Penyakit Ginjal Kronik Dan Indikasi Dialisis DR Ratih Tri KD MAJU

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Penyakit Ginjal Kronik dan

Indikasi Dialisis
Dr. Ratih Tri Kusuma Dewi Sp.PD
ANATOMI Anatomy
• 2 Kidneys
• 2 Ureters
• Bladder
• Urethra
Kidney Function
• Detoxify blood
• Increase calcium absorption
calcitriol
• Stimulate RBC production
erythropoietin
• Regulate blood pressure and electrolyte
balance
renin
• Definisi
(NKF KDOQI guidelines, 2002)
KDIGO 2012
• CKD is defined as abnormalities of kidney
structure or function, present for > 3 months,
with implications for health
(NKF KDOQI guidelines, 2002)
• KLASIFIKASI
(NKF KDOQI guidelines, 2002)
KDIGO 2012
(CGA) Cause..
Major causes of chronic renal failure.
Glomerulopathies Tubulointerstitial nephritis
Drug hypersensitivity
• Primary glomerular diseases: Idiopathic
Heavy metals
1. Focal and segmental glomerulosclerosis Analgesic nephropathy
2. Membranoproliferative glomerulonephritis Reflux/chronic pyelonephritis
3. IgA nephropathy
4. Membranous nephropathy Hereditary diseases
Polycystic kidney disease
• Secondary glomerular diseases: Medullary cystic disease
Alport's syndrome
1. Diabetic nephropathy Obstructive nephropathies
2. Amyloidosis Prostatic disease
3. Postinfectious glomerulonephritis Nephrolithiasis
4. HIV-associated nephropathy Retroperitoneal fibrosis/tumor
5. Collagen-vascular diseases Congenital
6. Sickle cell nephropathy Vascular diseases
7. HIV-associated membranoproliferative Hypertensive nephrosclerosis
glomerulonephritis
Renal artery stenosis
(Tierney, et.al; 2006)
Penyebab terbanyak PGK

 Di Indonesia, penyebab PGK yang


menjalani hemolisis tahun 2000 terbanyak
adalah :
 Glomerulonefritis (46%)
 Nefropati diabetik (18,6%)
 Infeksi Saluran Kemih (ISK) dan Batu saluran
kencing (BSK) (12,85%)
 Nefrosklerosis hipertensi (13,65 %)
 Ginjal polikistik (8,46 %)
ETIOLOGI PGK

Drug (1.50%)
BATU GINJAL
(9.20%) Policystic kidney
(3.10%) Glumerulonefritis
Diabetes melitus
HIPERTENSI (22%) GN (45%)
Hipertensi
Batu ginjal
DM (20%) Polycystic kidney
Drug induce

DATA ETIOLOGI RSCM. 2013


GFR
Problems with creatinine

Stevens L et al, NEJM 2006;


354:2473-2483
CKD- EPI
(Levy, et.al; 2009)
www.qxmd.com
GFR

NKF KDOQI guidelines, 2002


Albuminuria
False Positives in Microalbuminuria Interpretation

Functional Causes Contamination Other Causes


• Fever Menstrual Renal disease other
• Urinary infection contamination than diabetes
• Significant physical activity
in the preceding 24 hours Vaginal
• Severe hypertension discharge
• Heart failure stage IV
• Preeclampsia
• Post surgery (major)
Highly unstable diabetes

Donna Birbrager , 2013


Faktor Risiko Terkait Inisiasi dan Progresifitas PGK
Faktor Inisiasi Faktor Progresifitas
Hipertensi Usia tua
Diabetes melitus Laki-laki
Penyakit kardiovaskular Ras
Dislipidemia Predisposisi genetik
Sindrom metabolik Kontrol tekanan darah buruk
Hiperurisemia Kontrol glikemik buruk
Merokok Proteinuria
Status ekonomi rendah Penyakit kardiovaskular
Pajanan zat nefrotoksik (NSAID, Dislipidemia
analgetik, obat herbal, logam berat Merokok
Sindrom metabolik
Hiperurisemia
Status ekonomi rendah
Alkohol, zat neftrotoksik
Cedera ginjal akut

