PENYAKIT GINJAL KRONIK
PENYAKIT GINJAL KRONIKDr. Ian Effendi N, SpPD,K-GH Finasim
CRF = GGK = ESRD = GGT =CKD = PGKPenurunan fungsi ginjal
Bertahap / progresif (tak disadari)Sering tanpa gejala insidentil
medical check-up
Penyakit ginjal kronik (PGK) proses patofisiologis dengan
etiologi yang beragam fungsi ginjal yg progresif gagal ginjal
Gagal ginjal keadaan klinis ditandai fungsi ginjal yg
ireversibel perlu pengganti ginjal dialisis/transplantasi
ginjal
Kriteria PGKKerusakan ginjal > 3 bln, struktural atau
fungsional dengan atau tanpa penurunan LFGKelainan patologi
atauTanda kerusakan ginjal dalam darah ataupun urine atau pada
pemeriksaan imagingLFG < 60mL/m/1,73m2, > 3blnNormal: 120-130
ml / min / 1.73 m2Gangguan fungsi ginjalKlinisTanda, gejala,
pemeriksaan fisik.LaboratorisUreum , kreatitin , asam urat Tes
klirens kreatinin (TKK)
Rumus Cockrof-GaultKreatinin urin(mg/dL) x vol.urin(mL/24
jam)Kreatinin serum(mg/dL) x 1440LFG = (140-umur) x BB (Kg)72 x
kreatinin serum (mg/dLWanita = 0,85 x pria IncreaseDecreaseFactors
Affecting Serum Creatinine ConcentrationKidney Disease Ketoacidosis
Drugs: TrimethoprimCimetidineFlucytosineSome cephalosporinsReduced
Muscle Mass Malnutrition
Implementing NICE guidance 2011Prevalence of CKD by GFR in the
USA
StageDescriptionGFR(mL/min/1.73m2)PrevalencePrevalence
(%)1Kidney damage with normal or GFR> 905.9 million3.3%2Mild
GFR60-895.3 million3.0%3Moderate GFR30-597.6 million4.3%4Severe
GFR15-29400,0000.2%5Kidney Failure< 15 or dialysis
300,0000.2%Coresh, et al, Am J Kidney Dis. 2003; 41:
1-128Simplified Classification of CKD by DiagnosisDiabetic Kidney
Disease Nondiabetic Kidney DiseaseGlomerular disease autoimmune,
sytemic infections, drugs, neoplasia, idiopathic Vascular disease
ischemic renal disease, hypertensive nephrosclerosis,
microangiopathy Tubulointerstitial disease UTO, stones, UTI, drug
toxicity Cystic diseasePost-Transplant
Causes of ESRD in the USA: 2006 ADR: USRDS10This slide shows the
increasing prevalence of end-stage renal disease (ESRD)
patients.References1. Keith DS, Nichols GA, Gullion CM, Brown JB,
Smith DH. Longitudinal follow-up and outcomes among a population
with chronic kidney disease in a large managed care organization.
Arch Intern Med. 2004;164:659-663.2. U.S. Renal Data System, USRDS
2006 Annual Data Report: Bethesda, Md; 2006. Available at:
http://www.usrds.org. Accessed March 13, 2007. Transition to Next
SlideIt is important to note that CKD is also associated with high
mortality.1Penyebab pasien HDPenyebab Pasien HD se Indonesia Tahun
2009 ( 7748 pasien )
PatofisiologiTerjadi kerusakan dan penurunan progresif fungsi
nefron. Saat terjadi penurunan nilai GFR dan klirens serum ureum
dan kreatinin meningkat.
Nefron yang masih sehat mengalami hipertropi karena terus
menggantikan semua fungsi nefron yang rusak. Hal ini menyebabkan
ginjal kehilangan kemampuan untuk memekatkan urine secara
baik.Ginjal berupaya untuk mengeluarkan larutan urine dalam jumlah
besar sehingga pasien mengalami kekurangan cairan tubuh.
Kerusakan nefron terus terjadi, diikuti laju filtrasi ginjal
terus menurun.
Tubuh tidak mampu lagi membuang air, garam, dan produk-produk
sampah lainya melalui ginjal. Jika laju filtrasi ginjal < 10 20
mL/mnt secara klinis akan terlihat uremia dan tanda-tanda toksik
akibat produk sampah semakin terlihat.
