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

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

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  • A.Jenabi MD Ass. Professor of Medicine and Nephrology, iran University of medical Sciences Tehran, Iran CHRONIC KIDNEY DISEASE In the name of GOD
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  • 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).
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  • IRREVERSIBLE LOSS OF GFR DENOTES PROGRESSION EVEN WHEN THE UNDERLYING CAUSE HAS BEEN ELIMINATED chronic renal failure
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  • 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.
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  • MOST OF THE CKD PATIENTS ARE ASYMPTOMATIC AND ARE DETECTED DURING SCREENING EITHER ROUTINE OR FOR UNRELATED ILLNESS
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  • CKD ESRD 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.
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  • Uremia is a state of systemic poisoning Due to cumulative effects of failure of many functions of kidney ESRD?
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  • Pathophysiology of Chronic Kidney Disease Two broad sets of mechanisms of damage : (1) initiating mechanisms specific to the underlying etiology (immune complexes and mediators of inflammation in certain types of glomerulonephritis, or toxin exposure (2) a set of progressive mechanisms, involving hyperfiltration and hypertrophy of the remaining viable nephrons
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  • 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?
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  • 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-).
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  • CKD Causes CAUSE ADULTSCHILDREN 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+
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  • 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/1.73m 2 have CKD. However, since GFR declines normally with age (approximately 1ml/min/1.73 m 2 /year after age 20), a GFR between 60 - 90 ml/min/1.73m 2 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.
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  • 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.
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  • 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.
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  • 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 m 2, which is markedly abnormal, while the second has a GFR of 115 ml/min/1.73 m 2, well within the normal range.
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  • STAGEDESCRIPTIONGFR(ml/min) 0WITH RISK FACTORS>90 IKIDNEY DAMAGE (WITH NORMAL OR GFR) >90 IIMILD60-89 IIIMODERATE30-59 IVSEVERE15-29 VKIDNEY FAILURE
  • CKD death ComplicationsComplications Screening for CKD risk factors: diabetes hypertension age >60 family history US ethnic minorities CKD risk reduction; Screening for CKD Diagnosis & treatment; Treat comorbid conditions; Slow progression Estimate progression; Treat complications; Prepare for replacement Replacement by dialysis & transplant NormalNormal Increased risk Kidney failure DamageDamage GFR 11.3 m 5.6% 7.7 m 3.8% 0.3 m 0.2% Conceptual Model for CKD
  • Slide 18 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. Microalbuminuria refers 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. 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. Microalbuminuria refers 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. Measurement of albuminuria
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  • 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
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  • SYMPTOMS / SIGNS SYSTEM SYMPTOMSSIGNS GENERALFATIGUE, WELL BEINGWASTED,SALLOW COMPLEXION SKINITCHING / BRUISINGPALLOR, PIGMENTATION DRYNESSFROST, EXCORIATIONS GITANOREXIA / NAUSEAGI BLEED VOMITING / HICCUPS CVSEDEMA, CHEST PAINHT / CARDIOMEGALY DYSPNEARUB / CRACKLES MUSCULOBONE PAINDEFORMITIES / MYOPATHY SKELETALGROWTH FAILURE NSNUMBNESS / CRAMPSNEUROPATHY / ASTERIXIS INSOMNIA / IMPOTENCEMYOCLONUS / ACIDOSIS
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  • Volume expansion (I) Hyponatremia (I) Hyperkalemia (I) Hyperphosphatemia (I) Fluid and electrolyte disturbances
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  • Secondary hyperparathyroidism (I or P) Adynamic bone (D) Vitamin Ddeficient 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) 2 -Microglobulin associated amyloidosis (P or D) Endocrine-metabolic disturbances
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  • Bone Manifestations of CKD
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  • Flowchart for the development of bone, phosphate, and calcium abnormalities
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  • 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 Calcium, Phosphorus, and the Cardiovascular System
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  • 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.
