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CKD (December 2019jbkhjkj,gbkjhbljkbjhlk).pptx
- 1. CHRONIC KIDNEY DISEASES(CKD) Dr Manoj Aryal MBBS,MD DM-Resident Department of Nephrology NAMS (2080-09-03)
- 2. OUTLINE • DISEASE BURDEN •DEFINITION • ETIOLOGY • STAGING • MANAGEMENT - EVALUATION -TREATMENT
- 3. DISEASE BURDEN GlobalCKD prevalence 11 to 13%¹ Resource utilization is high Increased risk of cardiovascular complications 1. Hill , Lasserson , et al. (2016) Prevalence of Chronic Kidney Disease 2. SEEK (Screening and early evaluation of kidney disease) study
- 4. DEFINITION • CKD isdefined as abnormalities of kidney structure or function, present for 3 months Criteria for CKD (either of the following present for >3 months) Markers of kidney damage (one or more) • Albuminuria • Abnormalities detected by histology • Structural abnormalities detected by imaging Decreased GFR GFR < 60 ml/min/1.73 m² KDIGO Clinical Practice Guideline-Chronic Kidney Disease
- 5. COMMON ETIOLOGIES: INDIANPERSPECTIVE SEEK(Screening and early evaluation of kidney disease)study
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- 8. HISTORY AND EXAMINATION •Establishing chronicity • Establishing etiology: Past history, Drugs, Family history • Environmental exposure • Examination-Blood pressure Organ damage , oedema, Neuropathy, fundoscopy Signs of uremia/ fluid overload
- 9. INVESTIGATIONS • Lab parameter AetiologyComplications Blood • Diabetes- HbA1C • Viral markers- HCV,HBV,HIV • Autoimmune - ANA,dsDNA, C3/C4 • Inflammatory markers - ESR, CRP • Serum Electrophoresis • RFT/ LFT- Creatinine,Na,K, Bicarbonate , PO4, Uric acid, Ca, albumin • CBC-Hb,S.Fe,Ferritin, Peripheral smear, B12,Folate • Hormones- Vit.D,iPTH, • Lipid profile Urine • Active sediments • Urine electrophoresis • Proteins • Electrolytes: Na, K
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- 11. STAGING KDIGO Clinical PracticeGuideline for Chronic Kidney Disease
- 12. IMAGING Plane X-ray-stones IVU- vesico-uretericabnormalities USG- length-Normal -9-12 cm in length In CKD < 8cm -cortical echogenicity USG Finding Inference symmetric decrease in size • Systemic CKD Asymmetrical kidneys • UTI • Reflex uropathy Discrepancy >1 cm in length • Developmental abnormality • Reno vascular disease
- 13. IMAGING • Doppler sonography-forReno vascular disease • Radio nucleotide scanning- -DMSA- structural imaging -DTPA -MUGA • CT • Magnetic resonance imaging (MRI) • BIOPSY-Contraindicated in B/L contracted kidney Functional imaging
- 14. MANAGEMENT OF CKD •Identification &Treatment of reversible causes • slowing the progression of renal disease • Treatment of the complications of renal failure • Adjusting drug doses for e GFR • Identification and preparation for RRT
- 15. Reversible causes ofrenal failure CMDT-2017
- 16. Slowing the rateof progression Definition of CKD progression • Decline in GFR category • Rapid progression- eGFR > 5 ml/min/year. How? • Blood pressure control • Glycemic control • Protein restriction • Smoking cessation KDIGO Clinical Practice Guideline Chronic Kidney Disease
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- 18. Cardiovascular Morbidity • 10to 100 fold increase • CKD Causes- Ischemic heart disease Heart failure Left ventricular hypertrophy Hypertension Conduction abnormalities Pericardial disease Uremic syndrome KIDIGO-2013
- 19. Management of Cardiovascularcomplications Life style modification: BMI-20-25 kg/m2 DASH Physical exercise Protein restriction- 0.8 g/kg/day Salt intake<5 g/day Low alcohol intake KDIGO Clinical Practice Guideline-Chronic Kidney Disease
- 20. Anti-hypertensives Blood pressure • B.P<140/90mmof Hg if proteinuria<30 mg/24 hours • B.P<130/80 mm of Hg if proteinuria>30 mg/24 hours • Start with ACE or ARB • Later stages requires – Diuretics Calcium channel blockers(NIDP) Beta blockers, α2 agonist, α1 blocker. KDIGO-2013