Comprehensive clinical nephrology. 2010


Symptoms and signs of uremia
Organ System Symptoms Signs
General Fatigue, weakness Sallow-appearing, chronically ill
Skin Pruritus, easy bruisability Pallor, ecchymoses, excoriations,
edema, xerosis
ENT Metallic taste in mouth, epistaxis Urinous breath
Eye Pale conjunctiva
Pulmonary Shortness of breath Rales, pleural effusion
Cardiovascular Dyspnea on exertion, retrosternal pain on Hypertension, cardiomegaly,
inspiration (pericarditis) friction rub
Gastrointestinal Anorexia, nausea, vomiting, hiccups
Genitourinary Nocturia, impotence Isosthenuria
Neuromuscular Restless legs, numbness and cramps in
legs
Neurologic Generalized irritability and inability to Stupor, asterixis, myoclonus,
concentrate, decreased libido peripheral neuropathy

(Tierney, et.al; 2006)


Optimal PGK Patient Care
Deteksi dini
PGK

Interventions that Prevention of uremic Modification of Preparation for


delay progression complications comorbidity RRT

ACE inhibitors Malnutrition Cardiac disease Education

BP control Anemia Vascular disease Informed choice of


RRT
Blood sugar Osteodystrophy Neuropathy
control (in diabetics) Timely access
Acidosis placement
Protein restriction Retinopathy
(in diabetics) Timely initiation of
dialysis
NICE ESH/ESC ASH/ISH AHA/ACC/ JNC 7 JNC 8
CDC

BP target Not <140/85 <140/90 <140/90 <130/80 <140/90


for DM addressed
Low target
may be
considered

BP target Not CKD no <130/80 <130/80 <130/80 <140/90


for CKD addressed proteinuria (+proteinu
(<140/90 ria)
CKD +
proteinuria
<130/90
Th/ for Explana- Explana- Explana- Explana-tion Explana- No
resistent tion tion tion tion explana-
HTN tion

Controversy - Update Hypertension Guideline. JNC 8


Manajemen Anemia pada PGK
Indikasi :
• Hb < 10 g/gl ( penyebab lain anemia sdh disingkirkan )
• Syarat pemberian terapi ESA :
Tidak didapatkan defisiensi besi absolut ( ST < 20%, FS < 100 ng/ml PGK non
dialisis dan PGK dengan PD, FS < 200 ng/ml PGK HD) → target ST > 20 %
FS > 100 (Non Dialisis, PD) FS > 200 (HD)
• Bila ada defisiensi besi abosolut → koreksi besi dulu
( parenteral : iron sucrose, iron dextran ; oral : ferrous fumarate )
• Tidak ada infeksi berat
Terapi ESA
• Epoetin α dan β : mulai 2000-5000 IU 2x/minggu
atau 80-120 unit /kgBB/minggu SC
• Continous Erythropoesis Receptor Activator ( CERA ) : 0,6 µg/kbBB
atau 50-75 µg setiap 2 minggu
• (TARGET RESPON Hb naik 0,5-1,5 g/dl dalam 4 minggu) Hb 10-12 g/dl

PERNEFRI. Konsensus manajemen Anemia pada PGK. 2011


Penyakit ginjal kronik. Buku ajar penyakit alam.
Control of serum phosphorus, vitamin D, and parathyroid
hormone
• Hyperphosphatemia and low levels of 1,25-dihydroxyvitamin D3 (1,25-D) will lead to
secondary hyperparathyroidism and associated bone disease
• Hyperphosphatemia risk factor for mortality and adverse cardiovascular outcomes
Dietary management. Phosphate intake restricted to 800-1,000 mg/day
(26-32 mmol/L /day).
Target serum phosphorus levels CKD st 3 and 4 (2.7 and 4.6 mg/dL (0.9 and 1.5
mmol/L). CKD stage 5 on dialysis 3.5 and 5.5 mg/dL (1.1 and 1.8 mmol/L).
Phosphorus binders restrict total calcium intake 1500 mg per day (37mmol/L/Day)
minimize the risk of vascular calcification combined with sevelamer, lanthanum,
magnesium.
• Serum calcium levels CKD stages 3 and 4 maintained within the normal
CKD st 5 lower values (8.4-9.5 mg/dL [2.1-2.4 mmol/L]).
• Serum parathyroid hormone levels control of PTH secretion reduced hyperphosphatemia
• Vitamin D Target serum levels of 25-D in CKD. Serum levels of 25-D least 30 ng/mL (75
nmol/L) supplemented at least 800 IU of cholecalciferol per day
• Cinacalcet increases the sensitivity of calcium receptors on the parathyroid → decrease in
PTH secretion
Handbook of Dialysis 4th Edition 2007
National Cholesterol Education
Program.2012
• Prognosis
Initiation of Dialysis
Stages of chronic kidney disease: a clinical action plan
GFR
Stage Description (mL/min/1.73 m2) Action
1 Kidney damage with ≥ 90 Diagnosis and treatment. Treatment of
normal or ↑ GFR comorbid conditions.
Slowing of progression. Cardiovascular
disease risk reduction.
2 Kidney damage with 60–89 Estimating progression.
mildly ↓ GFR
3 Moderately ↓ GFR 30–59 Evaluating and treating complications.

