2.dr partini ckd batam 2013 97

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    Curriculum Vitae

    Nama: Partini Pudjiastuti Trihono

    Pendidikan:

    Dokter umum: FKUI 1979

    Spesialis Anak: FKUI 1989

    Master of Medicine (Paediatrics): University ofMelbourne 1996

    Pediatric Nephrology course: Royal ChildrenHospital Melbourne 1996

    Spesialis Anak Konsultan: IDAI 1999

    Doktor: FKUI 2007

    Jabatan sekarang:

    Ketua Program Studi IKA FKUI

    Ketua Divisi Nefrologi Departemen IKA FKUI

    Wakil Ketua Kolegium IKA Indonesia

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    CHRONIC KIDNEY DISEASE:DIANOSIS AND MANAGEMENT

    Partini Pudjiastuti TrihonoDepartment of Child Health

    Faculty of Medicine University of Indonesia

    Batam, 8 June 2013

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    Definition of CKD

    NKF-KDOQI CPG

    Structural or functional abnormalities of the kidneys for >3

    months, as manifested by either:

    1. Kidney damage, with or without decreased GFR, as defined

    bypathologic abnormalities

    markers of kidney damage, including abnormalities inthe composition of the blood or urine or abnormalities

    in imaging tests

    2. GFR

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    Stage 1 Kidney damage w/normal GFR

    GFR >= 90ml/min/1.73 m

    Stage 2 Kidney damage w/ mildGFR decrease

    60-89mild

    Stage 3 Moderate GFR decrease 30-59moderate

    Stage 4 Severe GFR decrease 15-29severe

    Stage 5 Kidney failure (ESRD) < 15 or on dialysis

    Classification of CKD

    NKF - K/DOQI (KIDNEY DISEASE OUTCOME QUALITY INITIATIVE) -Am J Kidney Dis 2002

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    PROGRESSION OF CHRONIC KIDNEY DISEASE

    Systemic

    hypertensionReduced nephron mass

    INTRAGLOMERULAR HYPERTENSION

    Increased filtration pressure

    ProteinuriaPodocyte

    injury

    Tubulointerstitial

    hypoxia

    Glomerular

    hypertrophy

    Hyperfiltration

    Vasoactive

    signaling

    Proinflamatory

    signaling

    Matrix deposition

    FIBROSIS

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    Causes of CKD

    Glomerulonephritis

    Primary: nephrotic syndrome, focal segmental glomerulosclerosis

    Secondary: SLE, Henoch-Schonlein

    Familial nephropathy

    Alport syndrome, congenital nephrotic syndrome

    CAKUT (congenital anomalies in kidney and urinary tract)

    Bilateral renal dyslasia, hypoplasia, polycystic kidney disease

    Reflux nephropathy

    Obstructive uropathy PUJO, VUJO, calculi

    Miscelaneous Bilateral Wilms tumor

    Renal cortical necrosis

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    Risk Factors for CKD

    VUR associated with recurrent UTI and renal scarring

    Obstructive uropathy

    Prior history of acute nephritis or nephrotic syndrome

    History of renal failure in perinatal period

    Family history of polycystic kidneys or genetic renal conditions

    Renal dysplasia or hypoplasia

    Low birth weight infants

    History of Henoch-Schonlein purpura

    Presence of diabetes, hypertension

    Systemic lupus erythematosus, vasculitis

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    DIAGNOSIS

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    Modes of presentation of CKD

    Antenatal ultrasoundscanning

    Abdominal mass

    Urinary tractinfection

    Enuresis

    Failure to thrive

    Short stature

    Lethargy and pallor

    Hematuria

    Nephrotic syndrome

    Hypertension

    Congestive cardiac

    failure Seizures

    Failure to recover fromacute renal failure

    Screening siblings ofindex cases

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    Simple assessment of GFR in children

    Schwartz formula:

    GFR= body height (cm) x K

    Pcr (mg/dL)

    K= 0.45 for babies < 1 year old

    K= 0.55 for boys and girls 1-13 year old

    K= 0.57 for girls > 13 year old

    K= 0.70 for boys > 13 year old

    This equation gives the GFR in ml/min./1.73 m2 BSA Theproblem is, the Schwartz formula does not work so goodin children with very high plasma creatinine levels.

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    Chronic renal failure

    Main consequences

    Mechanism Example Clinical Manifestation s

    Decreased

    excretion

    Uremic toxins

    Salt and water

    Phosphate

    Acid

    Potassium

    Uremic syndrome

    Volume overload, hypertension

    Hyperparathyroidism

    Metabolic acidosis

    Hyperkalemia

    Decreased

    biosynthesis

    Erythropoietin

    Activation of vitamin D

    Anaemia

    Osteomalacia,

    Hyperparathyroidism

    Altered

    metabolism

    Dyslipidaemia

    Glucose intolerance

    Atherogenesis

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    Uremic Syndrome: manifestations

