腎臟科病人的抽血檢驗值判讀 醫師彭清秀 CBC-- 紅血球系列 MCV (mean corpuscular volume) 平均血球容積 正常值 :82-100 MCV = HCTX10 RBC (10 12 /L) 依 MCV 值可將貧血分為 Macrocytic ( 大球性 ) anemia : MCV 100-160 Microcytic ( 小球性 ) anemia: MCV 50-82 Normocytic anemia: MCV 82-100
CBC-- 紅血球系列 Macrocytic anemia: Vitamin B 12 deficiency Folic acid deficiency Microctic anemia: Iron deficiency anemia (IDA) Thalassemia ( 地中海型貧血 ) Aluminum intoxication Sideroblastic anemia CBC-- 紅血球系列 Normocytic anemia: Blood loss Hemolytic anemia Anemia of chronic disease TB Rheumatic arthritis Chronic inflammation or infection Aplastic anemia Malnutrition
CBC-- 紅血球系列 RDW (red cell size distribution width) 紅血球大小分佈廣度 正常值 : 11.5-14.5 CV (coefficients of variation) 當紅血球大小較一致時 RDW 小, 大小不均時 RDW 大 可用以分辨 IDA 和 Thalassemia IDA 的病人 RDW 大 Thalassemia 的病人 RDW 正常 對沒有貧血的病人, 此數據無診斷幫助 CBC-- 紅血球系列 Reticulocyte ( 網狀紅血球 ) 血液中未成熟的紅血球, 以佔所有紅血球的百分比表示之 當紅血球破壞增加時, 網狀紅血球數增加 ; 當紅血球製造減少時, 網狀紅血球數降低 輸血後, 則無法如上判讀 正常值 : Reticulocyte Index (RI)=2-3 RI = reticulocyte (%) X patient Hct normal Hct 2
CBC-- 紅血球系列 Erythrocytosis in ESRD Polycystic kidney disease Acquired cystic disease RCC Profound anemia in ESRD Post nephrectomy Interstitial renal disease as cause of ESRD EPO resistance CBC-- 紅血球系列 EPO resistance Iron deficiency Vitamin B12 or Folic acid deficiency Chronic inflammation or infection Severe malnutrition Hemolysis or blood loss Inadequate EPO dosage Aluminum intoxication Hyperparathyroidism
CBC-- 血小板系列 正常值 : 150000-400000 血小板減小 in ESRD Drug side effect ( heparin, ticlopidine. ) SLE flare up Liver cirrhosis with splenomegaly Severe sepsis (DIC) or atypical infection 血小板增加 in ESRD Viral infection Hematological disease: essential thrombocytosis.. CBC 白血球系列 白血球增加 Infection ( PMN or seg 增加或 left shift ) 註 : Left shift: 表不成熟之 neutrophile 變多, 像 band form, blast cell 等 Inflammation 白血球減少 Severe sepsis or viral infection Liver cirrhosis related hypersplenism SLE activity 增加 白血病或其它血液疾病或葯物作用均可造成白血球增加或減少
Biochemistry liver function AST and ALT will decrease in patient with CRF or ESRD Abnormal liver function in ESRD patient Hepatitis B or hepatitis C Alcoholism Frequent transfusion ( due to hemolysis or hemosiderosis ) Drug-related Biochemistry liver function ALP : alkaline phosphatase From liver, biliary tract, bone, placenta, monocyte 高 ALP: Obstructive jaundice, cirrhosis, hepatoma Secondary hyperparathyroidism 低 ALP: Malnutrition Hypophosphatemia Hypothyroidism 小孩子的 ALP 正常值較成人高
Biochemistry albumin, globulin Albumin 是最重要也是目前唯一和洗腎病人的存活時間成正比的實驗數據 低 Albumin Poor nutrition Chronic inflammation or infection Liver cirrhosis A/G reverse: Chronic inflammation or infection ( like TB, shunt infection, hepatitis ) Multiple myeloma Biochemistry uric acid When and how to treat gout and hyperuricemia? When uric acid < 8.0 colchicine + NSAID prn for patient with gout When uric acid = 8.0-10.0 Gout hx(+): allopurinol (from low dose ½# qd) + colchicine + NSAID prn Gout hx (-): no treatment ( 因為 ESRD 造成的尿酸高很少會導致痛風發作 )
Biochemistry uric acid When uric acid > 10.0 Allopurinol from low dose Colchicine + NSAID prn if gout (+) In patient with ESRD or CRF, pseudogout is more seen than gout. Pseudogout: CPP(calcium pyrophosphate dihydrate) deposition in joint. Hydroxyapatite (Ca 10(PO4) 6OH) deposition disease: calcific deposits from X-ray Biochemistry uric acid 除了 allopurinol 以外, 其它可降尿酸的方法 Diet control Avoid alcohol consumption Avoid diuretics and other drugs which can elevate serum uric acid ( like, anti-tb drug ) Maintain adequate plasma volume Treat hypertension adequately Uricosuric agent ( urinorm, 但無尿病人不適用 )