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  • 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) Calciphylaxis
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  • Salt and pepper appearance skull And brawn tumor
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  • Sub periosteal bone resorbsion and arterial calcification
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  • Clavicles bone resorbsion
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  • Rugger jersey appearance of skeletal vertebrae
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  • Multiple brawn tumors of pelvic bone
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  • 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) Neuromuscular disturbances
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  • 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) Cardiovascular and pulmonary disturbances
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  • Correlation between the decline in kidney function, and the increasing incidence of cardiovascular (CV) complications and death from CV disease 75.0;, 60.074.9;, 45.059.9;, < 45
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  • 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
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  • HTN DM CKD MI
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  • Abnormal bone Age Oxidation (OxLDL) Diabetes HTN Advanced glycation end-products Smoking Genetics Dyslipidemia Carbonyl stress Low fetuin-A Traditional Risk FactorsNon-traditional Risk Factors Elevated IL-1, Il-6, TNF Homocysteine Abnormal mineral metabolism Fractures Cardiovascular disease in CKD
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  • Ischemic Vascular 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)
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  • Pallor (I) b Hyperpigmentation (I, P, or D) Pruritus (P) Ecchymoses (I) Nephrogenic fibrosing dermopathy (D) Uremic frost (I) Dermatologic disturbances
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  • Anorexia (I) Nausea and vomiting (I) Gastroenteritis (I) Peptic ulcer (I or P) Gastrointestinal bleeding (I, P, or D) Idiopathic ascites (D) Peritonitis (D) Gastrointestinal disturbances
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  • Anemia (I) b Lymphocytopenia (P) Bleeding diathesis (I or D) b Increased susceptibility to infection (I or P) Leukopenia (D) Thrombocytopenia (D) Hematologic and immunologic disturbances
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  • Causes of Anemia in CKD Relative deficiency of erythropoietin Diminished red blood cell survival Bleeding diathesis Iron deficiency Hyperparathyroidism/bone marrow fibrosis "Chronic inflammation" Folate or vitamin B 12 deficiency Hemoglobinopathy Comorbid conditions: hypo/hyperthyroidism, pregnancy, HIV-associated disease, autoimmune disease, immunosuppressive drugs
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  • 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.
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  • Desmopressin (DDAVP) Cryoprecipitate IV conjugated estrogens Blood transfusions EPO therapy Optimal dialysis Abnormal Hemostasis: Treatment
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  • Duration of symptoms / RF for months Absence of acute illness in face of very high urea and CREATININE Small kidneys on imaging Bone disease Neurological complications Skin / nail / eye changes Factors Suggesting CHRONICITY
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  • To confirm the primary renal diagnosis. A. Conditions that can be arrested / reversed. B. Conditions affecting dialysis / transplantation. C. Conditions FORESEE. Genetic counseling / screening. To establish CHRONICITY. To identify reversible factors. To detect INTERCURRENT illness. To detect COMORBID factors. To establish a baseline database. The Initial Assessment: Objectives
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  • UREMIA PATHOPHYSIOLOGY LOSS OF NEPHRONS Na+ BALANCEH 2 O BALANCE K+ BALANCE H+ BALANCE EXC. OF DRUGS EXC.OF NITROGENOUS WASTES Ca,Mg,,P,Vit D METABOLISM CATABOLSIM OF PEPTIDES ERYTHROPOIETIN
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  • Diagnosis: AETIOLOGY; Est.CHRONICITY ASSESMENT of severity ASSESMENT of nutritional status Conservative management PREDIALYSIS / transplantation evaluation Dialysis access / HBV vaccination Dialysis / transplantation Approach To The Patient With CKD
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  • History : symptoms of uremia Physical: wt/ supine - standing B.P Skin changes FUNDUS Cardiac size / rub Neurological Lab: biochemistry / RADIOLOGY / others Know about the varying natural history of different causes of CKD Parameters To Follow
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  • Systemic lupus ERYTHEMATOSIS Obstructive nephropathy ISCHEMIC nephropathy PYELONEPHRITIS GLOMERULONEPHRITIS HYPERTENSIVE NEPHROSCLEROSIS Treatable Causes Of CKD
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  • Follow Up Assessment Objectives: MONITOR PROGRESS OF PRIMARY DISEASE & RESPONSE TO SPECIFIC TREATMENT MONITOR PROGRESS OF CKD & RESPONSE TO NONSPECIFIC TREATMENT TO WATCH OUT FOR INTERCURRENT ILLNESS TO DETECT COMPLICATIONS OF CKD TO FORESEE NEED FOR DIALYSIS / TRANSPLANTATION & PREPARE
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  • AVOID AGGRAVATING RF CONSERVATIVE Mx OF CKD SLOW PROGRESSION OF RF TREAT. UREMIC SYMP.
