Ckd pre dialysis management

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  • The US NKF-DOQI (National Kidney Federation- Kidney Dialysis Outcomes Quality Initiative) guide lines defines CKD as
  • Premature cardiovascular death, not just ESRD, is a major risk for people with CKD. Recent studies have tightened the epidemiological link between CKD and CVD. These studies have reported a graded, inverse relation between initial renal function and subsequent risks of death and complications from cardiovascular disease. Some say, “Only the lucky CKD patients reach ESRD.”
  • Diagnosing CKD at an early stage can add 2 or more years of ESRD-free survival. In some patients ESRD may actually be prevented. Careful attention to classic cardiovascular risk factors, especially smoking cessation and lipids, is also important to prevent premature cardiovascular death.
  • The major factors are thought to be intraglomerular hypertension and glomerular hypertrophy (which are primarily responsible for the adaptive hyperfiltration described above), leading to glomerular scarring (glomerulosclerosis). Additional causes may include hyperlipidemia, metabolic acidosis, and tubulointerstitial disease.
  • Calcium carbonate, sevelamer and lanthanum carbonate
  • Target ferritin:>200mg/ml & transferrin >20%
  • Ckd pre dialysis management

    1. 1. CKD-PRE DIALYSISMANAGEMENTShruthi K
    2. 2. Chronic kidney disease Global health problem Rising incidence – doubled in last 15 years In India – 0nly 10% of patients with ESRD have access to RRT
    3. 3. CKD-definition GFR ≤ 60ml/min/1.73m that is present for ≥ 3months with or without evidence of kidney damageOR Evidence of kidney damage with or without decreased GFR that is present for ≥ 3months as evidenced by  Microalbuminuria  Proteinuria  Glomerular haematuria  Pathological abnormalities (e.g. abnormal biopsy)  Anatomical abnormalities (e.g. scarring seen on imaging or polycystic kidneys)
    4. 4. Pre dialysis management – Why? Optimal pre-dialysis care improve  Morbidity  Mortality  Dialysis and transplantation outcome
    5. 5. CKD Predicts CVD 40 36.6 Age-Standardized Rate of Cardiovascular 35 30 Events (per 100 person-yr) 25 21.8 20 15 11.29 10 5 3.65 2.11 0 ≥ 60 45-59 30-44 15-29 < 15 Estimated GFR (mL/min/1.73 m2)
    6. 6. Early Treatment Makes a Difference Brenner, et al., 2001
    7. 7. Goal To establish diagnosis Rule out reversible causes Slow down progression Evaluate and treat complications Treat co-morbidities Reduce cardiovascular risk Prepare for replacement therapy Select & start renal replacement therapy at appropriate time
    8. 8. Management Treatment of reversible causes Preventing or slowing the progression of disease Treatment of the complications Identification and adequate preparation of the patient in whom renal replacement therapy will be required
    9. 9. Treatment of reversible causes Decreased renal perfusion  Hypovolemia (such as vomiting, diarrhea, diuretic use, bleeding)  Hypotension (due to myocardial dysfunction or pericardial disease)  Infection /sepsis  Drugs which lower the GFR Urinary tract obstruction
    10. 10. Slowing the rate of progression Proteinuria < 1 gm/day or at least 60% of baseline values  Optimal level of protein intake  Not been determined  0.8 to 1.0 g/kg/day  ACEI/ARB  Smoking cessation
    11. 11.  Blood pressure  <130/80mmHg  <125/75mmHg if proteinuria >1g/day  Salt restriction  Antihypertensives  ACE,diuretics,CCB  Exercise
    12. 12. Treatment of complications Volume overload   Salt restriction  Loop diuretics
    13. 13.  Hyperkalemia  Developsin the patient who is oliguric or who has an additional problem such as a high potassium diet, increased tissue breakdown, or hypoaldosteronism  Low K+ diet – 40 to 70meq / day  Avoid NSAIDs
    14. 14.  Metabolic acidosis  Due to  Decreased ability to regenerate bicarbonate  Reduced ammonia production  Decreased hydrogen ion secretion  Decreased filtration of titrable acids – sulphate, phosphate, urate, hippurates  Decreased proximal tubular re-absorption of bicarbonate
    15. 15.  Treatment of academia is desirable  Bicarbonate supplementation may slow the progression of CKD  Bone buffering of the some of the excess hydrogen ion is associated with the release of calcium and phosphate from bone, contributing to worsening of renal osteodystrophy  Uremia acidosis can increase skeletal muscle breakdown and diminish albumin synthesis leading to loss of lean body mass and muscles weakness- contributing to malnutrition
    16. 16.  Therapy is targeted to maintain serum bicarbonate concentration above 23 mEq/Lit Drug of choice : sodium bicarbonate < 0.5-1.0 mEq/kg/day
    17. 17.  Hyperphosphatemia  Dietrestriction : 800mg/day  GFR<25 to 30 ml/min: oral phosphate binders  Stage 3 & 4 : between 2.7 and 4.6 mg/dL  Stage 5 : between 3.5 and 5.5 mg/dL
    18. 18.  Renal osteodystrophy High phosphate load and hypocalcemia stimulate PTH secretion Leads to sec hyper parathyroidism which increases bone resorption
    19. 19. Treatment Control serum phosphate CKD stage-specific target levels of intact PTH  CKD stage 3: treat elevated PTH to target 35-70pg/ml  CKD stage 4 to target 70-110 pg/ml  CKD stage 5 to target 150-300 pg/ml Next step is assessment of 25-(OH)D levels and replacement with vitamin D (ergocalciferol) if levels are lower than 30 ng/mL.
    20. 20.  If the intact PTH level is elevated and the serum 25- (OH)D level is higher than 30 ng/mL, treatment with an active form of vitamin D is indicated Available options  Calcitriol  Alfacalcidol  Doxecalciferol
    21. 21.  Cinacalcet Calcimimetic Used if elevated phosphorus/Ca limit use of vit D
    22. 22. Hypertension  Cause and complication of CKD Target <130/80 or <125 /75 mmHg if proteinuria is >1 gm /day or diabetes is + Non pharmacological  Lifestyle modification  Salt restriction  Exercise,weight reduction  Diet  Smoking cessation etc….
    23. 23.  Pharmacological May require 3 or more drugs Diabetes & proteinuria : treat with ACEI /ARB as 1st line therapy Monitor Creatinine & K+ on day 3 ,7 &weekly Loop and thiazide diuretics as an adjunct therapy CVD: beta blockers CCBs Alpha blockers : prazosin,doxazosin followed by direct vascular smooth muscle relaxant minoxidil is considered
    24. 24. Anemia Caused by insufficient erythropoietin production ,short life span of RBCs , iron deficiency Target Hb: 10 to 12gm% Correct iron deficiency EPO : 80 to 120units/kg/wk Alternative : darbepoietin alfa Longer acting agent Dose: 0.45µg/kg s/c once a week
    25. 25. Preparation for RRT Counselling HD,peritoneal dialysis / renal transplant If not for transplant : vascular access should be created in preferably native AV fistula in CKD stage 4 Venous preservation should start from stage 2 or 3 Vaccinate against hep B, pneumococcal and H influenza infection Drug dosage according to eGFR, avoid contrast

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