect CKD progression?

31 Tonelli et al JASN 2005;16:3748 Pravastatin reduces Absolute RR for CV events in DM & CKD – similar benefit seen in all-cause mortality Median F/U 64m

32 Bruce the Battler Commenced on perindopril/indapamide Seen 2 weeks later and reassessed:  BP 150 / 76 mmHg  Creatinine 189 umol/L (eGFR : 30 mL/min/1.73m 2 ) – Previously Creat 160 umol/L and GFR 37 mls/mt in Feb 2008.  K 5.8 mmo/L  Urine ACR9 mg/mmol

33 Do you : a.Cease the ACEi and commence another drug b.Cease the ACEi and check for a renal artery stenosis c.Continue the ACEi and check for a renal artery stenosis d.Add another drug for better BP control Question 2

34 My answer: Rationale: –A rise in creatinine of <30% is not unexpected after BP lowering and is a result of decreased perfusion –Target BP in CKD is <130/80 mmHg –ACEi may have particular benefit for kidney disease –K+ needs watching but not a concern at this level (? Give low K+ diet) d.Add another drug for better blood pressure control

35 Bruce the Battler Seen 1 month later –BP 134 / 68 mmHg –Creatinine 245 umol/LeGFR 23 mL/min –Ca 2.05 mmol/LPO 4 1.54 mmol/L –Hb 98 g/Lnormocytic/normochromic –Urine dipstick normal

36 What would you do? a.Refer for erythropoietin treatment b.Check iron studies c.Check Vit B12 and folate levels d.Check Vitamin D and PTH e.All of the above Question 3

37 Bruce the Battler My Answer: e. All of the above Results: –Ferritin996Tsat 55% –B12 and folate Normal –TSH Normal –PTH18 pmol/L(N <8 pmol/L) –Vit D25 nmo/L(mod deficiency)

38 CKD progression - Anaemia Anaemia due to CKD begins at GFR < 60 mL/min  common when GFR < 30 mL/min (30-40%) CKD anaemia is a diagnosis of exclusion  Need to ensure not Fe deficient or B12/folate deficient, or hypothyroid –Different reference range for Fe stores if on Erythropoietin  Ferritin > 300 ng/ml Tsat >20%  May respond to iv iron if stores low without need for erythropoietin  I.v. iron gives quicker and higher response than oral (and is better tolerated) Gouva et al, Kidney Int 2004;66:753-760

39 Anaemia is associated with mortality in dialysis patients Multiple observational studies show lower Hb associated with adverse outcome Adjusted RR of death due to any cardiac cause, according to Hct. Li & Collins, Kidney International 2004;65:626–633 n= 50,579

40 The target Hb for anaemia in CKD Optimal Hb level not known Observational – 110 – 120 g/L RCT – no benefit above 120 g/L

41 CKD & Anaemia Summary Common and important to correct Can’t start EPO till Hb <100g/L (PBS) Need to have nephrologist endorsement to start Ensure not iron deficient All respond – need to dose titrate Most self administer SC each 2- 4wks All will need extra iron (oral or i.v.)

42 Bruce the Battler Seen 1 month later –BP 134 / 68 mmHg –Creatinine 245 umol/leGFR 23 mL/min –Ca 2.05 mmol/LPO 4 1.54 mmol/L –Hb 98 g/Lnormocytic/normochromic –Urine dipstick normal

43 Why worry about Ca & PO 4 in CKD Stages 3-5? All patients develop Ca/PO 4 disturbance (by CKD Stage 5) Onset of Ca changes is early in CKD Ca/PO 4 disturbance causes Bone disease Soft tissue calcification (coronaries & valves) Pruritus Proximal myopathy Premature death

44 Increased PO 4 is associated with increased mortality even in normal Kidney Function Tonelli et al, Circulation 2006 S. PO 4 mg/dL Hazard ratio

45 PO4 and mortality in Dialysis

46 Mechanisms of Ca/PO 4 disturbance Phosphate retention with reduced GFR results in increased s PO 4 and suppresses Vit D3 production Reduced Vit D3 leads to reduced Ca absorption and this plus high s PO 4 leads to low s Ca Ca x PO 4 increases favouring tissue deposition PTH stimulated by low Ca, high PO 4 & low Vit D3 Clinical effects: Low s Ca High s PO 4 High s PTH Low Vit D3 [1,25 (OH) 2 D 3 = calcitriol]

47 Changes in serum levels CKD Stage PTHCalciumPhosphate1,25D GFR (mL/min/1.73m 2 ) 60-90 30-59 15-30 <15 2 3 4 5           2-fold  4-fold  8-fold Changes Ca/PO 4 parameters with reducing GFR

48 Assessment of Ca/PO 4 disturbance* (CKD Mineral and Bone disorder) What to measure –Calcium (corrected for albumin) –Phosphate –Alkaline phosphatase –Bicarbonate –PTH –(Vitamin D3) How often? –12 monthly in CKD Stage 3 –3 monthly in CKD Stage 4 *KDIGO position statement. Kid Intern 2006;69:1945

49 Goals of therapy for Ca/PO 4 disturbance Control s PO 4 to <1.65 mmol/L Keep s Ca in normal range (2.2-2.6 mmol/L) Keeps Ca x PO 4 <4mmol/L Keep s PTH to ~2-3 times normal

50 Therapy for Ca/PO 4 disturbance Control s PO 4  Dietary restriction  Phosphate binders (prevent uptake) Control s Ca  Adequate calcium intake  Calcitriol (increases uptake) Control s PTH  Calcitriol  Cinacalcet  Parathyroidectomy

51 Ca++ / PO4 2- / PTH / Vit D in CKD Changes by Stage of CKD Clinical effects

52 Mechanism for Vit D effect on CVS

53 Who may be considered for referral to a nephrologist? Anyone with –eGFR <30mL/min/1.73m 2 –Unexplained decline in kidney function (>15% drop in GFR over 3 months) –Proteinuria >1g/24hrs (protein:creatinine ratio of 100 mg/mmol  1g/24hrs) –Glomerular haematuria (particularly if proteinuria present) –CKD and hypertension that is hard to get to target –Diabetes with eGFR <60mL/min/1.73m 2 –Unexplained anaemia (<100g/L) with eGFR <60mL/min/1.73m 2 Anyone with an acute presentation and signs of acute nephritis should be regarded as a medical emergency and referred without delay Clinical tip When referring to a nephrologist ensure patient has had a recent kidney ultrasound, current blood chemistry and quantification of proteinuria

54 Who does not usually need to be referred to a nephrologist? Don’t refer CKD Stage 2-3 if: –Stable eGFR 30-89 mL/min/1.73m 2 –Minor proteinuria (<0.5g/d with no haematuria) –Controlled blood pressure In CKD Stages 2-3 –Don’t refer to nephrologist if targets of therapy are achieved –Pay attention to CVD risk reduction –Use ACE/ARB –Monitor 3-6 monthly The decision to refer or not must always be individualised. In younger patients the indications for referral may be less stringent e.g. minor proteinuria and in older patients they may be more selective.

55 Conclusion Early CKD is so common that it must be mainly managed in general practice Therapy overlaps significantly with best practice in CV risk reduction and diabetes care Key CKD management tasks  Lifestyle – Healthy diet & exercise, no smoking, weight control  Reduce CV risk  BP at target with ACE/ARB  Reduce proteinuria with ACE/ARB  Optimise haemoglobin, Ca/P and glycemia

56 THANK YOU


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