Penyebab Kerusakan NefronKehilangan fungsi ginjal
sebagianMenurunya GFR dan Clearance Meningkatkan fungsi ginjal yang
masih normalSisa yang normal hypertrofiFiltrasi solute
meningkatFungsi mengkonsentrasi urine menurunEkskresi hydrogen
Asidosis metabolicEkskresi fosfat HyperfosfatemiaEkskresi kalium
HyperkalemiaReabsorbsi Na Retensi airEkskresi sampah Nitrogen
UremiaPasien kehilangan cairan tubuhPerfusi pembuluh darah ginjal
menurunKerusakan renal meningkat, jumlah nefron normal
menurunPerfusi pembuluh darah ginjal menurunTotal GFR menurun lebih
lanjutTubuh tidak mampu membuang sisa garam dan sisa metabolisme
melalui ginjalSyndrome Uremia (GFR 10 20 mL/mnt)Pasien mengalami
Kehilangan fungsi non sekresi ginjal :Kerusakan fungsi
insulinKegagalan produksi erytropoetinKegagalan mengaktifkan
kalsiumGangguan reproduksiGangguan immunitasFungsi reabsorbsi
tubulus menurun secara berangsurEkskresi urin meningkat, cair
(Poliuria)Penyakit Ginjal KronikPerubahan yang
terjadi:Ketidakseimbangan cairanKetidakseimbangan
elektrolitKetidakmampuan mengekskresi metabolitKetidakmampuan
mengontrol tekanan darahPengurangan produksi eritrositManifestasi
KlinisSistemManifestasiPenyebab1.IntegumenKulitKukuRambutKulit
kekuninganPucat / pallorPruritasKering dan bersisikTipis dan
rapuhKering, rapuhPenimbunan urochromAnemiaPenurunan aktifitas
kelenjar keringat (semua kelenjar)Endapan fosfatTerbuangnya protein
dan Ca menurunAktifitas semua kelenjar menurunTerbuangnya
protein2.Gastro inestestinalOralLambungHalitosis / fetor
uremicumPerdarahan gusi, stomatitisMual, muntah, anoreksia,
gastritis, ulcreationUrea diubah menjadi anemia oleh bakteri
mulutPerubahan aktifitas plateletSerum uremit toxin akibat bakteri
ususMukosa usus lembab3.CardiovaskulerHipertensi, oedemConjunctiva
heart failureArteriosklerosis heart diseasePerikarditisOverload
cairan mekanisme rennin angiotensinKelebihan cairan,
anemiaHipertensi kronis, pengapuran jaringan lunakToxin uremic
dakam pericardium4. PulmonaryUremic lung atau pneumoniaToxin uremic
dalam pleura dan jaringan paru Retensi asam organic hasil
metabolismeToxin uremic
Tanda dan gejalaKemih : kencing malam, banyak kencing,
proteinuriaEkstremitas: edema tungkaiReproduksi: penurunan
libidoSaraf : mengantuk, kejang, komaHematologi : anemiaDefining
Kidney DamageMarkers of Kidney Damage
:ProteinuriaMicroalbuminuriaHematuria (especially when seen with
proteinuria)Isolated hematuria has a long differential: infection,
stone, malignancy, etc.Casts (especially with cellular
elements)
18Abnormal sediment
Red blood cell castWhite blood cell castGranular
castsHyperkalemia & EKGK > 5.5 -6Tall, peaked TsWide
QRSProlong PRDiminished PProlonged QTQRS-T merge sine wave
20
21Penatalaksanaan Konservatif
Tujuan:Mencegah menurunya faal ginjal yang progresifMeringankan
keluhan uremiaMengurangi gejala uremia dengan memperbaiki
metabolisme:Pengaturan cairan dan elektrolit dengan pengontrolan
yang ketat terhadap diit & cairan Pengontrolan tensi /
hipertensi dengan obatMeningkatkan kenyamanan pasien
Indikasi penatalaksanaan konservatif:PGK dan tahap insufisiensi
ginjalFaal ginjal 10 50 % atau creatinin serum 2 mg% - 10 mg%Bentuk
:Pengaturan keseimbangan cairan dan elektrolit:Penahanan kalium
& fosfat dapat terjadi pada GGK (oral dengan CaCo3)Kontrol
dapat dilakukan dengan mengurangi intake kalium dalam
diit.Pemberian alumunium hidroksida mengikat fosfat Pemberian
laksatifPemberian Vit.DKeseimbangan transport oksigenAnemia selalu
mengiringi GGK pasien cepat letih dan sesak nafas.Memberikan rasa
nyaman, istirahat dan tidurUmumnya tidak nyaman pada GGK meliputi
pruritus, kram otot, rasa haus, sakit kepala, kulit kering, stress,
emosional, insomnia.Mengurangi tingkat fosfat serum dengan
Alhydrokside mengurangi gatal-gatalMenjaga kulit lembabMemberikan
