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CHRONIC KIDNEY DISEASE

In the name of GOD. Jenabi MD Ass. Professor of Medicine and Nephrology, iran University of medical Sciences Tehran , Iran. CHRONIC KIDNEY DISEASE. CHRONIC KIDNEY DISEASE.

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CHRONIC KIDNEY DISEASE

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  1. In the name of GOD Jenabi MDAss. Professor of Medicineand Nephrology,iran University of medical Sciences Tehran , Iran CHRONIC KIDNEY DISEASE

  2. CHRONIC KIDNEY DISEASE • Chronic kidney disease (CKD) encompasses a spectrum of different pathophysiologic processes associated with abnormal kidney function, and a progressive decline in glomerular filtration rate (GFR).

  3. chronic renal failure • IRREVERSIBLE LOSS OF GFR • DENOTES PROGRESSION EVEN WHEN THE UNDERLYING CAUSE HAS BEEN ELIMINATED

  4. Why call it chronic kidney disease? why call it CKD as opposed to pre-ESRD, pre-dialysis or chronic renal failure ? • Pre-ESRD gives the impression that dialysis is the inevitable outcome of all kidney diseases and that there are no effective therapies to retard its progression. It is the equivalent of referring to life as pre-death. • The term renal failure also has a negative connotation and includes the term renal, which is not easily understood by patients and their families.

  5. MOST OF THE CKD PATIENTS ARE ASYMPTOMATIC AND ARE DETECTED DURING SCREENING EITHER ROUTINE OR FOR UNRELATED ILLNESS

  6. INCIDENCE OF CKD At least 6% of the adult population in the USA has CKD at stages 1 and 2. An unknown subset of this group will progress to more advanced stages of CKD. An additional 4.5% of the U.S. population is estimated to have stages 3 and 4 CKD. ESRD CKD

  7. Uremia is a state of systemic poisoning Due to cumulative effects of failure of many functions of kidney ESRD?

  8. Pathophysiology of Chronic Kidney Disease Two broad sets of mechanisms of damage: • initiating mechanisms specific to the underlying etiology (immune complexes and mediators of inflammation in certain types of glomerulonephritis, or toxin exposure • a set of progressive mechanisms, involving hyperfiltration and hypertrophy of the remaining viable nephrons

  9. Pathophysiology of Chronic Kidney Disease 2 • why a reduction in renal mass from an isolated insult may lead to a progressive decline in renal function over many years?

  10. Pathophysiology of Chronic Kidney Disease 3 • Increased intrarenal activity of the renin-angiotensin axis appears to contribute both to the initial adaptive hyperfiltration and to the subsequent maladaptive hypertrophy and sclerosis, the latter, in part, owing to the stimulation of transforming growth factor (TGF-).

  11. CKD Causes CAUSEADULTS CHILDREN GLOMERULONEPHRITIS 3+ 4+ DIABETES 4+ RARE HYPER TENSION 2+ RARE POLYCYSTIC KIDNEY 2+ 1+ INTERSTITIAL NEPHRITIS 2+ 2+ OBSRUCTIVE NEPHROPATHY 1+ 3+ RENAL HYPOPLASIA RARE 2+ HEREDITARY DISORDERS RARE 1+

  12. CKD –Some Definitions • CKD results when a disease process damages the structural or functional integrity of the kidney. • This is clinically detected using either physical exam (hypertension), laboratory (hematuria, proteinuria, microalbuminuria) or imaging studies (CT, MRI, IVP or renal ultrasound). • Almost all patients with a GFR 60 ml/min/1.73m2 have CKD. • However, since GFR declines normally with age (approximately 1ml/min/1.73 m2 /year after age 20), a GFR between 60 - 90 ml/min/1.73m2 in the elderly may not be indicative of the presence of CKD. • In order for patients to be classified as having CKD there must be some objective evidence on either physical exam, laboratory or imaging studies of kidney damage.

  13. Estimate the Glomerular Filtration Rate • Estimates of the glomerular filtration rate (GFR) based on the serum creatinine have a high degree of correlation with determinations of GFR based on inulin (gold standard) or iothalamate clearances. The later are more accurate but are cumbersome and costly. • These estimations also perform well when compared to collections of 24 hour urine which are difficult for patients to carry out and are often performed incorrectly. • Cockcroft-Gault equation- [140-age(yr)]  weight(kg)]/[72  serum Cr(mg/dl)] ( 0.85 for women). • MDRD equation 7-170  [serum creatinine (mg/dl)] - 0.999  [age] - 0.176  [0.762 if pt is female ] **[1.180 if pt is black ] **[BUN (mg/dl)] - 0.170  [albumin (g/dl)] + 0.318.

