Chronic Kidney Disease is defined as the irreversible loss of kidney function over a period of more than 3 months. The document discusses the pathophysiology, staging, risk factors, symptoms, complications, and management of Chronic Kidney Disease. Key points include: loss of nephron mass leads to decreased GFR and kidney function; common causes include diabetes and hypertension; later stages present with anemia, bone disease, and fluid/electrolyte imbalances; treatment focuses on controlling risk factors and addressing complications through medication and dialysis.
Chronic Kidney Disease is defined as the irreversible loss of kidney function over a period of more than 3 months. The document discusses the pathophysiology, staging, risk factors, symptoms, complications, and management of Chronic Kidney Disease. Key points include: loss of nephron mass leads to decreased GFR and kidney function; common causes include diabetes and hypertension; later stages present with anemia, bone disease, and fluid/electrolyte imbalances; treatment focuses on controlling risk factors and addressing complications through medication and dialysis.
Chronic Kidney Disease is defined as the irreversible loss of kidney function over a period of more than 3 months. The document discusses the pathophysiology, staging, risk factors, symptoms, complications, and management of Chronic Kidney Disease. Key points include: loss of nephron mass leads to decreased GFR and kidney function; common causes include diabetes and hypertension; later stages present with anemia, bone disease, and fluid/electrolyte imbalances; treatment focuses on controlling risk factors and addressing complications through medication and dialysis.
Chronic Kidney Disease is defined as the irreversible loss of kidney function over a period of more than 3 months. The document discusses the pathophysiology, staging, risk factors, symptoms, complications, and management of Chronic Kidney Disease. Key points include: loss of nephron mass leads to decreased GFR and kidney function; common causes include diabetes and hypertension; later stages present with anemia, bone disease, and fluid/electrolyte imbalances; treatment focuses on controlling risk factors and addressing complications through medication and dialysis.
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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
Diabetes Hypertension Chronic GN Cystic Disease Tubulointerstitial disease
Structural/ Functional Loss of Nephron Mass Hypertrophy of remnant nephrons
Sclerosis of remnant nephrons
Mediated by vasoactive molecules, cytokines and growth factors, renin angiotensin axis
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 Disease
Stage
Description
GFR (ml/min/1.73 m2)
At increased risk
90 (with CKD risk factors)
Kidney damage with normal or
increased GFR
90
Mildly decreased GFR
60-89
Moderately decreased GFR
30-59
Severely decreased GFR
15-29
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 Presentation
Cause
Clinical Presentation
Diabetic kidney disease
History of diabetes, proteinuria and retinopathy
Hypertension
Elevated BP, normal UA, family history
Non diabetic Nephritic or nephrotic presentations glomerular disease Cystic kidney 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
Symptoms 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 / 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
Neuromuscular
Restless legs, numbness and cramps in legs
Neurologic
Generalized irritability and inability to
concentrate, decreased libido
Isosthenuria
Stupor, asterixis, myoclonus,
peripheral neuropathy
Mineral Metabolism Calciphylaxis Calcemic uremic arteriopathy Extraosseous/metastatic calcification of soft tissues and blood vessels Devastating complication Treatment: controversial Sodium thiosulfate Parathyroidectomy calciphylaxis Calcemic uremik arteriopathy Extraosseous / metastatik kalsifikasi jaringan lunak dan pembuluh darah menghancurkan komplikasi Pengobatan: kontroversial natrium tiosulfat Parathyroidectomy
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
Coagulopathy
Chronic blood loss, hemolysis,
marrow suppression by uremic factors, and reduced renal production of EPO Normocytic, normochromic Rx: Iron and Epo as needed 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
Gastrointestinal
Endocrine
Dermatologic
Central, peripheral and autonomic neuropathy
Peripheral Sensory/Motor Neuropathy Stage 4 for more than 6 months Restless leg syndrome
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
ImbalanceKetidakseimbanga n
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)