obat anti gatal Penatalaksanaan Konservatif
Terapi Farmakologis
Diabetic Kidney Disease ACEI or ARB in all diabetic patients
with microalbuminuriaACEI (alt ARB) for Type 1 Diabetics with
macroalbuminuriaARB (alt. ACEI) in Type 2 Diabetics with
macroalbuminuria
Nondiabetic Kidney Disease ACEI/ARB recommended in all
proteinuric (>200 mg/g Cr on spot urine) patients with CKDMay
tolerate creatinine rise of 35% above baseline 902Mild GFR60-89TD
mulai meningkat3Moderate GFR30-59Hipefosfatemia,
HiipokalemiaAnemia, Hiperparatiroid, Hipertensi,4Severe
GFR15-29Malnutrisi, asidosis metabolikCenderung hiperkalemia,
dislipidemia5Kidney Failure< 15 Gagal jantunguremia31PTH and
Mineral Disorders in Patients With CKD
32IntroductionMineral and bone metabolism involves complex
interactions between P, Ca, PTH and vitamin DAbnormal mineral
metabolism in patients with CKD is associated withVascular
calcification1Renal bone disease2 and may lead to Increased
mortality31Goodman WG et al. N Engl J Med 2000;342:147883 2Moe S et
al. Kidney Int 2006;69:1945533Block GA et al. J Am Soc Nephrol
2004;15:220818Item code: 037/0052A Date of preparation: July
200633
www.kdigo.org34Definition of CKD MBDA systemic disorder of
mineral and bone metabolism due to CKD manifested by either one or
a combination of the following:Abnormalities of calcium,
phosphorus, PTH, or vitamin D metabolismAbnormalities in bone
turnover, mineralization, volume, linear growth, or
strengthVascular or other soft tissue calcification Moe et al
Kidney International June 200635Pathophysiology PTH & Mineral
Disorders in CKD 1,25(OH)2D3 P
Adapted from Skorecki K, et al. Harrisons Principles of Internal
Medicine. 15th ed. 2001:1551-1562. PTH
Ca2+36Pathophysiology of sHPT in Chronic Kidney DiseaseThe
pathogenesis of secondary hyperparathyroidism in chronic kidney
disease is multifactorial, with a number of different processes
contributing to disturbances in the regulation of PTH production
and secretion. With the progressive loss of kidney function, less
vitamin D is converted to its active form, calcitriol, resulting in
decreased serum calcitriol levels. Phosphorus is retained, so serum
phosphorus levels rise. Decreased serum vitamin D results in less
serum calcium absorption from the intestine, so serum calcium
levels may decrease.
The parathyroid gland is highly sensitive to even very small
changes in ionized extracellular calcium and rapidly releases PTH
in response to a decrease in calcium concentration.
Low serum calcium, elevated phosphorus, and decreased calcitriol
each contributes to chronic increases in PTH levels. The calcium
response is mediated by the calcium-sensing receptor (CaSR), the
primary regulator of PTH secretion. Calcitriol inhibits PTH gene
transcription, and therefore a decline in calcitriol leads to
increased PTH production. Decreased calcitriol has also been linked
to decreased expression of vitamin D receptors (VDR) and of CaSR in
parathyroid tissue, which also contributes to increases in serum
PTH levels.
Elevated PTH is known to contribute to pathogenesis of renal
osteodystrophy and has also been implicated in damage to other
systems, including cardiac, cutaneous, endocrine, immunologic, and
nervous systems. Associated imbalances in mineral homeostasis
probably also contribute to organ system damage.
References:Goodman WG. Recent developments in the management of
secondary hyperparathyroidism. Kidney Int. 2001;59:1187-1201.
Locatelli F, Cannata-Anda JB, Drueke TB, et al. Management of
disturbances of calcium and phosphate metabolism in chronic renal
insufficiency, with emphasis on the control of hyperphosphataemia.
Nephrol Dial Transplant. 2002;17:723-731.Skorecki K, et al.
Harrisons Principles of Internal Medicine. 15th ed.
