of 34/34
PATOFISIOLOGI GAGAL GINJAL KRONIK Dr. Daru Jaka S, M.Sc., SpPD

Patofisiologi & Penatalaksanaan Gagal Ginjal Kronik

  • View
    100

  • Download
    1

Embed Size (px)

DESCRIPTION

gagal ginjal kronik

Text of Patofisiologi & Penatalaksanaan Gagal Ginjal Kronik

  • PATOFISIOLOGI GAGAL GINJAL KRONIKDr. Daru Jaka S, M.Sc., SpPD

  • DEFINISIKidney damage for 3 months as defined by structural or functional abnormalities of the kidney, with or without decreased GFR, manifest by either: pathological abnormalities; or markers of kidney damage, including abnormalities in the composition of the blood or urine; or abnormalities in imaging tests. GFR < 60 mL/min/1.73m2 for 3 months, with or without kidney damage. (NKF-KDOQI)

  • CHRONIC KIDNEY DISEASE

  • PATOFISIOLOGI CKD

  • CKDManifest as a loss of renal reserveAs CKD progress Pt may remain asymptomaticAs renal function worsen susceptible to infection, poorly controlled hypertension

  • ESRDClinical state irreversible loss of endogenous renal function RRT permanent AzotemiaUremic syndrome: anemia, malnutrition; impaired carbohydrate metabolism,fats,and proteins; defective utilization of energy and metabolic bone disease

  • Symptoms & SignsDevelop slowly and nonspecificCan be asymptomatic until stage 5Manifestation: General: malaise, fatigue, weaknessGI: anorexia, nausea, vomitus, hiccupNeurologic: insomnia, irritable,twitch, paresthesia, restless legLibido , mens irregularityCardiopulmonary: cardiomegaly, oedema, pericarditisUremic encepahlopathy: asterixis, myoclonus, confusion-coma

  • PENYEBAB CKDNon-Diabetes:Hipertensi, Renal Artery StenosisPolicystic kidney diseaseGlomerular diseaseTubulointerstitial diseaseObstructive NephropathiesDiabetes Mellitus

  • DIABETIK NEFROPATIDef: laju ekskresi albumin urin>300mg/24jam pd Pt dg DM tanpa adanya penyakit ginjal lain Terjadi hampir 1/3 DM Tk albuminuria berhubungan dg tk gagal ginjalFaktor resiko perkembangan DN: Kontrol gula yg buruk, HT, intake protein ,smoking, ,cholesterolTreatment: Insulin terapi, ACE inhibitor, restriksi diet protein.Monitor: albuminuria, BP, komplikasi

  • COMPLICATIONSHYPERKALEMIAACID-BASE DISORDERCARDIOVASCULARHEMATOLOGIC NEUROLOGICDISORDERS OF MINERAL/ELECTROLIT METABOLISMENDOCRINE DISORDERSGI DISORDERHYPERURICEMIA

  • HYPERKALEMIAK balance usually remain intact until GFR < 10ml/minEndogenous causes: hemolysis, trauma, acidemic states, hyporeninemic hypoaldosteronismExogenous causes: diet, drugs that K secretion (spironolactone, ACE, NSAID)Hyperkalemia arytmia, ECG change (QRS widen)

  • ACID-BASE DISORDERInability of kidney to excrete acid generated from protein metabolismPrimarily due to loss of renal massAmmonia production & urine buffer production pH is maintained at 7,33-7,37 & bicarb 15meq/LExcess of H+ buffered by CaCO3 & CaPO4 Renal osteodystrophy

  • CARDIOVASCULARHYPERTENSIONPERICARDITIS UREMIACONGESTIVE HEART FAILURE

  • HYPERTENSIONCauses:Salt & water retention due to inability to excrete, adjust to variation in intake water, Na as renal failure worsenHyperreninemic statesExogenous erythropoetinFailure to control HT lead to progression of renal damage

  • PericarditisCause: retention of metabolic toxinsSymptoms & signs: chest pain, fever, pericardial effusionCO poor with distended Jugular Venous

  • Congestive Heart FailureHTMyocardial work O2 demand Atherosclerosis AnemiaCHFNa & water retention

