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Management of CKD basic to current update.pptx
- 1. Management of CKD BASICS TOCURRENT UPDATES Dr Shashikanth M DM Nephrology Assistant professor VIMS Bellary
- 2. Content Introduction Magnitudeof the problem Diagnosis Management • Summary
- 3. Introduction CKD isa worldwide public health problem, both for the number of patients and cost involved. With growing age of the population prevelence is increasing. Lack of knowledge to screen early and also to manage them rightly increasing morbidity and mortality among CKD patients.
- 4. Magnitude of the burden • Thereported prevalence of CKD in different regions of India ranges from <1% to 17%(ISN 2018). • Over 50% of patients with advanced CKD are first seen when the eGFR is <15 ml/min per 1.73 m2 . • This sobering number highlights the need for robust screening programs for those at risk for CKD
- 5. Diagnosis Chronic kidneydisease (CKD) is defined as either structural or functional impairment of the kidney for three or more months, irrespective of the cause.
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- 8. Gaps in CKD Diagnosis NotAppropriately Tested Appropriately tested - no diagnosis Appropriately tested - accurate diagnosis 0 10 20 30 40 50 60 CKD Screening in Primary Care (% of patients) % of Patients
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- 10. Creatinine & cystatin Noideal marker yet We have only functional marker no structural markers. No troponin or AST for kidney Both of them are late markers Hence rapid action is required once elevated. Serial values are important to know the rate of fall of GFR eGFR calculation – CKDEPI is preferred ( 2012) What’s new – cystatin in the formula
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- 12. Proteinuria/ Albuminuria Diagnostic &Prognositic .
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- 15. Imaging Ultrasonographyis the mainstay Small size is definitive ( 9.5 -12cm) Altered echogenecity. Loss of corticomedullary differentiation. Obstructive uropathies.
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- 17. Managemen t Treatment ofreversible causes of kidney failure Preventing or slowing the progression of kidney disease Treatment of the complications of kidney failure . Adjusting drug doses when appropriate for the level of estimated glomerular filtration rate (eGFR). Identification and adequate preparation of the patient in whom kidney replacement therapy will be required
- 18. Reversible causes of CKD Nephrotoxicdrugs Urinary tract obstruction Treating underlying cause. Preventing infections
- 19. Slowing the progression Lifestyle modifications Strict blood pressure and glycemic control RAAS inhibitors SGLT2 inhibitors No steroid MRA(Finerenone)
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- 21. Life style modification s Saltrestriction <2.5 gm /day Smoking cessation weight reduction (ORG) Dietary animal protein restriction.
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- 26. SGLT2 inhibitors The Game changers Decreasesblood sugars Decreases BP Slows progression of CKD 5th pillar for heart failure treatment Reduces hyponatremia
- 28. Finerenone The Forgotten ‘A’ of RAAS string Finerenone is a non-steroidal third generation Mineralocorticoid receptor antagonist. It has high affinity for the Mineralocorticoid receptor does not bind to androgen receptor It reduces albuminuria It improves cardiovascular outcomes and also renal outcomes Two major studies FIDELIO DKD and FIGARO DKD have shown significant improvement with respect to RENAL & CARDIOVASCULAR outcomes There is an increased risk of hyperkalaemia Use in combination with SGLT2 inhibitors requires further study
- 31. Too early not justearly . Protective therapy has the greatest impact if it is initiated before the plasma creatinine concentration exceeds 1.2 - 1.5 mg/dL
- 32. GFR of 50 yearold Indian male at different creatinine values S. Creatinine GFR 1.2 74ml/min/1.73m2 1.5 56ml/min/1.73m2 1.8 45ml/min/1.73m2 2.0 40ml/min/1.73m2 3.0 25ml/min/1.73m2 4.0 17ml/min/1.73m2 5.0 13ml/min/1.73m2 10.0 6ml/min/1.73m2
- 33. Complication s Metabolic acidosis Hyperkalemia Anemia Mineral bone disease Volume overload Dyslipidemia Malnutrition
- 34. Complication s Metabolic acidosis ImprovesGrowth in children Delays progression of CKD Preserves bone health Reduces inflammation Prevents cachexia Target above 22 meql/dl Caution about volume expansion Hyperkalemia DIET & DRUGS Food leaching RAASi ,MRA, Beta blockers,NSAIDS. Minimise with diuretics and alkali therapy
- 35. ANEMIA Worsens cardiacfailure , frequent hospitalisation, repeated transfusion, infections, sensitisation Relative deficiency of Erythropoietin and abnormal hypoxia sensing mechanism . Correct the iron ,B12, frolic acid deficiency. ESA – Erythropoetin, darbopetin, peqylated rHu EPO DUSTATS ( HIF STABILIZERS - desidustat, vadadustat, roxadustat,molidustat,daprodustat)
- 36. CKD MBD Triard Osteodystrophy, vascular calicification , high phosphate ,low calcium, high pth(paratharmone). Spectrum – a Dynamic bone disease to renal osteodystrophy Treatment - Correct vit D deficiency, hypocalcemia , hyperphosphatemia ( dietary restriction, oral phosphate binders, calcitriol, calcimmetics)
- 37. Dyslipidemia Mainly hypertriglycerdemiawith total cholesterol being normal. Screen all patients with CKD In DM, Nephrotic syndrome , metabolic syndrome may have elevated cholesterol , treatment is with statins and ezetimibe. Secondary prevention is similar to non CKD patients Primary prevention- 1. All patients with GFR <60ml/min 2. Patients with CKD and GFR >60ml/min and age>50yrs or other risk factors.
