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CKD complications and management
- 1. CHRONIC kidney disease UREMIC SYNDROME
- 2. Chronic kidney disease z CHRONIC IRREVERSIBLE and PROGRESSIVE LOSS OF RENAL FUNCTION. z REDUCED NUMBER OF FUNCTIONING NEPHRONS. z Hyperfiltration of the remaining nephrons
- 3. C k d z Results in : y Retention y Altered hormonal function y Deficiency state
- 4. CLINICAL EXPRESSION z Fatigue. z Anorexia, nausea, vomiting z Water and salt retention. Edema z Hypertension z Thirst dehydration z Organ related symptoms. z Pruritus z Mental and cognitive disorders
- 5. Retention SMALL MOLECULES z Water. z Sodium, potassium z Hydrogen ions. z Creatinine, urea. z Phosphate. z Oxalate z Calcium z Aluminum
- 6. UREMIC TOXINS Middle molecules: 300- 12000D z PTH z Beta 2 microglobulin z Homocysteine z Guanidin z Guanidin succinic acid z Phenol z (( phosphate ))
- 7. Parathyroid hormone (MW 9000) z HTN z CARDIOMYOPATY z OSTEODYSTROPHY z ANEMIA, PLT. z DISLIPIDEMIA z IMMUNE DEFFICIENCY z ENCEPHALOPATY
- 8. PTH z Glucose intolerance z T cell dysfunction z Prognostic factor
- 9. BETA 2 MICROGLOBULIN z Histocompatibility complex z DIALYSIS MEMBRANES z Bone z Joint z Tendon (Carpal Tunnel) z DIALYSIS CLEARANCE (P A N )
- 10. HOMOCYSTEINE z Cardiovascular morbidity z Progression of renal disease z Renovascular HTN
- 11. Uremic toxins z Guanidin z Guanidin succinic acid z Phenol
- 12. Deficiency z Malnutrition z Loss - Nephrotic Syndrome Hemodialysis Peritoneal Dialysis
- 13. deficiency z Albumin- Prognostic factor z Vitamins z Iron z Amino acids
- 14. Hormonal disturbances z PTH z INSULIN z RENIN z PROLACTIN z ENDOTHELIN z SEX HORMONS: Amenorrhea Azoospermia z GROWTH HORMON
- 15. Systemic damage z HYPERTENSION z Prevalence 70% z Cytosolic calcium z Water and Sodium z Renin z Endothelin z Atherosclerosis, z Physical inactivity
- 16. ACIDOSIS z CATABOLIC STATE z FATIGUE
- 17. Cardiovascular z ACCELERATED ATHEROSCLEROSIS z Hypertension z Hyperlipidemia z Vascular calcification - Calciphilaxis z Hyperhomocysteinemia
- 18. Cardiovascular z Incidence - 400 % higher then normal z First cause of death in ESRD (60%) z IHD: 50% (prevalence)
- 19. Myocardium z Systolic function - decreased (cytosolic calcium) z Diastolic function - decreased (interstitial precipitation) z Decreased ability of volume handling
- 20. MYOCARDIUM z Cardiomyopaty - v Concentric - HTN v Dilated - Volume overload - Anemia.
- 21. Coronary z Hypertension z Hyperlipidemia z Hyperhomocysteinemia z Calcification
- 22. PERICARDIUM Uremic Pericarditis z Under dialysis (50%) z Viral (50%) z Cause of death z Differential diagnosis z Treatment
- 23. Cardiac valves z Dilated cardiomyopathy z Calcification z SBE
- 24. NEUROLOGIC DISORDERS MENTAL: y FATIGUE y DEPRESSION y MEMORY y DECISION y CONCENTRATION
- 25. Neurologic involvement z UREMIC NEUROPATHY z UREMIC MYOPATHY z UREMIC ENCEPHALOPATHY
- 26. PERIPHERAL NEUROPATY z POLYNEUROPATHY z DISTAL > PROXIMAL z SYMETRIC z SENSORIAL >MOTOR
- 27. DISEQULIBRIUM SYNDROME z HYPEROSMOLAR STATE (HYPERGLICEMIA , HYPERNATREMIA) z IDIOPATHIC OSMOLS z AMINO ACID, URIC ACID, SORBITOL, z PHOSPHOCREATINE z BRAIN EDEMA - HERNIATION
- 28. ENCEPHALOPATHY z DIALYSIS DEMENTIA z ALUMINUM
- 29. ANEMIA z DECREASED EPO z BLOOD LOSS z DEFICIENCY(IRON,PROT,VIT) z SHORT SURVIVAL (Intrinsic-Extrinsic)
- 30. Immune system z DISTURBED PHAGOCYTOSIS (TB) z DIALYSIS LEUCOPENIA z ANTIBODY PRODUCTION z CELLULAR IMMUNITY (TB + Tumor) z PTH, PHENOL, INDOL z Chronic Infection (Bioincompatibility)
- 31. Coagulation z THROMBASTHENIA(PTH) z CHRONIC HEPARIN TREATMENT z HYPERCOAGULABILITY
- 32. SKIN z DRY SKIN z PRURITUS z UREMIC FETOR z UREMIC FROST z Ca, PO3H-, PTH, INDOL
- 33. UREMIC ENCEPHALOPATY z Early : EEG changes z Advance : Confusion, Convulsion, Coma and Death z Disequlibrium
