A. Jenabi MDAss. Professor of Medicine

and Nephrology,iran University of medical Sciences

Tehran , Iran

A. Jenabi MDAss. Professor of Medicine

and Nephrology,iran University of medical Sciences

Tehran , Iran

CHRONIC KIDNEY DISEASECHRONIC KIDNEY DISEASE

In the name of GOD

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).

IRREVERSIBLE LOSS OF GFR

DENOTES PROGRESSION EVEN WHEN THE UNDERLYING CAUSE HAS BEEN ELIMINATED

chronic renal failure

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.

MOST OF THE CKD PATIENTS ARE ASYMPTOMATIC AND ARE DETECTED DURING SCREENING

EITHER ROUTINE OR FOR UNRELATED ILLNESS

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.

Uremia is a state of systemic poisoning

Due to cumulative effects of failure of many functions of kidney

ESRD?

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

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?

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-).

CKD CausesCAUSE ADULTS 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+

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.

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.

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.

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.

STAGE DESCRIPTION GFR(ml/min)

0 WITH RISK FACTORS >90

I KIDNEY DAMAGE (WITH NORMAL OR GFR)

>90

II MILD 60-89

III MODERATE 30-59

IV SEVERE 15-29

V KIDNEY FAILURE <15

CLASSIFICATION OF CKD-NKF

CKDCKDdeathdeathCKDCKDdeathdeath

ComplicationsComplicationsComplicationsComplications

Screening for CKD

risk factors:diabetes

hypertensionage >60

family historyUS ethnic minorities

CKD riskreduction;

Screening forCKD

Diagnosis& treatment;

Treat comorbid

conditions;Slow

progression

Estimateprogression;

Treatcomplications;

Prepare forreplacement

Replacementby dialysis

& transplant

NormalNormalNormalNormal IncreasedIncreasedriskrisk

IncreasedIncreasedriskrisk

KidneyKidneyfailurefailureKidneyKidneyfailurefailureDamageDamageDamageDamage GFRGFR GFRGFR

11.3 m11.3 m5.6%5.6%

7.7 m7.7 m7.7 m7.7 m3.8%3.8%

0.3 m0.3 m0.2%0.2%

Conceptual Model for CKD

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

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

SYMPTOMS / SIGNSSYMPTOMS / SIGNSSYSTEM SYMPTOMS SIGNS

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

• Volume expansion (I)

• Hyponatremia (I)

• Hyperkalemia (I)

• Hyperphosphatemia (I)

Fluid and electrolyte 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)• β 2-Microglobulin associated amyloidosis (P or D)

Endocrine-metabolic disturbances

Bone Manifestations of CKD

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

• 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

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.

Calciphylaxis is a devastating condition seen almost exclusively in patients with advanced CKDthere 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

Salt and pepper appearance skullAnd brawn tumor

Sub periosteal bone resorbsion and arterial calcification

Clavicles bone resorbsion

Rugger jersey appearance of skeletal vertebrae

Multiple brawn tumors of pelvic bone

• 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

• 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

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

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

HTN DM

CKD

MI

Abnormal boneAbnormal bone

Age

Oxidation (OxLDL)

Diabetes

HTN

Advanced glycation end-products

Smoking

Genetics

DyslipidemiaCarbonyl stress

Low fetuin-A

Traditional Risk Factors Non-traditional Risk Factors

Elevated IL-1, Il-6, TNFElevated IL-1, Il-6, TNF

Homocysteine

Abnormal mineral metabolismAbnormal mineral metabolism

FracturesFracturesCardiovascular Cardiovascular disease in CKDdisease in CKD

Ischemic Vascular DiseaseAny 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)

• Pallor (I)b

• Hyperpigmentation (I, P, or D)• Pruritus (P)• Ecchymoses (I)• Nephrogenic fibrosing dermopathy

(D)• Uremic frost (I)

Dermatologic 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)

Gastrointestinal disturbances

• 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

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 B12 deficiency

• Hemoglobinopathy

• Comorbid conditions: hypo/hyperthyroidism, pregnancy, HIV-associated disease, autoimmune disease, immunosuppressive drugs

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.

• Desmopressin (DDAVP)• Cryoprecipitate• IV conjugated estrogens• Blood transfusions• EPO therapy• Optimal dialysis

Abnormal Hemostasis: Treatment

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

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

UREMIA PATHOPHYSIOLOGY

LOSS OF NEPHRONS

Na+ BALANCE H2O BALANCE K+ BALANCE

H+ BALANCE

EXC. OF DRUGS EXC.OF NITROGENOUSWASTES

Ca,Mg,,P,Vit DMETABOLISM

CATABOLSIM OFPEPTIDES

ERYTHROPOIETIN

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

• 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

Systemic lupus ERYTHEMATOSISObstructive nephropathyISCHEMIC nephropathyPYELONEPHRITISGLOMERULONEPHRITISHYPERTENSIVE NEPHROSCLEROSIS

Treatable Causes Of CKD

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

AVOID AGGRAVATING RF

CONSERVATIVE Mx OF CKD

SLOW PROGRESSION OF RF TREAT. UREMIC SYMP.