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  • AVOID VOLUME DEPLETION / EXCESS CAREFUL DRUG USAGE AVOID ELECTROLYTE IMBALANCE AVOID PREGNANCIES IN HIGH RISK CASES AVOID URINARY INSTRUMENTATION & CONTRAST STUDIES Measures To Avoid Aggravating RF
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  • CARDIAC FAILURE DRUGS: NSAIDS, ACEI, AG, CONTRASTS, ETC VOLUME DEPLETION HTN - UNCONTROLLED / OVER TREATMENT OBSTRUCTION INFECTION- RENAL / EXTRA RENAL CATABOLISM: INFECTION, GI BLEED, SURGERY, ETC ELECTROLYTE DISTURBANCES Reversible Factors Aggravating CKD
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  • CONTROL HTN / CARDIAC RISK FACTORS DIETARY PROTEIN RESTRICTION SCREEN & TREAT UTI CONTROL HYPERPHOSPHATEMIA / HYPERURICEMIA TREAT HYPERLIPIDEMIA ACE INHIBITORS TREATMENT OF PRIMARY CAUSE GLYCEMIC CONTROL IN DIABETES Measures To Slow Progression Of RF
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  • Degree of CKD GFR Action Mild 60-90 ml/min/1.73 m 2 Steps 1,2 Moderate30- 59 ml/min/1.73 m 2 Steps 1,2,3 Severe15- 29 ml/min/1.73 m 2 Steps 1,2,3,4 Step 1 - slow the progression of chronic kidney disease to end stage renal disease (ESRD) Step 2 - identify and treat co-morbid conditions (cardiovascular) Step 3 - identify and prevent complications of CKD (anemia, divalent ions, malnutrition) Step 4 - prepare the patient mentally and physically for renal replacement therapy Stepped-care Parallels Impairment of GFR
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  • 90KIDNEY DAMAGE (WITH NORMAL OR GFR) I >90WITH RISK FACTORS0 GFR(ml/mt)DESCRIPTIONSTAGE CLASSIFICATION OF CKD - NKF
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  • GFR (ref group GFR >80) Decrease in Hct (men) (women) 70-80 -0.1%-.03% 60-69-0.1%-0.3% 50-59-0.4%-0.7% 40-49-0.3%-2.2% 30-39-1.6%-2.9% 20-29-2.6%-3.8%
  • Blood Pressure TARGETS HYPERTENSION WITHOUT CRF1G/DAY
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  • AGEI/ARB RECOMMENDATIONS FOR USE IN CKD ACE INHIBITOR AS FIRST LINE THEPRAPY IN TYPE-1 & TYPE-2 DM PATIENTS WITH MICRO/ MACROALBUMINURIA EVEN WITHOUT HTN/RF ALL PATIENTS WITH HTN AND/OR PROTEINURIA ARB SAME INDICATIONS IF PATIENT INTOLERENT OF ACEI COMBINATION OF ACEI AND ARB MAY ALSO BE OF BENEFIT MONITOR CREATININE & K+ WEEKLY INITIALLY TOLERATE K + 5.5mEq/L INSTITUTE LOW K + DIET AND DOSE OF ACEI OR ARB TOLERATE RISE OF CREATININE OF < 20% ABOVE BASELINE AS LONG AS LEVEL PLATEUS IN 2-3 WEEKS DISCONTINUE DRUG IF EITHER K + >5.5 OR CRETININE>20% ABOVE BASELINE (CONSIDER RENAL ARTERY STENOSIS)
