2.dr partini ckd batam 2013 97
TRANSCRIPT
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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
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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
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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