    Cardiovascular Hypertension Cardiomyopathy Arrhythmias Cardiac failure

    Arteriosclerosis Pericarditis

    Central Nervous System Insomnia Fatigue/spasm

    Tremor asterixis, myoclonus Confusion, stupor, coma Encephalopathy EEG changes

    Coagulation System Bleeding Hypercoagulation

    Respiratory System Pneumonitis, uremic lung

    Lung edema Endocrinology and

    metabolism Glucose intolerance Abnormal lipid metab. Abnormal amino acids metab, Malnutrition

    Hypoalbuminemia Muscle wasting Growth retardation Hypothermia

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    Peripheral Nervous System Polyneuropathy Paresis Autonomic neuropathy Hypotension

    Hematology and Immunology Anemia Susceptible to infection Granulocyte dysfunction Lymphocyte dysfunction Immunodeficiency Malignancy

    Musculo-sceletal System Osteodystrophy, osteomalacia Hyperparathyroidism Pain and fracture Carpal Tunnel syndrome Amiloidosis Myopathy Muscle weakness

    Skin Skin dry Pruritus Hyperpigmentation Bleeding

    Delayed wound healing

    Gastrointestinal System Anorexia Nausea, vomiting Hiccup Stomatitis

    Gastritis Parotitis Colitis Bleeding Fetor uremicum

    Uremic Syndrome: manifestations

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    Diagnosis and Assessment Severity

    Investigations Urinalysis Blood: complete blood peripheral, urea,

    creatinine, Ca, PO4, alkaline phosphatase,PTH, iron, ferritin, blood gas

    Radiology: CXR, bone age ECG Kidney ultrasound: renal size, anomalies,

    obstruction MSU, DMSA (not helpful if GFR

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    PRINCIPAL MANAGEMENT

    1. Early detection and prompt treatmentkidney diseases

    2. Slowing progression of CKD3. Prevention and management of

    complications

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    100

    10

    0

    No Treatment

    Current Treatment

    Early Treatment

    4 7 9 11

    Time (years)

    GFR

    (mL/min/1

    .732)

    Kidney Failure

    Early treatment can make adifference

    [email protected]

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    Stage Description GFR Evaluation Management

    At increasedrisk

    Test for CKD Risk factor management

    1

    Kidneydamage with

    normal orGFR

    >90

    DiagnosisComorbidconditions

    CVD and CVD

    risk factors

    Specific therapy, based on diagnosisManagement of comorbid conditions

    Treatment of CVD and CVD risk factors

    2

    Kidneydamage with

    mild GFR60-89

    Rate ofprogression

    Slowing rate of loss of kidney function 1

    3Moderate

    GFR30-59 Complications Prevention and treatment of complications

    4 Severe GFR 15-29 Preparation for kidney replacement therapyReferral to Nephrologist

    5 Kidney Failure

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    Fluid and salts intake Nutrition Proteinuria

    Hypertension Anemia Metabolic acidosis Infection

    Secondary hyperparathyroidism Ca and P metabolisms/bone and mineral

    disorder

    Slowing progression and treatmentof complications

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    Maintain hydration

    Beware of polyuria

    Adequate hydration: attention to fluid intake and

    urine output Correct electrolyte disturbances

    Hyponatremia

    Hypo / hyperkalemia

    Hyperhosphatemia Hypo / hypercalcemia

    Fluids and salt intake

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    Nutritional and dietary management

    Adequate calorie intake formaintenance and catch-up growth

    Adequate protein intake for growth(RDA, higher biologic value protein)

    Low phosphate intake

    Salt / potassium restriction

    Vitamins and trace elementssupplementation

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    Proteinuria

    Screening:Test first morning urine sample Protein >+1: do protein to creatinine ratio

    Monitoring: protein to creatinine ratio on

    first morning urine sample Spot urine for albumin/creatinine ratio (mg:mg)

    Normal = 2

    Treatment: ACEI: captopril, enalapril

    ARB : losartan

    both

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    ACEI +/- ARB

    Beware of hypotension, deteriorationof kidney function, hyperkalemia

    Decrease in GFR, usually within 4weeks:

    Decrease < 30%: acceptable

    Decrease 30%-50%: dose adjustment

    Decrease > 50%: drug withdrawal

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    Hypertension

    Treatment should be aggressive

    Target: BP level < 90th centile for specificage, sex, and height

    Hypertension related to hypervolemia diuretics thiazide or furosemide

    Others anti-hypertensive agents:

    ACEI +/- ARB

    Ca channel blocker: amlodipine, nifedipine

    Selective -blocker: atenolol

    Vasodilators: hydralazine

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    Etiology of anemia in CKD:MULTIFACTORIAL

    Erythropoietin deficiency Erythropoiesis inhibitor Secondary hyperparathyroidism Blood loss Deficiency of hematinic agents (Fe,folic acid, B12) Shorter erythrocytes lifespan Primary renal diseases Cytokine inflammation Infection Aluminium toxicity

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    GFR < 60 mL/m/1.73 m2

    Hb level

    Hb < 11 g/dL

    Complete peripheral bloodIron index

    Normal Iron deficiency Refer to

    hematologist

    Treat with r-EPOIron supplement

    Anemia correctedAnemia persisted

    No No

    GUIDELINE NKF - K/DOQI

    Am J Kidney Dis, 2002 (mod)

