Chronic kidney disease results from the chronic and progressive loss of renal function and reduction in functioning nephrons. This leads to retention of waste products and toxins as well as hormonal and nutritional deficiencies. Clinical manifestations include fatigue, edema, hypertension, pruritus, and cognitive issues. Long-term complications involve multiple organ systems like the heart, bones, immune system, and brain. Management focuses on controlling risk factors, reducing retention and toxicity, and treating complications.
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
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
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
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
27. DISEQULIBRIUM
SYNDROME
z HYPEROSMOLAR STATE
(HYPERGLICEMIA , HYPERNATREMIA)
z IDIOPATHIC OSMOLS
z AMINO ACID, URIC ACID, SORBITOL,
z PHOSPHOCREATINE
z BRAIN EDEMA - HERNIATION
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)
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