Download
chronic renal failure n.
Skip this Video
Loading SlideShow in 5 Seconds..
Chronic Renal Failure PowerPoint Presentation
Download Presentation
Chronic Renal Failure

Chronic Renal Failure

180 Views Download Presentation
Download Presentation

Chronic Renal Failure

- - - - - - - - - - - - - - - - - - - - - - - - - - - E N D - - - - - - - - - - - - - - - - - - - - - - - - - - -
Presentation Transcript

  1. Chronic Renal Failure Niroj Obeyesekere 3rd year student notes

  2. What’s covered • The stages of CRF • Common causes of CRF • Modifiable and non modifiable RF for CRF • Approach to CRF diagnosis and management • Complications of CRF esp Renal bone disease and Anemia • Treatment of CRF complications • Basic understanding of dialysis hemodialysis and peritoneal dialysis

  3. Stages of CRF

  4. Clinical Classification

  5. Causes of CRF

  6. Incidence of RRT

  7. Prevalence

  8. Factors that affect progression Non modifiable- Age Sex – males higher incidence Race – In US African Americans higher incidence. In UK Indian subcontinent higher incidence. Aborigines in Australia Genetics – HT, DM PCKD, ACE polymorphism - In Homo sapiens, the gene encoding ACE is located on the longarm of chromosome 17 Polymorphism involving the presence(insertion, I) or absence (deletion, D) of a 287-bp sequenceof DNA in intron 16 of the gene DD, ID, II. DD have high ACE activity

  9. Factors that affect progression Modifiable Proteinuria Hypertension Metabolic factors Glycemia – initiation vs. progression Lipids – not in dialysis pts Smoking Alcohol and caffeine and HT not so robust

  10. Management RRT includes Transplantation

  11. Management step 1

  12. Reversible factors in acute on chronic renal failure

  13. Complications of Chronic Renal Failure • 1. Cardiovascular disease • 2. Anaemia • 3. Renal bone disease • 4. Metabolic acidosis • 5. Malnutrition • 6. Salt and water • 7. Hyperkalemia • 8. Bleeding diathesis

  14. Complications of CRF • 9. Skin – pruritis, dry xerotic skin • 10. CNS –uremic encephalopathy, restless legs, peripheral neuropathy, • 11. Endocrine – Hyperparathyroidism, GH reduced, Testosterone levels low, prolactin levels high infertility in women • 12. Immunity - low

  15. Renal Bone Disease

  16. Renal Bone disease • 1. osteitis fibrosa – increased PTH, increased osteoclast and osteoblast activity and peritrabecular fibrosis- rugger jersey spine • 2. osteomalacia – defective mineralisation • 3. adynamic bone disease – low bone turnover • 4. osteopenia or osteoporosis • 5. combination

  17. Prevalence of renal bone disease

  18. Pathogenesis – in osteitis fibrosa • Ca – bones (mineral), intracellular (protein bound) and extracellular (1/2 protein bound ½ free). • Vit D – reduced production in kidneys (1,25 from 25 by 1 -alpha hydroxylase) leads to decreased ca absorption from intestine. • PO4 retention occurs when GFR <20, prior to this increased PTH increases PO4 excretion in urine. • PTH – subperiosteal erosions

  19. Pathogenesis • Osteomalacia – Aluminium toxicity – reduced osteoblast function • Adynamic bone disease – use of vit d, high calcium dialysate.

  20. Clinical manifestation • Usually just biochemical abnormalities • Bone pain • Pruritis • Metastatic calcification and calciphylaxis.

  21. Treatment • Calcium replacement • Phosphate binders – caltrate, alutabs, mylanta, renagel, lanthunum. • ViT D replacement D3 and D2 –but increases Po4 absorption and Ca absorption PTH between 3 to 5 times of normal

  22. Treatment

  23. Anaemia • Normally normocytic normochromic • Reduced EPO • The EPO gene chromosome 7. Synthesised in fibroblast like interstitial cells in kidney and lesser degree liver.

  24. Why treat Anaemia

  25. Other causes of anaemia in CRF

  26. Investigations

  27. Iron status

  28. Treatment • 1. Replace iron – iron sulfate, iron gluconate, iron fumurate • 2. IV iron – iron polymatose, sodium ferric saccharate (sucrose). • 3. EPO – aim for Hb 10 – 12.

  29. Cardiovascular

  30. CVD • Increased strokes • Pericarditis – rare now. • IHD • Arrhythmias • LVH • HT

  31. Physiology of haemodialysis • HD describes the process whereby the solute composition of blood is altered by its contact with another solution through a semi-permeable membrane • HD removes solutes by: 1). Diffusion (mvt of solute across the membrane down a concentration gradient) 2). Convection (‘ultrafiltration’ solutes pushed through the membrane by a pressure gradient). Conventional HD relies mostly on diffusion.

  32. Access for dialysis • Vascath – temporary (max 5 days) for acute dialysis (femoral, subclavian or internal jugular vein) • Permacath – tunnelled catheter (subclavian or internal jugular) • Arteriovenous fistula • AV Graft

  33. Peritoneal Dialysis • PD uses the peritoneal membrane as a natural dialysis filter • PD solution is instilled into the peritoneal cavity and acts as the ‘dialysate’ • PD has some medical and lifestyle advantages over HD • Longterm technique survival after 5 years is low

  34. Peritoneal Dialysis • Continuous ambulatory PD (CAPD) – patients do 3 to 4 exchanges during the day and one dwell overnight • Automated PD (APD) – a machine cycles dialysate in overnight and patients may have a dwell in during the day. • Main complications: PD peritonitis, membrane failure