- 38. Malnutrition Protein diet.? Need customisation For Indian patients ICMR (2020) – 0.6gm/kg body weight. Restrict in glomerular disease in early stage. Restrict animal protein. Calorie - 30 to 35kcal /kg / day
- 39. Infection and vaccination Higherrisk of infections compared to general population Vaccination : Influenza – annual. Hepatitis B – 4 doses ( double dose) Pneumococcal ( prevenar 13 & pneumovac 23)
- 40. Medications in CKD CKDpatients at high risk for drug-related adverse events •Several classes of drugs renally eliminated •Consider kidney function and current eGFR (not just SCr) when prescribing meds •Minimize pill burden as much as possible •Remind CKD patients to avoid NSAIDs •No Dual RAAS blockade •Any med with >30% renal clearance probably needs dose adjustment for CKD •No bisphosphonates for eGFR <30 •Avoid GAD for eGFR <30
- 41. Referral to Nephrologist s When GFR< 30 ml/min/1.73m2. Earlier in whom GFR is falling rapidly and with albuminuric CKD Rapid fall - >5ml/min/1.73m2/ year . Why To Plan and counsel about renal replacement therapy Access(vascular & peritoneal Dialysis) To counsel about renal transplantation
- 42. Referral to Nephrologist s latereferral is associated with a significantly increased risk of all-cause mortality. Early referral enables discussion of the preferred mode of kidney replacement therapy to suit the patient's lifestyle. Helps in timely placement of a permanent dialysis access. Patients treated by nephrologists were significantly less likely to have required a temporary venous catheter for the first dialysis (36 versus 89 percent).
- 43. Most common cause of death 1.Cardiovascular. 2. Infections. 3. Access failure.
- 44. Kidney replacement therapy Hemodialysis (incentre / home ) Peritoneal dialysis ( intermittent/ continuous) Kidney transplantation – treatment of choice, as it improves quality of life and reduces mortality.
- 45. Hemodialysi s Pros Widely available Under government schemes Less patient involvement . Regular monitoring by Nephrologists Cons Thrice a week ( care giver fatigue) Not a continuous process(unphysiological) hemodynamic unstability Access issues.- Fistula first catheter kills Painful
- 46. Peritoneal dialysis Pros Homebased Patient involved in his own care More independent. More physiological and liberal food intake Less BP variations. Cons Abdominal discomfort. Peritonitis. Lack of Patient smartness. Less effective once patient is Anuric
- 47. Kidney transplantati on Treatment ofchoice As it replaces all the functions of the kidney. Live related / deceased donor(JSK). Swap transplantation program. Abo incompatible transplants. Cons. Cost Availability of the kidney Stigma in society (Donor and receipent) Immunosuppression risk for the recipient Graft loss ( rejection, recurrence of basic disease)
- 48. Take home Robustscreening of high risk patients for early diagnosis . Lifestyle modifications are equally important as pills. Use of Disease modifying drugs and regular monitoring. Timely referral to Nephrologists Preparing for kidney replacement therapy Encourage deceased donor and swap transplantation.
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Editor's Notes
- #4 Increases risk for all-cause mortality, CV mortality, kidney failure (ESRD), and other adverse outcomes.
- #10 Use of cystatin c along with creatnine strengthens the association between the eGFR and risk of death. Muscle mass All nucleated cells ( obesity smoking crp ) Epidemiology collaboration equation
- #18 Heart failure Liver failure Haematological diseases HBV HCV Glomerular disease
- #21 Hyperfiltration injury Nephron numbers are fixed
- #26 RAASi Diuretics MRA Beta blockers
- #37 Cheese, milk products, egg Red meat, beans nuts oats soft drinks
- #48 BP control erythropoesis, bone health