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  • Chronic Kidney Diseasedr. Tjatur Winarsanto SpPD

  • Chronic Kidney DiseaseDefinitionChronic, irreversible loss of kidney function attributable to loss of functional nephron mass pathophysiologic processes for more than 3 months.

    definisiKronis kerugian, tidak dapat diubah fungsi ginjal disebabkan hilangnya massa nefron fungsional - proses pathophysiologic untuk lebih dari 3 bulan.

  • Pathophysiology of CKDFinal Common Pathway is loss of nephron massMediated by vasoactive molecules, cytokines and growth factors, renin angiotensin axisDiabetes Hypertension Chronic GN Cystic Disease Tubulointerstitial disease

  • Estimation of GFRModification of Diet in Renal Disease (MDRD) FormulaEstimated GFR = 1.86 (Serum Creat) -1.154 X (age) -0.203Multiply by 0.742 for womenMultiply by 1.21 for African AmericansCockroft Gault Formula(140 age) X Body Weight (Kg)72 X Serum Creatinine (mg/dL)Multiply by 0.85 for women Modifikasi Diet di Penyakit Ginjal (MDRD) FormulaPerkiraan GFR = 1,86 (Serum Creat) -1,154 X (umur) -0,203Kalikan dengan 0,742 untuk wanitaKalikan dengan 1,21 untuk Afrika AmerikaCockroft Gault Formula(140 - umur) X Badan Berat (Kg)72 X serum kreatinin (mg / dL)Kalikan dengan 0,85 untuk wanita?

  • Staging of Chronic Kidney Disease

    StageDescriptionGFR (ml/min/1.73 m2)At increased risk90 (with CKD risk factors)1Kidney damage with normal or increased GFR902Mildly decreased GFR60-893Moderately decreased GFR30-594Severely decreased GFR15-295Renal Failure

  • Who is at Risk for CKD?Family history of heritable renal diseaseDiabetesHypertensionAuto-immune diseaseOld agePrior episode of ARFCurrent evidence of renal damage, even with normal or increased GFRRiwayat keluarga dari penyakit ginjal diwariskandiabeteshipertensiAuto-imun penyakittuaSebelum episode GGASekarang bukti kerusakan ginjal, bahkan dengan GFR normal atau meningkat

  • Etiology and Epidemiology6% of the US population has CKD (Stage 1 and 2)Additional 4-5% have Stage 3 and 4 CKDDiabetic nephropathyHypertension chronic ischemic nephropathyVery high CV disease burden6% dari penduduk AS telah CKD (Tahap 1 dan 2)4-5% tambahan memiliki Tahap 3 dan 4 CKDdiabetes nefropatiHipertensi - nefropati iskemik kronisSangat tinggi CV beban penyakit

  • Monitoring of CKDSerial measurements ofCreatinineGFRAlbumin Albumin-creatinine ratio in the 1st morning sampleElectrolytes including HCO3, Ca, Phos; alkaline phosphatase, iron studies, intact PTH Renal sonogramRenal biopsySerial pengukurankreatininGFRalbuminAlbumin-kreatinin rasio dalam sampel pagi 1Elektrolit termasuk HCO3, Ca, phos, fosfatase alkali, studi besi, PTH utuhsonogram ginjalbiopsi ginjal

  • Symptoms of CKDStage 1 and 2Asymptomatic, hypertensionStage 3 and 4Anemia loss of energyDecreasing appetite; poor nutritionAbnormalities in Calcium, Phosphorus metabolismSodium, water, potassium and acid base abnormalitiesStage 5All of the above accentuated; eventually overt uremiaTahap 1 dan 2Tanpa gejala, hipertensiTahap 3 dan 4Anemia - kehilangan energiPenurunan nafsu makan; gizi burukKelainan pada Kalsium, Fosfor metabolismeNatrium, air, kalium dan asam basa kelainantahap 5Semua hal di atas - ditekankan; uremia akhirnya terbuka

