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A brief overview of CKD A brief overview of CKD

A brief overview of CKD - PowerPoint Presentation

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A brief overview of CKD - PPT Presentation

Harshani D Perera Senior Registrar Nephrology SJGH 09012018 CKD definition Kidney damage or eGFR lt 60 mlmin173m2 persisting for 3 months despite the cause several classifications ID: 1033994

progression ckd egfr risk ckd progression risk egfr kidney patients esrf stage management min protein early dialysis blood control

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1. A brief overview of CKD Harshani D. Perera Senior Registrar – NephrologySJGH 09.01.2018

2. CKD – definition Kidney damage or eGFR < 60 ml/min/1.73m2 persisting for 3 months despite the cause several classifications KDOQI – by National Kidney Foundation KDIGO – by International Society of Nephrology

3. Classification - CKD KDOQI (Kidney Disease Outcome Quality Initiative ) guidelines , by NFK 5 stages of CKD suffix T for patients with allografts suffix D for patients on dialysis 2012 KDIGO guidelines by ISN 6 categories G1 to G5 G3 – split in to 3a, 3b A1, A2, A3 – 3 levels of albuminuria

4. Calculating eGFR MDRD (modification of diet in renal disease formula) : overall MDRD more accurate CKD-EPI Chronic kidney disease Epidemiology Collaboration) – gender, race, age, Cr : are parameters need in both MDRD , CKD- EPI Creatinine clearence : by Cockcrofr-Gault Equation : sex, age, weight, Cr, height (remains gold standard after 40 years) –less accurate than MDRD in obese and elderly

5. Limitations – classification CKD Current CKD classification based on eGFR MDRD , CKD-EPI – both are relatively inaccurate in reflecting measured GRF above 60 ml/min underestimate true GFR , thus over diagnose a large number of people having CKD stage 3 b Physiological age related decline in kidney function in elderly – in absence of associated micro albuminuria seldom progress to ESRF

6. Progression of CKD Current classification – not determined on progression of CKD KDIGO – suggest , to define Progressive CKD sustained decline in eGFR by 5ml/min per year Or declining eGFR category accompanied by 25% of drop in baseline eGFR

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8. Epidemiology - CKD Prevalence 10% - 14% among general population CAUSES : Hereditary – APCKD Acquired nephropathy : DM , HT, Glomerularnephritis, obstructive nephropathies

9. Rate of progression vary ! According to underlying etiology . Historically DM-nephropathy is the fastest , average decline around 10ml/min per year. In non diabetic CKD , chronic proteinuria GN having faster progression than low proteinuric CTIN-CKD. In APCKD, beyond stage 3b , more faster course. Majority reach from stage 3b to 5 progress to ESRF. Some patients in CKD-5 remain stable for number of years.

10. Risk factors - CKDModifiable Birth weightSystemic HTDiabetesCVDAlbuminuriaObesity / metabolic XnDyslipidemia/smoking HyperuricaemiaNephrotoxins – NSAID,herbal, Heavy metal Non- modifiableAge (older)Race (Non-caucasian)Genetics

11. Retarding progression of kidney disease ? Typically natural progression does not proceed until nephron loss exceeds 50%. Normal solitary kidney is vulnerable to natural progression if condition is congenital or acquired in early life. LBW esp males progress to ESRF due to defective nephron development.

12. Proteinuria magnitude and risk of CKD progression Magnitude of proteinuria is the strongest risk factor of CKD progression . When it exceeds 500mg/dl  it co relate the threshold of natural CKD progression. Exception is highly selective albuminuria which can persists in nephrotic range even 10 years with out causing structural renal damage.

13. Non proteinuric CKD CAUSES Early phase of diabetic CKD HT- GS ADPCK Chronic NSAIDs Obstructive uropathy Nephropathy of aging

14. Level 1 – kidney protective measures Control blood pressure ACEI or ARBS avoid dihydropyridine unless needed for BP control Control protein intake

15. Level 2 - recommendations Restrict NaCl intake and diuretic therapy NDHP –CCB control each component of metabolic syndrome Aldosterone antagonists Allopurinol therapy control serum PO4 alkali therapy Bata blockersAvoid over anti-coagulation with warfarin

16. Functions of kidney Fluid balance Regulate electrolytes Blood pressure regulation : RAAS Ca / P04 regulation- bone metabolism Acid base balance Endocrine function – erythropoietin / 1 OH CCF / Renin

17. Management of CKD Early referral to nephrologist Aim to slow down the progression : Management of complications related to CKD RRT counseling when CKD advances when eGFR – 20 ml/min Refer to vascular surgeon for access creation if dialysis is decided. Preserve non-dominant upperlimb for future AVF Hepatitis B vaccination - dual doses 0,1,6 months

18. Preventing CKD progression Most effective intervention is control of blood pressure : HT is very common among in patients with CKD Anti HT therapy Life style modifications : reduction of salt and alcohol maintenance of healthy weight regular exercise

19. Anti hypertensive therapy Fluid driven blood pressure (water and Na retention ) rise in advances CKD Activated RAAS usually multi drug regimens required. ACEI and ARBS are first line in proteinuric CKDrisk of hyperkalemia especially during intercurrent illnesses Choice of drugs depends on co-existing CVD, co-mobidities Target : 130/80

20. Dietary advice Obesity causes rapid progression of CKD, thus need weight loss. Malnutrition common in CKD , it is multifactorial. anorexia, acidosis, insulin resistance , inflammation , oxidative stress, urinary protein loss low serum Albumin, Cholesterol, transferrin – are markers Creatinine may stop rising due to reduction in muscle mass.