- 21. Management of Cardiovascular complications • Anti-platelet agents: Only for secondary prophylaxis • Hyperuricemia-Normal-7.0 mg/dl (420 mmol/l) • Anti hyperuricemics indicated in cases with gout, very high levels of hyperuricemia > 10 mg/dl • Allopurinol –low price, allergic reactions-rare KDIGO Clinical Practice Guideline-Chronic Kidney Disease
- 22. Dyslipidaemia • High LDL,VLDL, low HDL situation recommendation >50 years, GFR >60 Statin >50 years, GFR<60 not on RRT Statin <50 years, GFR<60 not on RRT Statin when associated with risk factors KDIGO Clinical Practice Guideline-Chronic Kidney Disease
- 23. Management of diabetesin CKD • May develop hypoglycemia • Target HbA1c- 7.0% • Look for –Diabetic retinopathy Peripheral vascular diseases KDIGO Clinical Practice Guideline-Chronic Kidney Disease
- 24. Class Drugs Doseadjustments Insulin Reduce dose as GFR decreases Biguanides Metformin • Normal dose GFR ≥45 ml/min/1.73 m2 • caution if GFR 30–44 ml/min/1.73 m2 • Contraindicated GFR <30 ml/min/1.73 m2 Sulphonylureas Glipizide No dose reduction Glimepiride 1 mg daily if GFR <60 ml/min/1.73 m2 Glyburide C/I if GFR <60 ml/min DPP4-inhibitors Linagliptin No dose reduction αGlucosidase Inhibitors Voglibose • Normal dose if GFR ≥30 ml/min/1.73 m2 • caution if GFR <30 ml/min/1.73 m2 Nature Reviews Nephrology
- 25. Anemia • Diagnosis &Evaluation • Treatment - use of iron - use of erythropoietin stimulating agents (ESAs) - red cell transfusion KDIGO Clinical Practice Guideline-Chronic Kidney Disease
- 26. Diagnosis & Evaluationof anemia • Definition in CKD - Male <13g/dL, Female <12g/dL • Evaluation of anemia -without anemia Annually in patients with CKD 3 Twice per year in patients with CKD 4–5ND Every 3 months in patients with CKD 5D -with anemia Every 3 months in patients with CKD 3–5ND &PD Monthly in patients with CKD 5HD • Hb target Range of 11.0 ~ 12.0 g/dL KDIGO Clinical Practice Guideline-Chronic Kidney Disease
- 27. Treatment of anemia- use of iron • TSAT ≤ 30% & Ferritin ≤ 500ng/mL CKD patients on dialysis : IV iron CKD patients not on dialysis : Oral iron ? IV iron? KDIGO Clinical Practice Guideline-Chronic Kidney Disease Benefits Risks • ↓ESAs • ↓Transfusions • Anaphylactoid • Acute reactions
- 28. Treatment of anemia- use of iron • I.V Iron Better than oral CKD Patients not on dialysis -Hb ≤ 10g/dL + Ferritin <100ng/mL or TSAT <20% CKD patients undergoing dialysis -Hb ≤ 11 g / dL + Ferritin <100 ng/mL or TSAT <20% • Oral iron-200 mg/day KDIGO Clinical Practice Guideline-Chronic Kidney Disease
- 29. Treatment of anemia-use of ESAs • Address all correctable causes of anemia • CKD patients not on dialysis: Hb >10g/dL not indicated • CKD patients on dialysis : Hb 9~10g/dL start using • Stop ESA if Hb>11.5 gm/dl KDIGO Clinical Practice Guideline-Chronic Kidney Disease Benefits Risks • ↓Transfusions • HTN • Stroke
- 30. Treatment of anemia-use of ESAs Agent Initial Dosing Epoietin alfa, beta Cost-1000IU-250 to 350rupees) 20 ~50 IU/kg three times a week (SC or IV) * SC > IV Darbepoietin alfa (long acting) (40 mcg-2200 rupees) 0.45 mcg/kg once weekly (SC or IV) 0.75 mcg/kg once every 2 weeks (SC) * SC = IV C.E.R.A (continuous erythropoietin receptor activator) 0.6 mcg/kg once every 2 weeks (SC or IV) KDIGO Clinical Practice Guideline-Chronic Kidney Disease
- 31. Treatment of anemia-red cell transfusion • Avoid– when impending plan for renal transplant Use with caution- volume overload, hyperkalemia • Benefits outweigh risk acute hemorrhage, unstable coronary artery disease, rapid pre-operative Hb correction is required KDIGO Clinical Practice Guideline-Chronic Kidney Disease
- 32. CKD-MBD (Mineral bonedisorder) Mineral metabolism abnormalitie s Vascular calcification Bone abnormalitie s Abnormalities of Ca, P, PTH, or vit.D metabolism, FGF- 23 Abnormalities in bone turnover, mineralization, volume, linear growth, or strength Vascular or other soft tissue calcification KDIGO Clinical Practice Guideline-Chronic Kidney Disease