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

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

CONTROL HTN / CARDIAC RISK FACTORSDIETARY PROTEIN RESTRICTIONSCREEN & TREAT UTICONTROL HYPERPHOSPHATEMIA /

HYPERURICEMIATREAT HYPERLIPIDEMIAACE INHIBITORSTREATMENT OF PRIMARY CAUSEGLYCEMIC CONTROL IN DIABETES

Measures To Slow Progression Of RF

Degree of CKD GFR ActionMild 60-90 ml/min/1.73 m 2 Steps 1,2 Moderate 30- 59 ml/min/1.73 m 2 Steps 1,2,3 Severe 15- 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

<15KIDNEY FAILUREV

15-29SEVEREIV

30-59MODERATEIII

60-89MILDII

>90KIDNEY DAMAGE (WITH NORMAL OR GFR)

I

>90WITH RISK FACTORS0

GFR(ml/mt)DESCRIPTIONSTAGE

CLASSIFICATION OF CKD - NKF

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%<20 -6.5% -11.2%

Rationale for a stepped-care action plan Degree of anemia parallels decline

in GFR

Kidney Int 2001; 59:725-731

Blood Pressure

TARGETS

HYPERTENSION WITHOUT CRF <130/85

HYPERTENSION WITH CRF& PROTEINURIA <1G/DAY <130/80

HYPERTENSION WITH CRF& PROTEINURIA >1G/DAY <125/75

Current Recommendations For Hypertension Control In CKD

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+ < 5.5. IF >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)

HTN CONTROL IN CKD

BP>15/10 >Goal, SCr <1.8 BP>15/10>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) Titrate to moderate dose

BP still not at goalBaseline pulse>82 Baseline pulse<82

Add low dose ß or α+βBlocker Add other group CCB

BP still not at goal

Add long acting α-Blocker?Ref.to Nephrologist

Protein Restriction

INITIATE WHEN SERUM CREATININE IS >2.0 mg/dL in Men and >1.5 mg/dL in WomenRESTRICT PROTEIN < 0.8G/Kg/DAYENCOURAGE PROTEIN OF HIGH BIOLOGICAL VALUEMONITOR NUTRITIONAL PARAMETERS (ALBUMIN, PREALBUMIN)

Cardiovascular Risk Factors In CKD

• SUSTAINED & REFRACTORY HTN• CHRONIC ANEMIA• DYSLIPIDEMIA S.PHOSPHATE &VASCULAR

CALCIFICATION• INCREASED OXIDANT STRESS• HYPERHOMOCYSTINEMIA

RECOMMENDATIONS FOR CVS RISK REDUCTION

AGGRESSIVE BP CONTROL (<130/80) MAXIMISE ACEI/ARB THERAPY DIURETICS AND SALT RESTRICTION NEEDED IN MOST ASSESS ANEMIA. USE EPOITEN WHEN HB<10-11G% KEEP PHOSPHATE CONTROL(<5.5mg%). DIET ADVICE AND

PHOSPHATE BINDERS ASSESS LIPID PROFILE AND USE DIET THERAPY, STATINS,

FISH OIL SUPPLEMENTS TO KEEP LDL-C < 70-100mg% DAILY ANTIOXIDANT VITAMINS VIT-E (MIXTURE OF

NATURAL ISOMERS) 400-800 IU,VIT-C 500mg, NATURAL - CAROTENE - UPTO 10,000IU

SCREEN FOR HOMOCYSTENEMIA. IF ELEVATED ADVICE FOLIC ACID , B6 & B12

Principles Of Divalent Ion Management In CKD

• CORRECTION OF HYPOCALCEMIA• CORRECTION OF ACIDOSIS• CORRECTION OF HYPERPHOPHATAEMIA• MONITORING PTH LEVELS AND

CONTROL OF RENAL OSTEODYSTROPHY

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(<5.5mg%)

DIET ADVICE, TO AVOID MILK & MILK PRODUCTS, PHOSPHATE BINDERS, BEST SEVELAMER - COSTLY, OTHERS CALCIUM CONTAINING - MONITOR S. CALCIUM, AVOID ALUMINIUM CONTAINING IN LONG TERM TRT.

PTH LEVELS GFR PTH>50ml UPPER NORMAL20-50ml/mt 1.0-1.5 TIMES<20ml/mt 1.5-2.0 TIMESDIALYSIS 2.0-3.0 TIMES

CORRECT HYPOCALCEMIA & HYPERPHOSPHATEMIACALCITRIOL THERAPY

• Anemia• Atherosclerosis• Anti-angiotensin therapy• Albumin• Anions and Cations• Arterial Blood Pressure• Arterial Calcification• Access• Avoidacne of Nephrotoxic Drugs• Allograft

10 A’s of CKD

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

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

• INTRACTABLE UREMIC SYMPTOMS• PERICARDITIS / PULMONARY OEDEMA• OSTEO DYSTROPHY• BLEEDING DIATHESIS• ENCEPHALOPATHY / NEUROPATHY• METABOLIC COMPLICATIONS

(ESP. HYPERKALEMIA)

Indications For Dialysis / TRANSPLANATATION

Renal replacement therapy

Hemodialysis

Peritoneal dialysis

Kidney transplantLiving donorCadaver transplant