2001:1551-1562.
Clinical Consequences of Mineral DysregulationRenal
osteodystrophyHyperphosphatemiaCardiovascular
calcificationExtraskeletal calcificationEndocrine
disturbancesNeurobehavioral changesCompromised immune systemAltered
erythropoiesis
37Risk Factors for Soft Tissue Calcification
HyperphosphatemiaIncreased Ca x P productExcessive calcium
loadSecondary hyperparathyroidismLocal tissue injuryRise in tissue
pH Decreased levels of calcification inhibitorsSystolic
hypertension (average 1 year systolic bp 160 mm Hg vs 120)Adipose
tissue (calcific uremic arteriolopathy)38Vascular Calcification,
Cardiovascular Complications, and CKDVascular Calcification
Associated With: Accelerated risk of stroke, amputation, MI Left
ventricular hypertrophy Poor coronary artery perfusion Increased
pulse wave velocity Increased pulse pressure
Contributory Factors: Deranged bone and mineral metabolism
Decreased levels of inhibitors of calcification such as fetuin-A
Stimulation of osteogenic pathways in endothelial cells by uremic
toxins Impaired endothelial repair mechanismsAdapted from Lederer E
and Ouseph R. Am J Kidney Dis. 2007;49:162-171.Block GA, et al.
Kidney Int. 2007;71(5):438-441.39Vascular Calcification,
Cardiovascular Complications, and CKDEnd-stage renal disease (ESRD)
is associated with a greatly increased risk of cardiovascular
mortality.1 Although patients develop cardiovascular abnormalities
early in the disease process and have substantial traditional risk
factors (diabetes, hypertension, dyslipidemia), a feature of many
patients in the years preceding a cardiovascular event is the
presence of extensive vascular calcification. This calcification
manifests as increased intimal calcification of atherosclerotic
plaques and extensive medial calcification of large elastic
arteries and small arterioles throughout the vascular tree.
Calcification at either site is associated with an increased risk
of myocardial infarction. Intimal calcification may increase the
risk of plaque erosion and rupture while medial calcification
increases arterial stiffness leading to high systolic and pulse
pressures.
Some risk factors for vascular calcification have been
identified in human, animal, or in vitro studies:2Clinical: age,
duration of dialysis, kidney function/uremia, diabetes, known
coronary artery disease, abnormal boneBiochemical:
hyperphosphatemia, hypercalcemia, abnormal parathyroid hormone, low
fetuin-A, elevated cytokines, oxidative stress, low pyrophosphate,
decreased matrix Gla protein (MGP), decreased bone morphogenetic
protein (BMP)-7Medications: calcium-containing phosphate binders,
high-dose vitamin D, Coumadin (decreases active
MGP)References:Shanahan CM. Vascular calcification. Curr Opin
Nephrol Hypertens. 2005;14:361-367. Moe SM. Vascular calcification:
hardening of the evidence. Kidney Int. 2006;70:1535-1537.Lederer E,
Ouseph R. Chronic kidney disease. Am J Kidney Dis.
2007;49:162-171.Block GA, Raggi P, Bellasi A, Kooienga L, Spiegel
DM. Mortality effect of coronary calcification and phosphate binder
choice in incident hemodialysis patients. Kidney Int.
2007;71:438-441.11.520.9All-Cause Death Hazard RatioSerum iPTH
(pg/mL)KDOQI recommended range: 150-300 pg/mLRisk of Death by
Quarterly Varying iPTH<
100100-200200-300300-400400-500500-600600-700 700Time-dependent
Case-Mix and MICS model Kalantar-Zadeh K, et al. Kidney Int.
2006;70:771-780.40Risk of Death by Quarterly Varying iPTHA 2-year
historical cohort study of prospectively collected data from
maintenance hemodialysis patients was performed to examine
associations between baseline values and survival.
Three types of models were examined based on the level of
multivariate adjustment: (1) unadjusted models included indicators
of osteodystrophy (Ca, P, Ca x P, iPTH, or alkaline phosphatase) as
the predicting variable, entry quarter as the covariate, and
mortality as the outcome variable; (2) case-mix adjusted models
included additional covariates: age, gender, race and ethnicity,
diabetes mellitus, vintage, primary insurance, marriage status, the
dialysis clinic mortality ratio, continuous values of Kt/V,
dialysate calcium, and vitamin D doses; and (3) case-mix and MICS
adjusted models also included 11 indicators of nutritional status
and inflammation, including the time-varying BMI, rHuEPO dose, and
the time-varying laboratory values.