- 33. Mineral metabolism abnormalities •K/DOQI™ Clinical Practice Guidelines on Bone Metabolism Target Levels CKD Stage 3 Stage 4 Stage 5 Phosphate (mg/dL) 2.7 - 4.6 2.7 - 4.6 3.5 - 5.5 Calcium (mg/dL) Normal Normal 8.4 - 9.5 PTH (pg/mL) 35 - 70 70 - 110 150 - 300
- 34. Mineral metabolism abnormalities •Hyperphosphatemia Management - Aluminum-containing phosphate binders - excellent phosphate binding capacity and low cost - aluminum accumulation osteomalacia & encephalopathy - Ca-containing phosphate binders - slightly lower phosphate-binding capacity - cost-effective, no risk of aluminum accumulation - increased Ca loading (hypercalcemia)
- 35. Treatment of hyperphosphatemia NonCa-based phosphate binders • Sevelamer hydrochloride/carbonate, Lanthanum • Relatively low phosphate binding capacity and high price KDIGO Clinical Practice Guideline-Chronic Kidney Disease DRUG DOSAGE COST PER TAB Sevelamer 3 X 700 -1500mg 18.00 rupees Lanthanum 3 X 750-1600 mg 19.00 rupees
- 36. Treatment of hyperparathyroidism •Prevention: control of hyperphosphatemia - Phosphate binders - Calcitriol : ↑Absorption of Ca & P - Paricalcitol : Less Hypercalcemia - Calcimimetics (Cinacalcet) KDIGO Clinical Practice Guideline-Chronic Kidney Disease
- 37. Bone abnormalities • High-turnoverbone diseases - Osteitis fibrosa cystica -↑P, ↓Ca, ↑PTH, ↓calcitriol - bone pain, fractures.
- 38. Bone abnormalities Low-turnover bonediseases - Adynamic bone disease -↓PTH (calcitriol, Ca-P binder) - Fractures, Increased risk -Osteomalacia (renal rickets) - Vit. D Deficiency, Al accumulation ,metabolic acidosis - spontaneous Fractures. KDIGO Clinical Practice Guideline-Chronic Kidney Disease
- 39. Vascular calcification KDIGO ClinicalPractice Guideline-Chronic Kidney Disease Early calciphylaxis Progressive calciphylaxis Advanced calciphylaxis
- 40. Electrolyte disturbances Na- IncreasedNa-HTN Dietary restriction <90mmol (<2 g) per day of sodium K- Decreased GFR Decreased aldosterone (Type IV RTA, ACE Inhibitor) Dietary restriction <60 meq/dl KDIGO Clinical Practice Guideline-Chronic Kidney Disease
- 41. Metabolic acidosis • Developswhen GFR is below 40ml/min • Association between acidosis and mortality • Metabolic Acidosis- Initial-Non anion gap acidosis Later-Anion gap acidosis KDIGO Clinical Practice Guideline-Chronic Kidney Disease
- 42. Alkali therapy • Randomizedtrials show benefits of alkali therapy Progression of CKD Bone health • Start bicarbonate < 22 meq/L • Daily dose of 0.5 to 1 meq/kg per day • Sodium bicarbonate -500 - 1300 mg oral 3 times a day KDIGO Clinical Practice Guideline-Chronic Kidney Disease
- 43. Volume overload • Sodiumand intravascular volume balance maintained until - e GFR 10 to 15 mL/min/1.73 m2 . • Can present as • sodium restriction + diuretic therapy • Sodium intake <2 g/day • Salt- 5gm/day KDIGO Clinical Practice Guideline-Chronic Kidney Disease
- 44. Diuretics • Loop diuretics-Furosemide GFR20~50 ml/min/1.73m2 - starting dose iv 40mg ( po 80mg ) - ceiling dose iv 120~160mg ( po 240~320mg ) GFR <20 - starting dose iv 80mg ( po 160mg ) - ceiling dose iv 160~200mg ( po 320~400mg ) • Thiazide diuretics decreased effect if GFR < 30ml/min Metolazone used in GFR<30 ml/min KDIGO Clinical Practice Guideline-Chronic Kidney Disease
- 45. Infection and vaccination •Increased risk for infection -All stages of CKD are annual influenza vaccination -CKD 4,5-Hepatitis B Pneumococcal PCV13-8 weeks later PPSV23 Booster PPSV-23 every 5 years KDIGO Clinical Practice Guideline-Chronic Kidney Disease
- 46. Referral to specialistservices • AKI or abrupt sustained fall in GFR; • GFR <30 ml/min/1.73 m2 (GFR categories G4-G5), • Significant albuminuria (ACR >300 mg/g PCR >500 mg/g) • Rapid progression of CKD • Urinary red cell casts, RBC >20 per high power • CKD and hypertension refractory to treatment • Persistent abnormalities of serum potassium; • Recurrent or extensive nephrolithiasis; • Hereditary kidney disease.
