Chronic Kidney Disease.ppt
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Transcript of Chronic Kidney Disease.ppt
Chronic Kidney Disease
dr. Tjatur Winarsanto SpPD
Chronic Kidney Disease
• Definition– Chronic, irreversible loss of kidney
function attributable to loss of functional nephron mass – pathophysiologic processes for more than 3 months.
• definisi• Kronis kerugian, tidak dapat
diubah fungsi ginjal disebabkan hilangnya massa nefron fungsional - proses pathophysiologic untuk lebih dari 3 bulan.
Pathophysiology of CKD
• Final Common Pathway is loss of nephron mass
Structural/ Functional Hypertrophy of remnant nephrons
Sclerosis of remnant nephrons
Loss of Nephron Mass
Mediated by vasoactive molecules, cytokines
and growth factors, renin angiotensin axis
Diabetes Hypertension
Chronic GN Cystic Disease
Tubulointerstitial disease
Estimation of GFR
• Modification of Diet in Renal Disease (MDRD) Formula– Estimated GFR = 1.86 (Serum
Creat) -1.154 X (age) -0.203
• Multiply by 0.742 for women• Multiply by 1.21 for African
Americans
• Cockroft 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) Formula
• Perkiraan GFR = 1,86 (Serum Creat) -1,154 X (umur) -0,203
• Kalikan dengan 0,742 untuk wanita• Kalikan dengan 1,21 untuk Afrika
Amerika• Cockroft Gault Formula• (140 - umur) X Badan Berat (Kg)• 72 X serum kreatinin (mg / dL)• Kalikan dengan 0,85 untuk wanita?
Staging of Chronic Kidney DiseaseStage Description GFR (ml/min/1.73 m2)
At increased risk 90 (with CKD risk factors)
1 Kidney damage with normal or increased GFR
90
2 Mildly decreased GFR 60-89
3 Moderately decreased GFR 30-59
4 Severely decreased GFR 15-29
5 Renal Failure <15 (or dialysis)
Who is at Risk for CKD?
• Family history of heritable renal disease
• Diabetes• Hypertension• Auto-immune disease• Old age• Prior episode of ARF• Current evidence of renal
damage, even with normal or increased GFR
• Riwayat keluarga dari penyakit ginjal diwariskan
• diabetes• hipertensi• Auto-imun penyakit• tua• Sebelum episode GGA• Sekarang bukti kerusakan
ginjal, bahkan dengan GFR normal atau meningkat
Etiology and Epidemiology
• 6% of the US population has CKD (Stage 1 and 2)
• Additional 4-5% have Stage 3 and 4 CKD
• Diabetic nephropathy• Hypertension – chronic
ischemic nephropathy• Very high CV disease
burden
• 6% dari penduduk AS telah CKD (Tahap 1 dan 2)
• 4-5% tambahan memiliki Tahap 3 dan 4 CKD
• diabetes nefropati• Hipertensi - nefropati
iskemik kronis• Sangat tinggi CV beban
penyakit
Monitoring of CKD• Serial measurements of
– Creatinine– GFR
• Albumin • Albumin-creatinine ratio in
the 1st morning sample• Electrolytes including HCO3,
Ca, Phos; alkaline phosphatase, iron studies, intact PTH
• Renal sonogram• Renal biopsy
• Serial pengukuran• kreatinin• GFR• albumin• Albumin-kreatinin rasio
dalam sampel pagi 1• Elektrolit termasuk HCO3, Ca,
phos, fosfatase alkali, studi besi, PTH utuh
• sonogram ginjal• biopsi ginjal
Symptoms of CKD• Stage 1 and 2
– Asymptomatic, hypertension• Stage 3 and 4
– Anemia – loss of energy– Decreasing appetite; poor
nutrition– Abnormalities in Calcium,
Phosphorus metabolism– Sodium, water, potassium and
acid base abnormalities• Stage 5
– All of the above – accentuated; eventually overt uremia
• Tahap 1 dan 2• Tanpa gejala, hipertensi• Tahap 3 dan 4• Anemia - kehilangan energi• Penurunan nafsu makan; gizi
buruk• Kelainan pada Kalsium, Fosfor
metabolisme• Natrium, air, kalium dan asam
basa kelainan• tahap 5• Semua hal di atas - ditekankan;
uremia akhirnya terbuka
Common Causes and PresentationCause Clinical Presentation
Diabetic kidney disease
History of diabetes, proteinuria and retinopathy
Hypertension Elevated BP, normal UA, family history
Non diabetic glomerular disease
Nephritic or nephrotic presentations
Cystic kidney disease
Urinary symptoms, abnormal sediment, radiologic findings
Tubulointerstitial disease
UTI, reflux, chronic med use, drugs, imaging abnormalities, urine concentrating defects
Clinical Features of Diabetic CKD
Clinical Features of Non-Diabetic CKD
Pathophysiology of Uremia• Azotemia – refers to the retention
of nitrogenous waste products. Uremia – advanced stages of azotemia with end organ dysfunction
• Accumulation of products of protein metabolism– Urea – anorexia, malaise, vomiting
and headaches• Loss of other renal functions
– Erythropoietin deficiency – anemia– Metabolic bone disease; endocrine
abnormalities– Fluid, electrolyte and acid base
disorders
• Azotemia - mengacu pada retensi produk limbah nitrogen. Uremia - stadium lanjut azotemia dengan disfungsi organ akhir
• Akumulasi produk dari metabolisme protein
• Urea - anoreksia, malaise, muntah dan sakit kepala
• Kehilangan fungsi ginjal lainnya• Erythropoietin kekurangan - anemia• Tulang metabolik penyakit; kelainan
endokrin• Cairan, elektrolit dan asam basa
gangguan
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 / fetor