  • HEMATOLOGICANEMIACOAGULOPATHY

  • ANEMIACharacteristic: normochromic, normocyticCause: Erythropoetin production, Fe deficiencyLow grade hemolysisBlood loss from platelet dysfunctionHDGI bleeding

  • CoagulopathyPlatelet dysfunctionBleeding is prolongPlatelet shows abnormal adhessiveness and aggregationSign: petechiae, purpura

  • NEUROLOGICUremic encephalopathyOccur at CKD stage 5 or ESRDCause: hiperPTH; Ca >12-15mg/dLSymptoms: difficulty in concentrating, lethargy,confusion, comaPhysical: nystagmus, weakness, asterixis, hypereflexiaNeuropathy: can be peripherally (restless legs, distal pain, lost of tendon reflexes) and others (impotence, autonomic dysfunction)

  • DISORDERS OF MINERAL METABOLISMRenal Osteodystrophy: disorder of Ca, P and bone. Form: osteomalacia, osteitis fibrosa cysticaGFR falls
  • OTHERSGI DISORDERS include: nasea, vomiting, anoreksia, gastric/duodenal ulcerHYPERURICEMIA; impaired excretion of uric acid as renal function worsen

  • ENDOCRINE DISORDERRenal insulin clearance insulin levelGlucose intolerance can occur when GFR
  • PHARMACOTHERAPYTreating Reversible Causes of Renal DysfunctionSlowing the Progression of Renal DiseaseTreating Complications

  • Treating Reversible CausesFactors responsible for acute decrements in renal function in CKD: volume depletion, CHF, nephrotoxic drugs, radiocontrastHypovolemia treatment: repletion, dose of diuretic, Na intakeCKD + CHF treatment: Loop diuretic (maintaining fluid balance)Use of Nephrotoxic drug: adjust dose, avoidRadiocontrast: use non-ionic contrast,hydration 12 hours before procedure

  • Slowing the Progression of RDSystemic HTGenerates intraglomerular pressures and accelerate glomerular sclerosis and RD Antihypertensive protect both renal & cardiovascularAntihypertensive in non-proteinuric CKD unable to slow the progressionAgents: ACE,ARB, diuretic, Diltiazem, Verapamil, -blockerDietary Protein intakeProtein restriction to 0,6g/kg/day in pt not on dialysisGlycemic controlStrict glycemic control

  • Treating ComplicationHYPERKALEMIATreatment: iv Ca gluconate, insulin + glucose, Nabic, ion exchange resin, dialysisACIDOSISTreatment: Nabic 0,50 mEq/kg/d target Nabic level>22mEq/LHEMATOLOGIC Anemia: erythropoetin started 50U/kg 1-2 x/week s.c.(iron stores must be adequate), iron supplementaion if ferritin < 100g/ml with 1-3 x 325mg FeSO4DISORDER OF MINERAL METABOLISMPTH, Ca Calcitriol, Ca CO3

  • Treating ComplicationHIPERURICEMIAKrn kegagalan ginjal mengekskresi as urat.Terapi: Allopurinol atau dialisis.

    ABNORMALITAS GI Karakterisitik: anoreksia, gastric/duodenal ulcerPenyebab: prod.amonia, siklus internal amonia-ureumTerapi: H2-bloker, sukralfat, PPI

  • PHARMACEUTICAL CARE

  • TREATMENT OUTCOMEPREVENT PROGRESSION OF RENAL DISEASEPREVENT & MANAGE COMPLICATIONS

  • Estimate Renal FunctionModified Diet in Renal Disease (MDRD)GFR (mL/min/1.73 m 2) = 186 x [Cr] 1.154 x (Age) 0.203 x (0.742 if female) x (1.210 if African American) SCr: serum creatinine in mg/dL; age in years

  • Estimate Renal Function

    COCKROFT-GAULTCrCl = (140-umur) x BB 72 x Serum creatinine(mol/L)

    Goal: to assess the need of dossage adjustment

  • MONITORING BIOKIMIA:Cr, BUN, elektrolit (Na, K, Ca, PO4), keseimbangan asam-basa, albumin, asam urat.Hematologi:Hb, platelet, hematokrit, white cell count, profil koagulasiKarakteristik Pasien:BP, BB, temp.,KU, kulit.Terapi Obat: TDM, dosis, efek, adverse drug reaction, nefrotoksisitas