- 47. Preparation for renalreplacement therapy • Choice of RRT-Educate patient if GFR < 30 ml/min/1.73m2 • Preparation for hemodialysis -primary arteriovenous fistulas -cuffed tunnel catheters • Preparation for peritoneal dialysis • Preparation for renal transplantation
- 48. Initiation of RRT •Pericarditis or pleurites • Progressive uremic encephalopathy • Bleeding diathesis attributable to uraemia • Metabolic disturbances refractory to medical therapy • Fluid overload refractory to diuretics • Hypertension unresponsive to medications • Persistent nausea and vomiting • Evidence of malnutrition
- 49.
Editor's Notes
- #2 A BREIF NOTE ON THE PROBLEM STATEMENT
- #3 1 in every 10 individuals are suffering from CKD,
- #4 AER or ACR > 30 mg/24 hr or 30 mg/gm
- #5 Quote study as ref. mention the pitfalls of this being not very representative as a study Diabetes and hypertension cause 40–60% cases CKD of unknown etiology-CKDu-2nd most common –CKD hot spots –cause may be genetical, environmental,socio economical factors Prevalence of CKD is expected to rise 1. Singh et al. BMC Nephrology 2013, 14:114 2. Indian Journal of Nephrology, Vol. 25, No. 3, May-June, 2015, pp. 133-135
- #7 Stage 1,stage 2 are asymptomatic.start develops symptoms by stage 3 ,it effects bone skeletal,cardiovascular,cns ,dermatological systems
- #8 If pt come to OPD with raisesd creatine –look for previous history suggestive of KIDNEY DISEASE. Other symptoms like joint pais,blood transfusion,old age presentsd with bone pains like multiple myeloma, and In past look for systemic disease dm,htn,
- #9 Lab investigations-clues to an underlying causative or aggravating disease Uriine examination for electrolytes
- #10 WHAT ARE THE VARIOUS EQUATIUONS THAT YPUR ARE AWARE OF FOR FINDING CKD, THE MOST PREFEERD ONE/? WHY? Ckd-epidemiology collaberation Immuno dilution mass spectoscopy
- #11 How do we stage cks While the earlier staging sytsme took only gr=fr into account th epitfall was.. Hence now we condier staging in terms of 2 variabnle g anoithe ra. Anothe The terminology has been changed from micro to modertely increased proteinuria, to highlight the increased risk of ckd associated complications even at micro proteinuria Proteinuria is an independent risk factor for morbidity Why Ckd 3a and 3b why because g3 b there is difference in disese progression G5 is when uremic toxins which cause the classic uremic syndrome unless there is dialysis Next coming to albuminuria 30 mg per gram of creat based on spot acr Do you see any difference theres is a definite reason
- #12 If the history of Mri sequences for uro
- #13 CT-look for renal stones ,cystic diseases,ct-angio for vessels MRA-renal artery stenosis,vessels,masses,early stages of infection
- #15 Bp, pulse, ivc Drug or other toxins Fundus Emergency
- #17 Now that we have talked about the satiging what kind of disease profile do patoemyts of differentr stages have. Ckd 1 and 2 are asymptomatic Based on gfr value Include fgf 23 Other early markers Stage 1 and 2 non specific or asymptomatic
- #19 Dash emphasis on vegetables ,fruits and low fat food ,moderate amount of grains nuts,fish poultry products.,Alchol role how much permissible look up
- #21 Secondary prophylaxis+
- #31 Allosensitisation.
- #33 KIDIGO stage 5 requires 2-9 times PTH
- #34 INITIAL MANAGEMENT IS phosphate reduction-800 -1000 mg /day excessive inhibition of PTH adynamic bone disease : vascular calcification
- #35 Temporary discontinuation of potentially nephrotoxic and renally excreted (>70% via renal route) drugs in people with a GFR <60 ml/min
- #40 Full frorm
- #48 or neuropathy, with signs such as confusion, asterixis, myoclonus, wrist or foot drop, or, in severe, cases, seizures hyperkalemia, hyponatremia, metabolic acidosis, hypercalcemia, hypocalcemia, and hyperphosphatemia)