This graph shows the association between the time-varying serum
intact PTH values and the relative risk of death in 58,058 MHD
patients as derived in the case-mix and MICS adjusted model. This
analysis includes time-dependent Cox models with time-varying
repeated measures. PTH values outside the KDOQI-recommended range
are associated with increased hazard ratios of 1.31.4.
Reference:Kalantar-Zadeh K, Kuwae N, Regidor DL, et al. Survival
predictability of time-varying indicators of bone disease in
maintenance hemodialysis patients. Kidney Int.
2006;70:771-780.Corrected Serum Calcium (mg/dL)< 8.08.0 to8.58.5
to9.09.0 to9.59.5 to10.010.0 to10.510.5 to11 11.00.7231All-Cause
Death Hazard Ratio8.0 to0.72310.72310.71.5231Risk of Death by
Quarterly Varying Albumin-Adjusted CalciumKDOQI recommended range
8.4-9.5 mg/dLTime-dependent Case-Mix and MICS model Kalantar-Zadeh
K, et al. Kidney Int. 2006;70:771-780.41Death Risk by Quarterly
Varying Albumin-Adjusted CalciumA 2-year historical cohort study of
prospectively collected data from maintenance hemodialysis patients
was performed to examine associations between baseline values and
survival.
Three types of models were examined based on the level of
multivariate adjustment: (1) unadjusted models included indicators
of osteodystrophy (Ca, P, Ca x P, iPTH, or alkaline phosphatase) as
the predicting variable, entry quarter as the covariate, and
mortality as the outcome variable; (2) case-mix adjusted models
included additional covariates: age, gender, race and ethnicity,
diabetes mellitus, vintage, primary insurance, marriage status, the
dialysis clinic mortality ratio, continuous values of Kt/V,
dialysate calcium, and vitamin D doses; and (3) case-mix and MICS
adjusted models also included 11 indicators of nutritional status
and inflammation, including the time-varying BMI, rHuEPO dose, and
the time-varying laboratory values.
This graph shows the association between the time-varying
adjusted serum Ca2+ values and the relative risk of death in 58,058
MHD patients as derived in the case-mix and MICS adjusted model.
This analysis includes time-dependent Cox models with time-varying
repeated measures. Calcium values above 10.5 mg/dL are associated
with increased hazard ratios 1.4, while within and near the
KDOQI-recommended range the hazard ratio is less. When considered
with the relative stability of serum Ca2+ during the course of
chronic kidney disease, these data suggest that fluctuation of
serum ionized calcium is not a major determinant of mortality in
ESRD.Reference:Kalantar-Zadeh K, Kuwae N, Regidor DL, et al.
Survival predictability of time-varying indicators of bone disease
in maintenance hemodialysis patients. Kidney Int.
2006;70:771-780.
Risk of Death by Quarterly Varying Phosphorus0.72341Serum
Phosphorus (mg/dL)234123412341< 3.03.0 to3.994.0 to4.995.0
to5.996.0 to6.997.0 to7.998.0 to8.99 9.0KDOQI recommended range:
3.5-5.5 mg/dLAll-Cause Death Hazard RatioKalantar-Zadeh K, et al.
Kidney Int. 2006;70:771-780.Time-dependent Case-Mix and MICS model
42Reference:Kalantar-Zadeh K, Kuwae N, Regidor DL, et al. Survival
predictability of time-varying indicators of bone disease in
maintenance hemodialysis patients. Kidney Int. 2006;70:771-780.
Risk of Death by Quarterly Varying PhosphorusA 2-year historical
cohort study of prospectively collected data from maintenance
hemodialysis patients was performed to examine associations between
baseline values and survival.
Three types of models were examined based on the level of
multivariate adjustment: (1) unadjusted models included indicators
of osteodystrophy (Ca, P, Ca x P, iPTH, or alkaline phosphatase) as
the predicting variable, entry quarter as the covariate, and
mortality as the outcome variable; (2) case-mix adjusted models
included additional covariates: age, gender, race and ethnicity,
diabetes mellitus, vintage, primary insurance, marriage status, the
dialysis clinic mortality ratio, continuous values of Kt/V,
dialysate calcium, and vitamin D doses; and (3) case-mix and MICS
adjusted models also included 11 indicators of nutritional status
and inflammation, including the time-varying BMI, rHuEPO dose, and
the time-varying laboratory values.