- 34. Renal Osteodystrophy DECREASED PHOSPHATE EXCRETION Decreased 1 alpha hydroxylase Decreased Ca absorption Ca x P increased PTH stimulation Decreased PTH inhibition
- 35. 1- Alpha hydroxylase deficiency z Acidosis z Secondary hyperparathyroidism. z Skeletal resistance to PTH
- 36. ACIDOSIS z Bone buffering z Bone resorption
- 37. Amyloid z Beta2 microglobulin z Bone fracture
- 38. Osteodystrophy z Aluminum z Immobilization z Heparin z Malnutrition z Drugs z Osteoporosis
- 39. RENAL OSTEODYSTROPHY z Osteitis fibrosa cystica (HIGH) z Osteomalacia (low) z Aluminnum (low) z Adynamic bone disease (low) z Mixed z Amyloid
- 40. RENAL OSTEODYSTROPHY z Hemodialysis - High turn over (Osteoclasts) z Peritoneal Dialysis - Low turn over
- 41. TREATMENT z Accepted level of PTH z Phosphate : diet, chelation ,dialysis perscription z Calcium : dialysate, intake z Vitamin D z Pulse therapy z PTX z Desferioxamin z Nutrition
- 42. Natural History of CKD z NORMAL: From 40 years of age z 1 ml/year z ACTIVE RENAL DISEASE z KIDNEY DONOR z NEPHRECTOMY 3/4
- 43. PATOPHYSIOLOGY z Over work of the remaining nephrons z Hyperfiltration z Afferent arteriole vasodilation (DM, Protein intake) z Efferent arteriole vasoconstriction (angiotensin )
- 44. Hyperfiltration z Increased filtration pressure z Increased mechanical stretch and strain z Activation of AT2, TGF z Increased synthesis of collagen z Glomerulosclerosis and fibrosis z Increased tubular flow, reabsorption and and solute precipitation z Interstitial fibrosis
- 45. TREATMENT z Blood pressure z Proteinuria z Protein intake z Glycemia z Dietary Na z Hyperlipidemia z Smoking z Homocysteinemia
Editor's Notes
- can get utimate dx by doing renal biopsy\n- not simple- is last stage of investigation\n\n\n
- chronic renal failure:\n- defined mainly by irreversibility of the disease\n- can never cure- and have normal renal fnxn\n- is a progressive disease\n- progression depend on several causes:\n- HTN \n- diabetes\n- primary renal disease\n- coexistence of other diseases \n- diabetes- most common dx of renal disease- which brings pts to end stage disease\n- bc of the great prevalence of diabetics in the pop\n- used to not accept daibetics for dialysis, and now its the main cause for dialysis in the western world (bc in africa- malaria is more common than diabetics)\n\n-reduced number of functioning nephrons\n- but blood supply to kidney is the same- same blood, less nephrons\n- so each nephron now has work to do now\n- each nephron filtrates more: hyperfiltration\n\nhyperfiltration- not only a mechanical problem- but also some physiology/pharmacological changes in the kidney\n\n- each mm higher causes damage to the cap membrane epithelium\n-diff btw blood pressure and intraglomerular pressure\n- glomer cap pressure- is not not always the systemic pressure: ACEI- reduce bp - reduce glomer pressure than other drugs\n- aff arterioles, in situation of hyperfiltration: dilate more than the efferent- this is good thing\n\n
- result in renal function:\n- retention: \n- main fnxn of kidney is exretion of water, and salt, and urea, metabolites, toxins, ammonia, aids...\n- so retention of these things\n- altered hormonal fnxn\n- PTH\n- erythropoietin\n- vit D\n- deficiency state\n- \n\n\n- decrease in GFR (more than 30% decrease) one of first things that happen in normal way: retention of K\n\nretention: \n- k (advanced state of renal failure)\n- first stage- dont see hyperkalemia- only seen in the pre-dialysis situation-- EXCEPT in situation of drugs (k sparing diuretics, ACEI, ARBS, NSAIDS, Spironolactone, diet, )\n- nephrologists dont like spironolactone- bc scared of the hyperkalemia, but cardiologists like it\n\n
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