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    Indikasi : Hb < 10 g/dl atau Ht 30 % (PERNEFRI) Dosages: start with 50 unit/kg SC, twice a week

    Pre-requisite:1. Adequate iron storage: feritin serum >100 g/L

    transferin > 20%2. No infection/inflammation3. No hyperparathyroidisms4. Avoid iron overload

    TREATMENT ANEMIA WITH r-HuEPO

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    Packed Red Cell Transfusion

    Indications

    1. Acute bleeding

    2. Hb< 7 g/dl but r-EPO is not available

    3. Hb

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    Acid base status

    Maintenance of acid base balance is important

    Metabolic acidosis associated with

    Failure to thrive, muscle degradation, bone

    demineralization, hyperkalemia Correction:

    Reducing protein intake ( S- containingamino acids)

    Reduce endogenous acid production Sodium bicarb. supplementation (dose

    adjusted to BGA)

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    Feedback Loops in 2nd Hyperparathyroidism

    Ca = calcium; CVD = cardiovascular disease; P = phosphorus.Courtesy of Kevin Martin, MB, BCh.

    PTH

    Bon e Disease

    Fractures

    Bone pain

    Marrow fibrosisErythropoietin resistance

    1,25DCalcitriol

    Renal Failur e

    PTH

    Systemic Toxic i ty

    CVD

    Hypertension

    Inflammation

    Calcification

    Immunological

    25D

    Ca++

    Decreased Vitamin D Receptorsand Ca-Sensing Receptors

    Serum P

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    Ca and PO4 metabolism in CKD

    Monitor Ca, PO4, alkaline phosphatase,PTH, Xray renal osteodystrophy view (kneeor wrist)

    Restrict dietary phosphate Phosphate binder

    CaCO3 50-100 mg/kg BW taking during meals

    Ca acetate

    Sevelamer

    Vitamin D3 (1,25 diOH cholecalciferol)

    Calcium supplement (watch carefully for

    hypercalcemia)

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    Target ranges for blood biochemicalparameters in children with CKD

    Camg/dL

    Pmg/dL

    Ca x P PTHpg/mL

    ALPmg/dL

    Age 1-12 yrs

    CKD 2-3 9-10.2 4-6

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    Vaccination of Patients with ChronicRenal Disease

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    Factors affecting renal diseaseprogression

    CKD

    Progression

    Hypertension Proteinuria

    Renal

    anemia,dyslipide

    mia

    Altered

    mineralhomeostasis

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    Anemia of Renal Failure

    [email protected]

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    KDOQI RECOMMENDATION

    Ca

    Maintain in normal range

    PO4

    CKD stage 5:

    > 12 year 3.4-5.5 mg/dL

    1-12 year 4 6 mg/dL

    PTH

    CKD stage 4: 70-110 pg/ml

    CKD stage 5: 200-300 pg/ml

    Ca x PO4

    > 12 year : 55 mg2/dL2

    < 12 year : 65 mg2/dL2

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    Growth

    Possible factors contributing to growth retardation in CRF

    Inadequate energy intakeInappropriate protein intakeDisturbance of water and electrolyte balanceMetabolic acidosisRenal osteodystrophyHypertensionInfectionAnemiaHormonal abnormalities

    Corticosteroid therapyPsychosocial factors

    Recombinant human growth hormone when optimal management fails

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    Vaccination of Patients with ChronicRenal Disease

    Recommended:

    BCG

    Hepatitis B

    Varicella zoster

    Pneumococcus

    Influenza

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    Chronic Kidney Disease

    Common condition

    Most etiology:

    Glomerulonephritis

    Reflux nephropathy Obstructive uropathy

    Significant morbidity

    Expensive

    Effective treatment can slow progression Teamwork: primary physicians, pediatricians,

    renal specialists

    Infection Congenital UT anomalies

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    CKD

    death

    Stages in Progression of Chronic KidneyDisease and Therapeutic Strategies

    Complications

    Screeningfor CKD

    risk factors

    CKD riskreduction;

    Screening for

    CKD

    Diagnosis& treatment;

    Treat

    comorbid

    conditions;

    Slow

    progression

    Estimateprogression;

    Treat

    complications;

    Prepare for

    replacement

    Replacementby dialysis

    & transplant

    NormalIncreased

    risk

    Kidney

    failureDamage GFR

    AJKD 2002: 39(2)

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    Chronic kidney disease

    Hyperparathyroidism

    Phosphate retention FGF23 1,25(OH)2D3

    PTH resistanceof bone

    Hypocalcemia Acidosis

    Parathyroid Careceptor expression

    Parathyroid 1,25(OH)2D3receptor expression

    Pathophysiology

    of2nd

    h

    yperparathyroidism

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    Recommended target ranges forserum PTH and Ca-Po4 product

    Targetrange

    Chronic Kidney Disease Stage

    II III IV VSerum PTHlevel

    35-70pg/ml

    35-70pg/ml

    70 -110pg/ml

    200-300pg/ml

    Ca-PO4

    productlevel

    Age < 12 years < 65 mg2/dL2

    Age > 12 years < 55 mg2/dL2