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Chronic Renal Failure Niroj Obeyesekere 3 rd year student notes.

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Presentation on theme: "Chronic Renal Failure Niroj Obeyesekere 3 rd year student notes."— Presentation transcript:

1 Chronic Renal Failure Niroj Obeyesekere 3 rd 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- 1. Age 2.Sex – males higher incidence 3.Race – In US African Americans higher incidence. In UK Indian subcontinent higher incidence. Aborigines in Australia 4.Genetics – HT, DM PCKD, ACE polymorphism - In Homo sapiens, the gene encoding ACE is located on the long arm of chromosome 17 Polymorphism involving the presence (insertion, I) or absence (deletion, D) of a 287-bp sequence of DNA in intron 16 of the gene DD, ID, II. DD have high ACE activity

9 Factors that affect progression Modifiable 1.Proteinuria 2.Hypertension 3.Metabolic factors a.Glycemia – initiation vs. progression b.Lipids – not in dialysis pts c.Smoking d.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



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

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

23 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

24 Treatment

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

26 Why treat Anaemia

27 Other causes of anaemia in CRF

28 Investigations

29 Iron status

30 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.

31 Cardiovascular

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

33 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.

34 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




38 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

39 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

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