21. Recommendation - diet Reduce protein intake slow the CKD progression – evidence based. Protein energy malnutrition is common. KDIGO – protein 0.8 g/KBW/day when GFR < 30 ml/min Avoid high protein intake >1.3g/KBW/d in patients at risk of CKD progression. Salt restriction : < 5g NaCl (90mmol) per day.In stage 4,5 – restrict K ,and PO4 .

22. Anemia in CKD Common in stage 3a and above low Epo levels reduced availability of iron chronic inflammation Monitor Hb levels annually till stage 3 a , then 6 monthly in advanced CKD.

23. Recommendation - anemia Rule out other causes of anemia Fe studies, blood picture, Vit B12, foalte levels, stool occult blood, UGIE / LGIE IV Iron : when T. Sat < 30 % Correct deficiencies , if Hb still < 10g/dl, start EAS ( Erythropoetin stimulating agents)If benefits overweigh potential harm – increased risk of stroke/thromboembolism, malignancies, hypertension

24. Benefits of anemia correction Cardio- vascular benefits : regression of LVH, reduction of myocardial ischemia, reduced HR / CO Increased quality of life : improved exercise capacity, sleep patterns, immune functions, cognition, depression Target Hb < 11.5 g/dl should be maintained. Hb > 11.5 carry higher risk of cardiovascular events : stroke/ MI

25. Bone and mineral metabolism Renal bone disease may already be manifested in CKD stage 3 b, and well established in ESRF. Even it is well established patient may remain asymptomatic. Active early management of CKD-BMD will prevent some of cardio-vascular complications.

26. Recommendations - BMD check serum ionized Ca, PO4 , intact PTH levels when eGFR < 45 ml/min optimal PTH target : 3 times upper range correct hyperphosphatemia, hypocalcemia, and Vit D deficiency Vit D suppliments / analogue Phosphate binders dietary phosphate restriction (dairy products, processed foods )

27. Complications of BMD Coronary vessels calcification  higher cardio-vascular risk Heart valve calcification soft tissue calcifications – calciphilaxis : indicating very poor prognosis in CKD. Renal osteodystrophy

28. Metabolic acidosis in CKD Failure of H+ excretion , may be compounded by accumulation of organic acids and bicarbonate loss in interstitial kidney diseases. clinical manifestations rare till stage 5, dyspnoea occur due to respiratory compensation .

29. Metabolic acidosis … aggravate hyperkalemia inhibits protein anabolism accelerate Ca loss from bone correction of acidosis also slow the progression of kidney diseaseKDIGO - recommends if HCO3 < 22 mmol/L oral bicarbonate supplementations to maintain HCO3 level above 22 .

30. Cardiovascular risk high prevalence of CVD among CKD patients. most likely to die due to CV event than progress to ESRF. KDIGO – recommends :level of coronary care should not be reduced by their CKD state. Anti platelets in secondary prevention of CVD. accelerate atherosclerosis : lipid lowering drugs for all above 50 yr, and young CKD patients with additional risk factors for dyslipidemia.

31. Risk of infection Infection is second commonest cause of death in ESRF. state of chronic immunosuppression ,defect in both cellular and humoral immunity. Annual influenza vaccine when eGFR < 30 Pneumococal vaccine for those who are high risk Hepatitis vaccination : early as possible , preferably eGFR > 30

32. Avoid risks of AKIs among CKD All patients with CKD are at increased risk of AKI Avoid nephrotoxins: NSAIDs, aminoglycosides, vancomycin , drugs causing interstitial nephritis Iodinating contrast for imaging better avoid unless benefits outweigh the risk of contrast AKI. poor renal perfusion : volume depletion , over diuresis , diarrhoea, vomiting sepsis heart failure , MI, tachyarrythmias

33. Increased bleeding risk Uremic platelet dysfunction mild to moderate thrombocytopenia is commonly seen among ESRF Inadequate dialysis anemiaHeparin use for dialysis Options :adequate hemodialysis, correction of anemia, platelet transfusion, cryopercipitate, desmopressin nasal spray, tranexamic acid

34. Timing and initiation of RRT All patients with eGFR < 20 , or who are likely to progress to ESRF in 12 months should receive education and counseling to aid their decision on best RRT modality. If HD is preferred  AVF referrel If PD is preferred  CAPD catheter insertion 3 weeks prior. Kidney transplant : Pre-emptive is the best , offer when eGFR <20 , before dialysis. explore the possibility of live donor if KT opted.

35. “Conservative” Management Potential burden of commencing RRT in terms of high short term mortality rates Recurent hospitalizationsTime spent for travellingLimited improvement of quality of lifeMultiple co-morbidities Advanced malignancy Offer active medical management and follow up with out starting dialysis. distressful advanced uremic symptoms – need palliative care to facilitate suffering free death.

36. Conclusion Rising global trend of CKD during last few decades. Diagnosis of CKD is challenging and by exclusion of AKI when there is no baseline Cr available. CKD management guidelines are freely available which is helpful to provide standards of care. Asses the progression of CKDDelay the progression of CKD while managing CKD related complication. Early referral to nephrologist and on time RRT counseling are key in successful management.

37. Thank You.