  14. Why can ’t one just use the serum creatinine ? • The serum creatinine alone is not an accurate measure of glomerular filtration rate. Creatinine, unlike inulin, is secreted by renal tubules; and as renal function worsens the amount secreted increases. Normal ranges for serum creatinine are misleading because they do not take into account the age, sex, or weight of the patient.

  15. Clinical examples • Consider the following two patients with identical serum Cr of 1.2 mg/ dL. • Patient 1 -a 60 year old 50 kg woman • Patient 2 - a 30 year old 90 kg man • The first patient has a GFR of 39 ml/min/1.73 m2, which is markedly abnormal, while the second has a GFR of 115 ml/min/1.73 m2, well within the normal range.

  16. CLASSIFICATION OF CKD-NKF

  17. 7.7 m 11.3 m 5.6% 7.7 m 3.8% 0.3 m 0.2% Conceptual Model for CKD Complications Normal Increasedrisk Damage  GFR Kidneyfailure CKDdeath Screening for CKDrisk factors: diabeteshypertension age >60family history US ethnic minorities CKD riskreduction;Screening forCKD Diagnosis& treatment;Treat comorbidconditions;Slow progression Estimateprogression;Treatcomplications;Prepare forreplacement Replacementby dialysis& transplant

  18. Measurement of albuminuria Albuminuria is also helpful for monitoring nephron injury apy in many forms of CKD While an accurate 24-h urine collection is the "gold standard" for measurement of albuminuria, the measurement of albumin-to-creatinine ratio in a spot first-morning urine sample is often more practical to obtain and correlates well. Persistence in the urine of >17 mg of albumin per gram of creatinine in males and 25 mg albumin per gram of creatinine in females usually signifies chronic renal damage. Microalbuminuriarefers to the excretion of amounts of albumin too small to detect by urinary dipstick or conventional measures of urine protein. It is a good screening test for early detection of renal disease, in particular, and may be a marker for the presence of microvascular disease in general.

  19. Pathophysiology and Biochemistry of Uremia The uremic syndrome can be divided into manifestations in three spheres of dysfunction: (1) those consequent to the accumulation of toxins normally undergoing renal excretion, including products of protein metabolism. (2) those consequent to the loss of other renal functions, such as fluid and electrolyte homeostasis and hormone regulation. (3) progressive systemic inflammation and its vascular and nutritional consequences Hundreds of toxins that accumulate in renal failure have been implicated in the uremic syndrome; nitrogenous excretory products include guanido compounds, urates and hippurates, products of nucleic acid metabolism, polyamines, myoinositol, phenols, benzoates, and indoles

  20. SYMPTOMS / SIGNS SYMPTOMS / SIGNS SYMPTOMS SIGNS SYSTEM GENERAL FATIGUE, WELL BEING WASTED,SALLOW COMPLEXION SKIN ITCHING / BRUISING PALLOR, PIGMENTATION DRYNESS FROST, EXCORIATIONS GIT ANOREXIA / NAUSEA GI BLEED VOMITING / HICCUPS CVS EDEMA, CHEST PAIN HT / CARDIOMEGALY DYSPNEA RUB / CRACKLES MUSCULO BONE PAIN DEFORMITIES / MYOPATHY SKELETAL GROWTH FAILURE NS NUMBNESS / CRAMPS NEUROPATHY / ASTERIXIS INSOMNIA / IMPOTENCE MYOCLONUS / ACIDOSIS

  21. Fluid and electrolyte disturbances • Volume expansion (I) • Hyponatremia (I) • Hyperkalemia (I) • Hyperphosphatemia (I)

  22. Endocrine-metabolic disturbances • Secondary hyperparathyroidism (I or P) • Adynamic bone (D) • Vitamin D–deficient osteomalacia (I) • Carbohydrate resistance (I) • Hyperuricemia (I or P) • Hypertriglyceridemia (I or P) • Increased Lp(a) level (P) • Decreased high-density lipoprotein level (P) • Protein-energy malnutrition (I or P) • Impaired growth and development (P) • Infertility and sexual dysfunction (P) • Amenorrhea (I/P) • β2-Microglobulin associated amyloidosis (P or D)

  23. BoneManifestationsof CKD

  24. Flowchart for the development of bone, phosphate, and calcium abnormalities

  25. Calcium, Phosphorus, and the Cardiovascular System • Recent epidemiologic evidence has shown a strong association between hyperphosphatemia and increased cardiovascular mortality in patients with stage 5 CKD and even in patients with earlier stages of CKD • Hyperphosphatemia and hypercalcemia are associated with increased vascular calcification

  26. Fibroblast growth factor 23 (FGF-23) is part of a family of phosphatonins that promotes renal phosphate excretion. Recent studies have shown that levels of this hormone, secreted by osteocytes, increases early in the course of CKD. It may defend normal serum phosphorus in at least three ways: (1) increased renal phosphate excretion; (2) stimulation of PTH, which also increases renal phosphate excretion; and (3) suppression of the formation of 1,25(OH)2D3, leading to diminished phosphorus absorption from the gastrointestinal tract. Interestingly, high levels of FGF-23 are also an independent risk factor for left ventricular hypertrophy and mortality in dialysis patients. Moreover, elevated levels of FGF-23 may indicate the need for therapeutic intervention (e.g., phosphate restriction), even when serum phosphate levels are within the normal range.