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  • HTN CONTROL IN CKD BP>15/10 >Goal,SCr15/10>Goal,SCr>1.8 ACEI/ATB+(Thiazide)ACEI/ATB+(Loop diuretic) BP still not at goal(130/80) Add Long Acting CCB(Pref-Non-DHP)Titrateto moderate dose BP still not at goal Baseline pulse>82 Baseline pulse
  • Protein Restriction INITIATE WHEN SERUM CREATININE IS >2.0 mg/dL in Men and >1.5 mg/dL in Women RESTRICT PROTEIN < 0.8G/Kg/DAY ENCOURAGE PROTEIN OF HIGH BIOLOGICAL VALUE MONITOR NUTRITIONAL PARAMETERS (ALBUMIN, PREALBUMIN)
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  • Cardiovascular Risk Factors In CKD SUSTAINED & REFRACTORY HTN CHRONIC ANEMIA DYSLIPIDEMIA S.PHOSPHATE &VASCULAR CALCIFICATION INCREASED OXIDANT STRESS HYPERHOMOCYSTINEMIA
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  • RECOMMENDATIONS FOR CVS RISK REDUCTION AGGRESSIVE BP CONTROL (
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  • Principles Of Divalent Ion Management In CKD CORRECTION OF HYPOCALCEMIA CORRECTION OF ACIDOSIS CORRECTION OF HYPERPHOPHATAEMIA MONITORING PTH LEVELS AND CONTROL OF RENAL OSTEODYSTROPHY
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  • RECOMMENDATIONS FOR DIVALENT IONS MANAGEMENT HYPOCALCEMIA - MONITOR, ORAL CaCO3+/- CALCITRIOL ACIDOSIS - 1-4G OF NaHCO3 IF NOT CONTRAINDICATED BY HTN CONTROL AND FLUID BALANCE HYPERPHOSPHATAEMIA - MONITOR TARGET(50mlUPPER NORMAL 20-50ml/mt1.0-1.5 TIMES
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  • Anemia Atherosclerosis Anti-angiotensin therapy Albumin Anions and Cations Arterial Blood Pressure Arterial Calcification Access Avoidacne of Nephrotoxic Drugs Allograft 10 As of CKD
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  • Treatment Of UREMIC Symptoms GI SYMPTOMS: Protein Restriction Correct Acidosis Small Frequent meals Antiemetics / Cisapride H2 Antagonists AL.OH Gel ITCHING: Protein Restriction Phosphate Restriction Antihistaminics Emollients UV Radiation Cholestyramine Boluso of Xylocaine Erythropoietin
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  • NEUROMUSCULAR: Protein Restriction Vitamins Exercise Muscle Relaxants Tranquilizers Quinine Anti-depressants Correction of Anemia SKELETAL: Decrease & Bind Phosp Treat acidosis Calcium Supplements Clacitriol / 1 Alpha Treat severe hyperuricemia ANEMIA Iron, Folate & B12 Erythropoietin Transfusion
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  • INTRACTABLE UREMIC SYMPTOMS PERICARDITIS / PULMONARY OEDEMA OSTEO DYSTROPHY BLEEDING DIATHESIS ENCEPHALOPATHY / NEUROPATHY METABOLIC COMPLICATIONS (ESP. HYPERKALEMIA) Indications For Dialysis / TRANSPLANATATION
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  • Renal replacement therapy Hemodialysis Peritoneal dialysis Kidney transplant Living donor Cadaver transplant