This graph shows the association between the time-varying serum
phosphorus values and the relative risk of death in 58,058 MHD
patients as derived in the case-mix and MICS adjusted model. This
analysis includes time-dependent Cox models with time-varying
repeated measures. Phosphorus values above and below the
KDOQI-recommended range are associated with increased hazard
ratios.Nutrition GuidelinesLimit dietary phosphorus to 800-1000
mg/d with consideration for protein needs, ie, as low as possible
while allowing for a recommended level of protein intakeLimit
elemental calcium from calcium-based binders to 1500 mg/dLimit
total (dietary and medication) elemental calcium to 2000 mg/d Avoid
calcium fortified foods as directedModerate application of
cardiovascular dietary recommendations, not to the detriment of
nutrition statusNational Kidney Foundation. Am J Kidney Dis.
2002;39(Suppl 1):S1-S266.43Nutrition GuidelinesAccording to KDOQI
guidelines1, dietary phosphorus should be restricted to 800 to 1000
mg/day (adjusted for dietary protein needs) when the serum
phosphorus levels are elevated (> 4.6 mg/dL) at Stages 3 and 4
of CKD, and > 5.5 mg/dL in those with kidney failure (Stage 5).
This same restriction should be observed when the plasma levels of
intact PTH are elevated above target range of the CKD stage. The
serum phosphorus levels should be monitored every month following
the initiation of dietary phosphorus restriction.
The average daily dietary intake of phosphorus is about 1550 mg
for males and 1000 mg for females.2 In general, foods high in
protein are also high in phosphorus. Phosphates are added to many
processed foods including meats, cheeses, dressings, beverages, and
bakery products. Such additives may increase the phosphorus intake
by as a much as 1 g/day.
Dietary calcium intake is low in patients with CKD. Intake of
calcium in adults with advanced CKD ranged between 300 and 700
mg/day; in those treated with hemodialysis, calcium intake averaged
549 mg/day. When dietary calcium intake was less than 20 mg/kg/day,
patients with CKD had negative net intestinal calcium balance, but
neutral calcium balance was achievable with calcium intake around
30 mg/kg/day.
References:National Kidney Foundation. K/DOQI clinical practice
guidelines for chronic kidney disease: evaluation, classification,
and stratification. Am J Kidney Dis. 2002;39(2 suppl
1):S1-S266.Uribarri J, Calvo MS. Hidden sources of phosphorus in
the typical American diet: does it matter in nephrology? Semin
Dial. 2003;16:186-188. InterventionResultCaPO4PTHPhosphate
Binders(Ca-based)Therapeutic Interventions forManaging CKDAdapted
from Goodman WG. Nephrol Dial Transplant. 2003;18(suppl
3):iii2-iii8.
44Therapeutic Interventions for Managing Secondary HPTPhosphate
binders are useful for control of serum phosphorus, but
calcium-based binders can also increase serum calcium
concentration.Reference:Slide: Adapted from Goodman WG. Medical
management of secondary hyperparathyroidism in chronic renal
failure. Nephrol Dial Transplant. 2003;18(suppl 3):iii2-iii8.
Nefropati DiabetikPenderita diabetes melitus sangat cenderung
untuk mengalami gangguan ginjal.Dibagi menjadi 5 stadium:Stadium
hipertropi-hiperfungsi; dimana GFR meningkat 3-40% disertai
pembesaran ukuran ginjal, reversibelNefropati diabetikaStadium
sepi; perubahan glomerular telah melanjut, akan tetapi fungsi tidak
memburuk pada pemeriksaan standar. GFR tetap tinggi (20-30% di atas
normal), ekskresi albumin akan meningkat setelah latihan fisis.
Stadium awal nefropati diabetik; meningkatnya ekskresi albumin
di urin (mikroalbuminuria), walaupun secara klinis tetap tanpa
proteinuria dengan pemeriksaan standarNefropati diabetikaStadium
nefropati diabetik nyata; ditandai oleh proteinuria yang menetap,
peningkatan tekanan darah dan penurunan GFR
Stadium gagal ginjal terminalPemeriksaan laboratoriumPemeriksaan
yang penting:urinalisis (mikroalbuminuria,albuminuria,
glukosuria)pemeriksaan fungsi ginjalelektrolit serumHemoglobin dan
hematokrit
Pemeriksaan LaboratoriumPemeriksaan fungsi ginjalKadar Ureum
serum Ureum adalah hasil akhir dari metabolisme proteinHanya ginjal
yang mensekresi ureumSehingga kadar ureum dapat menggambarkan
fungsi ekskresi ginjal
Pemeriksaan LaboratoriumPemeriksaan fungsi ginjalKreatinin
serumKadar kreatinin dalam darahKreatinin adalah hasil terakhir
metabolisme kreatin ( zat yang sangat diperlukan untuk kontraksi
otot rangka)Hanya ginjal yang mengekskresi kreatinin, sehingga
dapat menggambarkan fungsi ekskresi ginjal.Dapat dijadikan nilai
pemantau perburukan fungsi ginjal.
