1 تفسیر میکروآلبومین / کراتینین در بیماران دیابتی ( معرفی )CASE کنگره غدد و متابولیسم دانشگاه علوم پزشکی اصفهان یکم اردیبهشت 1396 سخنران: دکتر مژگان کریمی فر فوق تخصص غدد و متابولیسم استادیار دانشگاه علوم پزشکی اصفهان INTRODUCTION • Diabetic nephropathy occurs in: • type 1 • type 2 diabetes mellitus, and • in other secondary forms of diabetes mellitus, in which duration of diabetes is long-enough and level of glycemia high enough to result in complications. Diabetic nephropathy • is a common problem that is most likely to occur in patients • • • • • who have: Worse glycemic control Hypertension Glomerular hyperfiltration or A genetic predisposition The lifetime risk of nephropathy is roughly equivalent in type 1 and type 2 diabetes CLINICAL FEATURES • Diabetic kidney disease is defined by characteristic • • • • structural and functional changes. The predominant structural changes include: Mesangial expansion Glomerular basement membrane thickening Podocyte injury Glomerular sclerosis Clinical Features of Diabetic kidney disease Mesangial expansion Glomerular basement membrane thickening Podocyte injury Glomerular sclerosis The major clinical manifestations of diabetic nephropathy are • Albuminuria • Hematuria (less often), • progressive chronic kidney disease, which can be slowed with optimal therapy. Measurement of albumin alone • Measurement of a spot urine sample for albumin alone (whether by immunoassay or by using a sensitive dipstick test specific for albuminuria) without simultaneously measuring urine creatinine (Cr) is less expensive but susceptible to falsenegative and false positive determinations as a result of variation in urine concentration due to hydration. Persistent Albuminuria • because of biological variability in urinary albumin excretion, two of three specimens of UACR collected within a 3- to 6month period should be abnormal before considering a patient to have albuminuria Additional causes of kidney disease • An active urinary sediment (containing red or white blood • • • • cells or cellular casts) Rapidly increasing albuminuria or Nephrotic syndrome Rapidly decreasing eGFR, or The absence of retinopathy (in type 1 diabetes) may suggest alternative or additional causes of kidney disease. Albuminuria • moderately increased albuminuria, formerly called "microalbuminuria" (defined as urinary albumin excretion between 30 and 300 mg/day or between 30 and 300 mg/g creatinine on a random urine sample) or albumin excretion rate 20-200 mcg/min • and severely increased albuminuria, formerly called "macroalbuminuria" (defined as urinary albumin excretion above 300 mg/day or above 300 mg/g creatinine on a random urine sample). Degree of albuminuria • For reasons that are not understood, the degree of albuminuria is not necessarily linked to disease progression in patients with diabetic nephropathy associated with either type 1 or type 2 diabetes Hematuria • — The urine sediment in diabetic nephropathy is usually bland • but microscopic hematuria can occur • as it can in any form of glomerular disease, including disorders such as membranous nephropathy that are not associated with glomerulonephritis. This is an important issue in diabetic nephropathy since nondiabetic renal disease, either alone or with diabetic nephropathy, is occasionally seen in patients with diabetes. Red blood cell casts have also been described in patients with diabetic nephropathy The urine dipstick is a relatively insensitive marker for albuminuria, not becoming positive until albumin excretion exceeds 300 to 500 mg/da DETECTION OF ALBUMINURIA • Establishing the diagnosis of moderately increased albuminuria (formerly called "microalbuminuria") requires the demonstration of: • an elevation in albumin excretion (30 to 300 mg/day) that persists over a three- to six-month period. Approach to detection of the urine albumin-to-creatinine ratio • Measurement of the urine alb/cr ratio in an untimed urinary sample is the preferred screening strategy for moderately increased albuminuria in all diabetic patients Transient elevations in the excretion of albumin • Fever • Infection • Exercise • Heart failure • Nonspecific joint inflammation • Poor glycemic control (hemoglobin A1c greater than 8 percent) • Elevation in blood pressure (greater than 160/100 mmHg) • Hyperlipidemia (LDL cholesterol greater than 120 mg/dL) Recommendations Measurement of the urine albumin-tocreatinine ratio • in an untimed urinary sample is the preferred screening strategy for moderately increased albuminuria . • خانم 60ساله ای با دیابت تیپ ( 2از 7سال پیش) و هیپرکلسترولمیا جهت پیگیری و معاینات دوره ای مراجعه نموده است.داروهای مصرفی وی شامل متفورمین 500میلیگرم و گلیکالزید 80میلیگرم دو بار در روز میباشد .در معاینه اگاه به زمان و مکان واشخاص میباشد .قد 165 سانتی متر ،وزن 82/6کیلوگرم ،فشار خون mmhg 130/80و ضربان 76ضربه در دقیقه دارد .روی شکم استریا ندارد و تیروئید نرمال است بدون ندوالریتی و زخم پا ندارد و نبضها به خوبی لمس میشوند .سایر معاینات طبیعی است .نتایج آزمایشات وی به شرح زیر است: FBS = 192 mg/dL Hemoglobin A1C = 9.5 % Sodium = 138 mEq/L Potassium = 4.5 mEq/L Creatinine = 0.8 mg/dL Total Cholesterol = 165 mg/dL Triglyceride = 157 mg/dL HDL Cholesterol = 38 mg/dL LDL = 104 mg/ dL Urine Micro Albumin (Random) = 1.9 mg/dL Urine Creatinine (Random) = 380 mg/L • تفسیر شما از تست آلبومین اوری بیمار فوق چیست؟ • • • • • • • • • • • Urine Micro Albumin (Random) = 1.9 mg/dL Urine Creatinine (Random) = 380 mg/L )• Urine Albumin(mg/L)/ Urine Creatinine(g/L • ابتدا برای بدست اوردن نسبت باید واحد حجم را یکسان کنید .مثال واحد البومین را به لیتر تبدیل کنید ،که میشودmg/L 19 : سپس واحد البومین به میلیگرم و واحد کراتینین را به گرم تبدیل کنید که واحد کراتینین میشودg/L0/38 : اینک نسبت را محاسبه کنید: 19تقسیم بر 0/38برابر mg/g 50میزان میکرو البومین اوری بیمار محاسبه میشود. • ولیکن با توجه به اینکه در حال حاضر قند خون بیمار کنترل نیست و HbA1c باالتر از %8دارد انجام تست مجدد را تا بعد از کنترل مناسب قند خون ،موکول میکنید. • در صورتیکه مجددا باال بود طی 3تا 6ماه بعد مجددا چک شود.
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