  • Common Causes and Presentation

    Cause Clinical PresentationDiabetic kidney diseaseHistory of diabetes, proteinuria and retinopathyHypertensionElevated BP, normal UA, family historyNon diabetic glomerular diseaseNephritic or nephrotic presentationsCystic kidney diseaseUrinary symptoms, abnormal sediment, radiologic findingsTubulointerstitial diseaseUTI, reflux, chronic med use, drugs, imaging abnormalities, urine concentrating defects

  • Clinical Features of Diabetic CKD

  • Clinical Features of Non-Diabetic CKD

  • Pathophysiology of UremiaAzotemia refers to the retention of nitrogenous waste products. Uremia advanced stages of azotemia with end organ dysfunctionAccumulation of products of protein metabolismUrea anorexia, malaise, vomiting and headachesLoss of other renal functionsErythropoietin deficiency anemiaMetabolic bone disease; endocrine abnormalitiesFluid, electrolyte and acid base disordersAzotemia - mengacu pada retensi produk limbah nitrogen. Uremia - stadium lanjut azotemia dengan disfungsi organ akhirAkumulasi produk dari metabolisme proteinUrea - anoreksia, malaise, muntah dan sakit kepalaKehilangan fungsi ginjal lainnyaErythropoietin kekurangan - anemiaTulang metabolik penyakit; kelainan endokrinCairan, elektrolit dan asam basa gangguan

  • Symptoms of Uremia

    Organ SystemSymptomsSignsGeneralFatigue, weaknessSallow-appearing, chronically illSkinPruritus, easy bruisabilityPallor, ecchymoses,excoriations, edema, xerosisENTMetallic taste in mouth, epistaxisUrinous breath / fetor EyePale conjunctivaPulmonaryShortness of breathRales, pleural effusion CardiovascularDyspnea on exertion, retrosternal pain on inspiration (pericarditis)Hypertension, cardiomegaly,friction rubGastrointestinalAnorexia, nausea, vomiting, hiccupsGenitourinaryNocturia, impotenceIsosthenuriaNeuromuscularRestless legs, numbness and cramps in legsNeurologicGeneralized irritability and inability to concentrate, decreased libidoStupor, asterixis, myoclonus, peripheral neuropathy

  • Mineral MetabolismCalciphylaxisCalcemic uremic arteriopathyExtraosseous/metastatic calcification of soft tissues and blood vessels Devastating complicationTreatment: controversialSodium thiosulfateParathyroidectomycalciphylaxisCalcemic uremik arteriopathyExtraosseous / metastatik kalsifikasi jaringan lunak dan pembuluh darahmenghancurkan komplikasiPengobatan: kontroversialnatrium tiosulfatParathyroidectomy

  • Cardiovascular AbnormalitiesLeading cause of morbidity and mortality in patients with CKD at all stagesIschemic CADHypertension and LVHCongestive heart failureUremicPenyebab utama morbiditas dan mortalitas pada pasien dengan CKD pada semua tahapiskemik CADHipertensi dan LVHGagal jantung kongestifuremic perikarditis pericarditis

  • Hematological AbnormalitiesAnemiaChronic blood loss, hemolysis, marrow suppression by uremic factors, and reduced renal production of EPONormocytic, normochromicRx: Iron and Epo as neededCoagulopathyMainly platelet dysfunction decreased activity of platelet factor III, abnormal platelet aggregation and adhesiveness and impaired thrombin consumptionIncreased propensity to bleed post surgical, GI Tract, pericardial sac, intracranialIncreased thrombotic tendency nephrotic syndromeanemiaDarah kronis kerugian, hemolisis, penekanan sumsum oleh faktor uremik, dan produksi ginjal berkurang EPONormositik, normokromikRx: Besi dan Epo sesuai kebutuhankoagulopatiTerutama trombosit disfungsi - aktivitas penurunan III faktor platelet, agregasi platelet abnormal dan kelengketan dan konsumsi trombin gangguanPeningkatan kecenderungan untuk berdarah - posting bedah, GI Tract, pericardial sac, intrakranialPeningkatan trombotik kecenderungan - sindrom nefrotik