Biochemistry Lipid profile Factor HD PD Total cholesterol Normal LDL cholesterol Normal HDL cholesterol Triglycerides Apo A1 protein Apo B protein Lp(a) LDL oxidation Biochemistry Lipid profile Lipoproteins and cardiovascular risk Atherogenic lipoproteins Chylomicron remnants VLDL remnants IDL LDL Lp (a) Antiatherogenic lipoproteins HDL
Biochemistry Lipid profile Treatment based on LDL-cholesterol With CAD LDL 130 drug therapy LDL 100-130 dietary therapy Without CAD and 2 risk factors LDL 160 drug therapy LDL 130-160 dietary therapy Without CAD and < 2 risk factors LDL 190 drug therapy LDL 160-190 dietary therapy Biochemistry Lipid profile Nonlipid risk factors for CAD Modifiable factors Smoking Hypertension Obesity Decreased physical activity DM Nonmodifiable factors Age Male gender Family history of premature CAD
Biochemistry Lipid profile Treatment of hypertriglyceridemia Borderline-high triglycerides ( 200-400 ) should be treated when Total cholesterol > 240 and HDL-C < 35 Established CAD Family history of premature CAD Genetic forms of hypertg associated with increased CAD risks LDL-C/ HDL-C > 5 Biochemistry Lipid profile Lipid lowering agents Fibric acid derivatives ( Fenofibrate) TG (20-60%), HDL Side effect: myopathy or rhabdomyolysis ( monitoring CK level closely ) HMG-CoA reductase inhibitor ( Lipitor, Zocor ) cholesterol (20-30%), LDL (20-40%), TG (10%), HDL (10%) risk of myopathy if liver disease (+) or combined with fibric acid derivatives.
Biochemistry Lipid profile Other managements of hyperlipidemia in ESRD patients Lifestyle modification ( diet, exercise, reduce alcohol, quit smoking, reduce weight ) Dialysis-related modification ( more biocompatible, high-flux, LMW heparin, reduction in use of hypertonic solution in PD ) Correction of hyperparathyroidism, anemia, homocysteinemia L-carnitine or fish oil (lowering TG), aspirin, antioxidants ( Vit C, Vit E ) Biochemistry potassium Hyperkalemia in HD patients Inappropriate dietary intake Hemolysis or GI bleeding Heparin-related ( 因抑制 aldosterone 活性 ) Hypoaldosteronism Inadequate dialysis High-glucose dialysate ( glucose-free dialysate 可比 glucose 200mg/dL dialysate 多移除 30% 的鉀 )
Biochemistry Sodium Hyponatremia in HD patient Water retension Combined with CHF or liver cirrhosis Diuretics effect ( esp. thiazide ) Poor nutrition SIADH ( rare ) Biochemistry Aluminum HD patient 會造成鋁高的原因 透析液中的鋁含量高 含鋁的制酸劑服用過量 Aluminum intoxication Encephalopathy (rare but may be severe) Early: stuttering, dyspraxia ( 反應遲鈍 ) Late: Speech disturbance, myoclonus, seizures, personality changes, global dementia. Anemia: microcytic Bone disease
Biochemistry Aluminum Aluminum related bone disease Symptoms and signs: bone pain, muscle weakness ( esp. 大腿 ), spontaneous fracture Lab findings: serum aluminum, serum Ca ( 特別是服用 vit D 後, 開完副甲狀腺仍高 ), i- PTH 和 ALP 都正常 Diagnosis: bone biopsy Aluminum intoxication 無明顯治療方法只有靠預防 Biochemistry Ca, P, i-pth 腎衰竭後, 磷排除減少, 加上 vit D 在腎臟製造減少, 故 Ca 低 Ca 低會刺激 i-pth 生成, 久而久之就會造成副甲狀腺功能亢進, 甚至產生 tumor, 此時體內 i-pth 及 Ca 均高, 稱次發性副甲狀腺功能亢進, 可用 vit D 來抑制副甲狀腺活性 食物中均含磷, 故需用磷結合劑來降磷, 必須在飯中嚼碎服用效果最佳, 含鋁之磷結合劑效果佳但不宜長期使用, 含鈣之磷結合劑有時會造成血鈣升高, 但可以將透析液中的鈣離子濃度降低以輔助治療