Eye Pale conjunctiva
Pulmonary Shortness of breath Rales, pleural effusion
Cardiovascular Dyspnea on exertion, retrosternal pain on inspiration (pericarditis)
Hypertension, cardiomegaly,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 concentrate, decreased libido
Stupor, asterixis, myoclonus, peripheral neuropathy
Symptoms of Uremia
Mineral Metabolism• Calciphylaxis
– Calcemic uremic arteriopathy– Extraosseous/metastatic calcification of soft tissues
and blood vessels – Devastating complication– Treatment: controversial
• Sodium thiosulfate• ParathyroidectomycalciphylaxisCalcemic uremik arteriopathyExtraosseous / metastatik kalsifikasi jaringan lunak dan
pembuluh darahmenghancurkan komplikasiPengobatan: kontroversialnatrium tiosulfatParathyroidectomy
Cardiovascular Abnormalities
• Leading cause of morbidity and mortality in patients with CKD at all stages
• Ischemic CAD• Hypertension and LVH• Congestive heart failure• Uremic• Penyebab utama morbiditas dan
mortalitas pada pasien dengan CKD pada semua tahap
• iskemik CAD• Hipertensi dan LVH• Gagal jantung kongestif• uremic perikarditis pericarditis
Hematological Abnormalities• Anemia
– Chronic blood loss, hemolysis, marrow suppression by uremic factors, and reduced renal production of EPO
– Normocytic, normochromic– Rx: Iron and Epo as needed
• Coagulopathy– Mainly platelet dysfunction – decreased
activity of platelet factor III, abnormal platelet aggregation and adhesiveness and impaired thrombin consumption
– Increased propensity to bleed – post surgical, GI Tract, pericardial sac, intracranial
– Increased thrombotic tendency – nephrotic syndrome
• anemia• Darah kronis kerugian, hemolisis,
penekanan sumsum oleh faktor uremik, dan produksi ginjal berkurang EPO
• Normositik, normokromik• Rx: Besi dan Epo sesuai kebutuhan• koagulopati• Terutama trombosit disfungsi - aktivitas
penurunan III faktor platelet, agregasi platelet abnormal dan kelengketan dan konsumsi trombin gangguan
• Peningkatan kecenderungan untuk berdarah - posting bedah, GI Tract, pericardial sac, intrakranial
• Peningkatan trombotik kecenderungan - sindrom nefrotik
Other Abnormalities• Neuromuscular
– Central, peripheral and autonomic neuropathy– Peripheral Sensory/Motor Neuropathy– Stage 4 for more than 6 months– Restless leg syndrome
• Gastrointestinal– Uremic fetor– Gastritis, peptic disease, mucosal ulcerations, AVMs
• Endocrine– Glucose metabolism– Estrogen levels – amenorrhea, frequent abortions– Male: oligospermia, germinal cell dysplasia, delayed sexual
maturation• Dermatologic
– Pallor, ecchymoses, hematomas, calciphylaxis, pruritus, uremic frost
• neuromuskular• Tengah neuropati, perifer dan otonom• Peripheral Sensory / Motor Neuropati• Tahap 4 selama lebih dari 6 bulan• Restless leg syndrome• gastrointestinal• uremic bau mulut• Gastritis, penyakit lambung, ulserasi mukosa, AVMs• kelenjar endokrin• glukosa metabolisme• Tingkat estrogen - amenore, aborsi sering• Pria: oligospermia, displasia sel germinal,
kematangan seksual tertunda• Dermatologic• Pucat, ekimosis, hematoma, calciphylaxis, pruritus
es, uremik
Therapeutics in CKD
• Non Pharmacologic– Risk Factor Modification
• Pharmacologic• Treatment of complications
Therapeutics in CKD
• Non Pharmacologic– Risk Factor Modification
• Pharmacologic• Treatment of complications
Therapeutics in CKD
• Non Pharmacologic– Risk Factor Modification
• Pharmacologic• Treatment of complications
Sodium and water ImbalanceKetidakseimbangan
• Glomerulotubular 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 diuretics
Umpan 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 Imbalance• Potassium
– GI excretion is augmented– Constipation, dietary intake,
protein catabolism, hemolysis, hemorrhage, transfusion of stored blood, metabolic acidosis,
– Drugs: ACE inhibitors, ARBs, B blockers, K sparing diuretics and NSAIDs
– Hyporeninemic hypoaldosteronism: Diabetes, sickle cell disease
Acid Base Imbalance• Damaged 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 mass– Decreased filtration of titrable acids
– sulfates, phosphates– Decreased proximal tubular bicarb
reabsorption, decreased positive H ion secretion
• Arterial pH: 7.33 - 7.37; serum HCO3 rarely below 15 – buffering offered by bone calcium carbonate and phosphate
• Should be maintained over 21• Treatment: Sodium bicarbonate,
calcium carbonate, sodium citrate
Bone Disease
Treatment of Secondary Hyperparathyroidism
• Phosphorus control in diet• Phosphate binders
– Calcium acetate (Phoslo), calcium carbonate (TUMS), sevelamer (Renagel) , lanthanum (Fosrenol)
• Oral Vitamin D • Calcimemetic agent:
Cinacalcet (Sensipar)
• Fosfor kontrol dalam diet• fosfat binder• Kalsium asetat (Phoslo),
kalsium karbonat (Tums), sevelamer (Renagel), lantanum (FOSRENOL)
• Oral Vitamin D• Calcimemetic agent:
cinacalcet (Sensipar)