Pemeriksaan laboratoriumPemeriksaan fungsi ginjalBersihan
kreatinin (Creatinine clearance)Jumlah kreatinin yang dalam urin
selama 24 jam.Rumus : Cockcroft-Gault (140 - umur) x Berat Badan
(Kg)Creatinine clearance =(pria)72 x Kreatinin serum
(wanita) = 0,85 x Bersihan kreatinin priaRumus :
MDRDPenatalaksanaanPemantauan status cairan melalui:Penghitungan
pemasukan dan pembuangan cairan.Pengukuran berat badanPengukuran
tekanan darahPengaturan diet:Pembatasan pemasukan protein, natrium,
kaliumPemberian suplementasi besi, folat, vit B12Pengobatan:
pemberian Epo, antihipertensi, obat lain sesuai gejalaPada PGT
dibutuhkan dialisis atau transplantasi
Pilihan Terapi PenggantiDIALISISDefinisiMetode yang dilakukan
untuk mengeluarkan senyawa toksik dan sampah metabolisme yang
normal dieksresi oleh ginjal yang sehatPeritoneal
DialisisHemodialisisDialisis dilakukan bila pasien tidak respon
terhadap terapi konservatif
Ruang HD RS. RK Charitas PalembangHEMODIALISISMenggantikan
fungsi ginjal dengan alat dialiser (ginjal buatan).Menggunakan
mesin dialiser, darah dikeluarkan dari tubuh, masuk mesin dialiser;
dibersihkan, kemudian setelah bersih masuk kembali ke dalam
tubuh.
CARA KERJA
BERAPA SERING ?Sebaiknya 2-3 kali seminggu, selama 3-5
jam.Seumur hidup, kecuali bila dilakukan transplantasi ginjal.
PERITONEAL DIALISISProses dialisis dengan memakai selaput rongga
perut sebagai alat pembersihnya (saringannya).Cara kerja :
memasukkan cairan pembersih ke dalam rongga perut melalui suatu
kateter atau selang khusus yang ditanam ke dalam rongga
perut.Karena tidak mencuci darah secara langsung, hemodinamik tidak
terganggu.Dilakukan setiap hari 3-4 kali, di rumah, sehingga
sosialisasi tidak terganggu.Penyakit Ginjal KronikPeritoneal
dialisis
Penyakit Ginjal KronikPeritoneal dialisis
Penyakit Ginjal KronikTransplantasiTerapi terbaik dibanding
dialisisMemindahkan ginjal dari seorang donor yang sehat atau dari
kadaver pada seorang dengan PGT yang membutuhkan dialisis.Angka
keberhasilannya bervariasi, faktor yang sering mempengaruhi
kesuksesan adalah respon imun (penolakan). Donor dari famili lebih
besar angka keberhasilannya dibandingkan donor kadaver
Dialisis vs Transplantasi
Complications of CKDAnemiaBone
diseaseHTNCVDChart10.150.230.010.310.010.010.110.080.060.02
Column1
Sheet1Column1E1 (Glumerulopati Primer) (GNC)15%E2 (Nefropati
Diabetika)23%E3 (Nefropati Lupus) (SLE)1%E4 (Penyakit ginjal
Hipertensi)31%E5 (Ginjal Polikistik)1%E6 (Nefropati Asam Urat)1%E7
(Nefropati Obstruksi)11%E8 (Pielonefritis Chronic0 (PNC)8%E9
(Lain-Lain)6%E10 (Tidak Diketahui)2%
Transplantasi ginjalDialisis
Prosedur
Kualitas hidup
Biaya
Bila gagalSatu kali
Baik sekali
Sekali saja, lebih kecil
Dapat dialisis kembali atau transplantasiSeumur hidup
Cukup baik
Cukup besar
Meninggal