  • Other AbnormalitiesNeuromuscularCentral, peripheral and autonomic neuropathyPeripheral Sensory/Motor NeuropathyStage 4 for more than 6 monthsRestless leg syndromeGastrointestinalUremic fetorGastritis, peptic disease, mucosal ulcerations, AVMsEndocrineGlucose metabolismEstrogen levels amenorrhea, frequent abortionsMale: oligospermia, germinal cell dysplasia, delayed sexual maturationDermatologicPallor, ecchymoses, hematomas, calciphylaxis, pruritus, uremic frostneuromuskularTengah neuropati, perifer dan otonomPeripheral Sensory / Motor NeuropatiTahap 4 selama lebih dari 6 bulanRestless leg syndromegastrointestinaluremic bau mulutGastritis, penyakit lambung, ulserasi mukosa, AVMskelenjar endokringlukosa metabolismeTingkat estrogen - amenore, aborsi seringPria: oligospermia, displasia sel germinal, kematangan seksual tertundaDermatologicPucat, ekimosis, hematoma, calciphylaxis, pruritus es, uremik

  • Therapeutics in CKDNon PharmacologicRisk Factor ModificationPharmacologicTreatment of complications

  • Therapeutics in CKDNon PharmacologicRisk Factor ModificationPharmacologicTreatment of complications

  • Therapeutics in CKDNon PharmacologicRisk Factor ModificationPharmacologicTreatment of complications

  • Sodium and water ImbalanceKetidakseimbanganGlomerulotubular feedback is disrupted sodium retention, contributes to hypertension; hyponatremia is unusual. Higher than usual doses for diuretics. In situations with volume depletion can be severe, because of inadequate sodium retention.Treatment: Salt restriction; high doses of diureticsUmpan balik Glomerulotubular terganggu - retensi natrium, memberikan kontribusi untuk hipertensi; hiponatremia tidak biasa.Lebih tinggi dari dosis biasa untuk diuretik. Dalam situasi dengan penurunan volume - mungkin parah, karena retensi natrium memadai.Pengobatan: pembatasan garam; dosis tinggi diuretik

  • Potassium ImbalancePotassiumGI excretion is augmentedConstipation, dietary intake, protein catabolism, hemolysis, hemorrhage, transfusion of stored blood, metabolic acidosis, Drugs: ACE inhibitors, ARBs, B blockers, K sparing diuretics and NSAIDsHyporeninemic hypoaldosteronism: Diabetes, sickle cell disease

  • Acid Base ImbalanceDamaged kidneys are unable to excrete the 1 mEq/kg/d of acid generated by metabolism of dietary proteins. NH3 production is limited because of loss of nephron massDecreased filtration of titrable acids sulfates, phosphatesDecreased proximal tubular bicarb reabsorption, decreased positive H ion secretionArterial pH: 7.33 - 7.37; serum HCO3 rarely below 15 buffering offered by bone calcium carbonate and phosphateShould be maintained over 21Treatment: Sodium bicarbonate, calcium carbonate, sodium citrate

  • Bone Disease

  • Treatment of Secondary HyperparathyroidismPhosphorus control in dietPhosphate bindersCalcium acetate (Phoslo), calcium carbonate (TUMS), sevelamer (Renagel) , lanthanum (Fosrenol)Oral Vitamin D Calcimemetic agent: Cinacalcet (Sensipar)Fosfor kontrol dalam dietfosfat binderKalsium asetat (Phoslo), kalsium karbonat (Tums), sevelamer (Renagel), lantanum (FOSRENOL)Oral Vitamin DCalcimemetic agent: cinacalcet (Sensipar)

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