  27. Calciphylaxis • Calciphylaxis is a devastating condition seen almost exclusively in patients with advanced CKD • there is evidence of vascular occlusion in association with extensive vascular calcification: • advanced hyperparathyroidism • increased use of oral calcium as a phosphate binder • Warfarin is commonly used in hemodialysis pts, (decrease the vitamin K–dependent regeneration of matrix GLA protein)

  28. Salt and pepper appearance skull And brawn tumor

  29. Sub periosteal bone resorbsion and arterial calcification

  30. Clavicles bone resorbsion

  31. Rugger jersey appearance of skeletal vertebrae

  32. Multiple brawn tumors of pelvic bone

  33. Neuromuscular disturbances • Fatigue (I)b • Sleep disorders (P) • Headache (P) • Impaired mentation (I)b • Lethargy (I)b • Asterixis (I) • Muscular irritability • Peripheral neuropathy (I or P) • Restless legs syndrome (I or P) • Myoclonus (I) • Seizures (I or P) • Coma (I) • Muscle cramps (P or D) • Dialysis disequilibrium syndrome (D) • Myopathy (P or D)

  34. Cardiovascular and pulmonary disturbances • Arterial hypertension (I or P) • Congestive heart failure or pulmonary edema (I) • Pericarditis (I) • Hypertrophic or dilated cardiomyopathy (I, P, or D) • Uremic lung (I) • Accelerated atherosclerosis (P or D) • Hypotension and arrhythmias (D) • Vascular calcification (P or D)

  35. Correlation between the decline in kidney function, and the increasing incidence of cardiovascular (CV) complications and death from CV disease 75.0;    , 60.0–74.9;    , 45.0–59.9;    , < 45

  36. U.S. Renal Data System showing increased likelihood of dying rather than starting dialysis or reaching stage 5 chronic kidney disease (CKD). Death , ESRD/D , event-free

  37. CKD DM HTN MI

  38. Homocysteine Traditional Risk Factors Non-traditional Risk Factors Diabetes Elevated IL-1, Il-6, TNFa Smoking Genetics Oxidation (OxLDL) HTN Advanced glycation end-products Age Dyslipidemia Carbonyl stress Cardiovascular disease in CKD Fractures Low fetuin-A Abnormal bone Abnormal mineral metabolism

  39. IschemicVascular Disease Any stage of CKD is a major risk factor for ischemic cardiovascular disease, including occlusive coronary, cerebrovascular, and peripheral vascular disease • Traditional (classic) • hypertension, hypervolemia, dyslipidemia, sympathetic overactivity, and hyperhomocysteinemia • Nontraditional (CKD-related) risk factors • anemia, hyperphosphatemia, hyperparathyroidism, sleep apnea, and generalized inflammation • circulating acute-phase reactants(cytokines and CRP • negative acute-phase reactants(serum albumin and fetuin)

  40. Dermatologic disturbances • Pallor (I)b • Hyperpigmentation (I, P, or D) • Pruritus (P) • Ecchymoses (I) • Nephrogenic fibrosing dermopathy (D) • Uremic frost (I)

  41. Gastrointestinal disturbances • Anorexia (I) • Nausea and vomiting (I) • Gastroenteritis (I) • Peptic ulcer (I or P) • Gastrointestinal bleeding (I, P, or D) • Idiopathic ascites (D) • Peritonitis (D)

  42. Hematologic and immunologic disturbances • Anemia (I)b • Lymphocytopenia (P) • Bleeding diathesis (I or D)b • Increased susceptibility to infection (I or P) • Leukopenia (D) • Thrombocytopenia (D)

  43. Abnormal Hemostasis • Patients with later stages of CKD may have a prolonged bleeding time: • Decreased activity of platelet factor III, • Abnormal platelet aggregation and adhesiveness • Impaired prothrombin consumption. • Interestingly, CKD patients also have a greater susceptibility to thromboembolism, especially if they have renal disease that includes nephrotic-range proteinuria. The latter condition results in hypoalbuminemia and renal loss of anticoagulant factors, which can lead to a thrombophilic state.

  44. Abnormal Hemostasis: Treatment • Desmopressin (DDAVP) • Cryoprecipitate • IV conjugated estrogens • Blood transfusions • EPO therapy • Optimal dialysis

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