4 Severely ↓ GFR 15–29 Preparation for kidney replacement


therapy.
5 Kidney failure < 15 (or dialysis) Replacement (if uremia is present).
1
From National Kidney Foundation, KDOQI, chronic kidney disease guidelines.
2 2
Chronic kidney disease is defined as either kidney damage or GFR < 60 mL/min/1.73 m for 3 or more months. Kidney damage is defined as
pathologic abnormalities or markers of damage, including abnormalities in blood or urine tests or imaging studies.

(Tierney, et.al; 2006)


When to start dialysis in ESKD

The current K/DOQI (USA) and European guidelines when the


GFR is <15ml/min (patients have any symptoms from ESKD)
definitively before GFR = 6ml/min.

The UK Renal Association guidelines


when the GFR is <10ml/min.

(Levy, et.al; 2009)


Treatment modalities for ESKD
• Hemodyalisis
centre
satellite
home
• Peritoneal Dyalisis
continuous ambulatory PD (CAPD)
automated PD (APD)
• Transplantation
cadaver
living related donor
living unrelated donor (emotionally related)
• Conservative management
best supportive care.

(Levy, et.al; 2009)


Indikasi Dialisis
A. Inpatients with laboratory evidence of impaired renal function e.g. creatinine
clearance < 15 mL/min/1.73m2
1. Symtoms known to be associated with uremic:
a. Nausea, vomiting, impaired nutrition because of poor appetite;
another gastrointestinal symptoms, including gastritis with hemorrhage,
ileus dan colitis with or without hemorrhage.
b. Altered mental status (e.g. lethargy, somnolence, malaise, stupor, coma, or
deliriumsor sign of uremic enchepalopathy, asterixis, tremor, multifocal
myoclonal, seizure)
c. Pericarditis, high risk of hemorrhage and/ or tmponade
d. Bleeding diarthosis associated with uremic platelet dysfunction
2. Refractory or progressive fluid overload
3. Uncontrolable hyperkalemia
4. Severe metabolic acidosis, especially in an oliguric patient

B. Worsening of renal function with blood urea nitrogen exceeding 70-100 mg/dl or
decreased creatinine clearance <15-20 mL/min/1,73m2.
(Levy, et.al; 2009)
Indikasi Dialisis

Complications that may prompt initiation of kidney replacement therapy


• Intractable extracellular volume overload and/or hypertension
• Hyperkalemia refractory to dietary restriction and pharmacologic treatment
• Metabolic acidosis refractory to bicarbonate treatment
• Hyperphosphatemia refractory to dietary counseling and to treatment with
phosphorus binders
• Anemia refractory to erythropoietin and iron treatment
• Recent weight loss or deterioration of nutritional status accompanied by
nausea, vomiting

Urgent Indications
• Neurologic dysfunction
(neuropathy, encephalopathy, psychiatric disturbance)
• Pleuritis or pericarditis without other explanation
• Bleeding diathesis manifested by prolonged bleeding time
a
Modified from the National Kidney Foundation's 2006 Kidney Disease Outcomes Quality Initiative (KDOQI) hemodialysis adequacy guidelines

(Daugirdas, et.al; 2007)


Assessment of patients for dialysis:
when not to dialyse

 dementia, unless there are family members who are


dedicated to helping with treatment and care
 severe peripheral arterial disease
 severe hypotensive heart failure
 severe mental illness, so the patient has no awareness of the
treatment and is unable to comply
 malignant disease with poor prognosis

(Levy, et.al; 2009)

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