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Chronic renal Failure

Chronic renal Failure. Dr. Jumana Albaramki. Chronic renal failure. Plasma Cr does not rise until renal function has fallen to less than half normal levels Cr affected by muscle bulk GRF= height x k /creat in mg/dl ml/min/1.73 m2. Normal progression of GFR with age. Creatinine with age.

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Chronic renal Failure

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  1. Chronic renal Failure Dr. Jumana Albaramki

  2. Chronic renal failure Plasma Cr does not rise until renal function has fallen to less than half normal levels Cr affected by muscle bulk GRF= height x k /creat in mg/dl ml/min/1.73 m2

  3. Normal progression of GFR with age

  4. Creatinine with age

  5. presentation Asymptomatic Anorexia,lethargy Polydipsia,polyuria Anemia,HTN FTT,bone osteodystrophy Causes: 1.Structural congenital malformations 2.Hereditary nephropathy 3.Glomerulonephritis

  6. Management Investigations:FBC,iron studies EUC, biocarbonte,Ca,PO4,ALP,PTH Urine protein,lipid profile Attention: Nutrition,fluid.growth,anemia,HTN,renal osteodystrophy

  7. Prevention of progression of CRF 1.Proteinuria:due to hyperfilteration,ACEI,ARB dilate afferent art and reduce intraglomerular pressure ACEI cause anemia,high K,Cr, cough 2.HTN 3.Dyslipidemia

  8. Bone disorders in CKD

  9. PTH Mobilizes Ca from bones Decrease renal tubular absorption of PO4 Increase renal tubular absorption of Ca Promote 1 alpha hydroxylase

  10. Disorders of Bone Mineral Metabolism in CKD Reduced 1,25 OH vit D impairs intestinal Ca absorption leads to low Ca and increase PTH stimulates 1hydroxylase increase Vit D,Ca. Calcemic response to PTH is reduced CKD Ca major regulator of parathyroids High PO4 increase FGF23 increase excretion High PO4 stimulte PTH,lowers Ca Acidosis impairs bone mineralization

  11. Clinical Manifestations Bone pain Myopathy due uremic toxins,carnitine def Skeletal deformities:bowing,genu valgum,ricket changes of widening of metaphyseal regions Slipped epiphyses,proximal femur,presents as limping,waddling gait Fractures Vascular calcification (maintain PO4 X Ca <65 mg2/dl2)

  12. Biochemistry Ca low or normal,high in low turn over,tertiary hyperparathyroidism, Tx with calcitriol,volume depletion PO4 high is age dependant PTH high,ALP high Xrays detect subperiostal resorption,

  13. Treatment Optimal control of PO4 by diet ,phosphate binders (Ca carbonate 40%elemental Ca),dialysis not enough,to be taken with meals. Sevelamer HCL.:lower risk of hypercalcemia,lower lipids,same efficacy as CaCO3 in lowering PO4. maintain PO4 X Ca <55mg2/dl2 in adults, <65mg2/dl2 in chidren Vitamin D:10-60ng/kg/day,increase PO4,Ca,given daily or intermittent Calimimetic,parathyroidectomy

  14. Target PTH in children with CKD

  15. Histologic classification of renal osteodystrophy

  16. Anemia in CRD Erythropoietin Deficiency Blood loss (HD lines,GIT losses due to impaired platelet function) Decreased RBC survival Hyperparathyroidism decrease BM production. Aluminum toxicity Iron deficiency Vitamin B12,folate deficiency Inflammation,infection

  17. Clinical effects of anemia Systemic symptoms of fatigue,loss of appetite,decrease exercise tolerance CVD:LVH Anemia increase mortality Evaluation:FBC,ret,ferritin,iron,TIBC TSAT:Iron/TIBC should be >20% Target Hb levels based on KDOQI guidelines is between 11-13 Ferritin be above 100 in predialysis patients

  18. ESA rHuEPO s.c. as 100 U/kg/week in two doses in predialysis,PD rHuEPO i.v. as 150 U/kg/week in three doses in HD. S.c. longer half life than iv Complications:HTN,seizures,iron defiency,thrombosis,EPO antibodies New darbepoetin-:longer T1/2, every 2 wk

  19. Iron thearpy iron not to be given with food,phosphate binders 3-5mg/kg elemental iron IV iron in HD as iron sucrose Various oral preparations as ferrous sulphate,ferrous gluconate

  20. nutrition Adequate nutrition to promote growth,prevent complications of uremia,bones. Protein intake 1.1 g/day 1-6 y Higher protein in dialysis Low phosphate,potassium diet Vitamin but vit A,minerals as folic acid Special formula low in K,PO4,increase energy by adding lipid,sugar Salt supplements in tubular losses

  21. Growth and puberty in CKD

  22. Causes of growth failure in CKD Genetic factors:gender,parental height,syndromes Age of onset of CKD Residual renal function Treatment modality Energy malnutrition Water and electrolyte disturbances:renal dysplasia needs salt. Metabolic acidosis Anemia,renal osteodystrophy

  23. Gonadotropic hormone axis Growth hormone levels are normal to high GH resistance due to low GH receptor expression or post-receptor signaling defect. IGF1 levels are high and there is resistance to its action

  24. Treatement of growth failure Adequate caloric intake to 100% of RDA Treatment with alkali,salt Calcitriol Growth hormone:benefit more in pre endsatge CKD,than dialysis Prepubertal start cause a marked pubertal growth spurt.

  25. Treatment of ESRD Peritoneal dialysis:CAPD,NIPD CCPD :Uses an automated machine with 7 night cycles with a long day time dwell Acute intermittent hemodialysis:needs vacular acsess as AV fistula,permcath Requires 3 X 5 hour sessions/week Diffusion through a semipermeable membrane,ultrafilteration of fluids

  26. Transplantation Living or cadervic donons,HLA matching Needs long immunosuppression with steriods,CNI, mycophenolate acetate Problems :rejection,hypertension,infection,obstruction,chronic allograft nephropathy LRD 1 year graft survival of 91%,5 years of 74 % CRD 1 year graft survival of 80%,5 years of 60 %

  27. Dialysers

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