| Objective: In the current world, along with the rapid economicdevelopment, the continuous growth of people’s living standard, theacceleration of industrialization, modernization of lifestyle and the greying ofsociety, the prevalence of diabetes is increasing rapidly. The following chroniccomplications has been posing a great threat to patients’ length and quality oflife, and bring huge economic pressure and burden to medical and health care.Diabetic nephropathy is the most diabetic specific chronic complication indiabetic kidney disease (DKD), and is one of the major causes of death inpatients with Diabetes Mellitus. Early discovery and therapy is very importantin delaying the progression of diabetic nephropathy. Persistentmicroalbuminuria has been shown to be a well-established marker forsystemic endothelial dysfunction and macroangiopathy, and a sensitive markerfor early stage of diabetic nephropathy. Screening for increased urinaryalbumin excretion can be performed by measurement of thealbumin-to-creatinine ratio in a random spot collection (uACR). Markedhyperglycemia, marked hypertension, exercise within24h, infection, fever,CHF may elevate uACR over baseline values. While the visiting patients withdiabetes, especially hospitalized patients, usually show a higher blood glucoselevel, and as a result, the influence of high glucose on uACR detection isparticularly significant. The purpose of this study was to clarify the decreaseof uACR levels after short-term glycaemic control, and to explore itsmechanism: whether the remission of glomerular hyperfiltration state or theimprovement of renal structure damage, and to explore for correctionparameters that can eliminate the influence of hyperglycemia on uACR.Podocalyxin(PCX) is one of the markers of podocytes, and urinary PCX content can reflect the damage state of podocyte. Hepatic fatty acid bindingprotein (L-FABP) is secreted by renal proximal tubule epithelial cells, and itscontent in urine can reflect the damage state of renal tubular. These twosubstances were used in this study to reflect the damage state of kidneystructure. Glomerular filtration rate (eGFR) was estimated using theModification of Diet in Renal Disease (MDRD) study equation.Methods: This study recruited60patients with type2Diabetes Mellitus(29male,31female) with mean age56.95±11.50years old, poor glycaemiccontrol (FBG>7.0mmol/L,2h-postprandial blood glucose>10.0mmol/L) and auACR level30-299ug/mg (uACR was evaluated in a morning first clean catchmidstream urine without glycaemic therapy on the first day after admission) inthe First Hospital of Qin Huangdao from January,2013to January,2014,excluding those with acute complications of diabetes, infections, dysfunctionof heart, liver and renal, as well as other kidney disease except diabeticnephropathy. Patients with history of hypertension were required for a bloodpressure control under130/80mmHg and no change of antihypertensivetherapy during the study. All patients’ gender, age, family history of diabetes,duration of diabetes, history of hypertension, history of smoking and drinkingwere collected, and height, weight, HbA1c,25-(OH)VitD, LDL-C weremeasured on the second morning after admission, while diabetic neuropathywas evaluated by clinical symptoms, signs and electromyogram, diabeticretinopathy was evaluated by fundus examination. Blood pressure, serumcreatinine, uACR, urinary PCX and L-FABP were measured both on the firstmorning after admission and the second morning after glycaemic control, andestimated glomerular filtration rate (eGFR) was calculated by MDRD formula,and separately recorded as uACR1, uACR2, eGFR1, eGFR2. OneTouch UltraVue was used to detect capillary blood glucose (CBD). Preprandial and2h-postprandial blood glucose of nummet and supper on the admission day andof breakfast on the first day after admission were detected, and the average ofthese six CBD was recorded as average blood glucose1(ABG1). Preprandialand2h-postprandial blood glucose of nummet and supper on the first day after glycaemic control and of breakfast on the second day after glycaemiccontrol were selected, and the average of these six CBD was recorded asaverage blood glucose2(ABG2).Statistical analysis was performed using SPSS13.0software package.P<0.05was considered significant for all statistical analysis. The normaldistribution data was described by Mean±SD. T-test was employed to comparedifference between two groups. Rectilinear correlation and multiple linearregression analysis were employed to analyze those elements.Results：1The average time that patients reached glycemic targets was5.73±2.72days，and the interval time between two uACR detections was8.73±2.72days.The uACR levels were obviously decreased after glycaemic control comparedwith the levels before (133.71±86.29ug/mg vs78.95±64.94ug/mg), with adecreasing amplitude of43.24±22.07%, with statistical significance (P<0.01).2The changes of urinary PCX, L-FABP, eGFR, the average blood glucose(ABG) and fasting blood glucose (FBG) before and after glycaemic control,and the correlated analysis between these changes and the decrease of uACR.2.1The levels of eGFR, ABG and FBG were obviously decreased afterglycaemic control compared with the levels before, with statisticalsignificance (P<0.01). While the urinary PCX and L-FABP concentrationshowed no statistically significant change after glycaemic control (P>0.05).2.2The pearson correlation coefficients between the decreasing amplitude ofuACR, eGFR, ABG and FBG were as follows:0.648(decreasing amplitude ofeGFR and uACR, P＜0.05);0.520(decreasing amplitude of eGFR and FBG, P＜0.05);0.360(decreasing amplitude of eGFR and ABG, P＜0.05);0.648(decreasing amplitude of FBG and uACR, P＜0.05);0.468(decreasingamplitude of ABG and uACR, P＜0.05);0.360(decreasing amplitude of ABGand FBG, P＜0.05).3Analysis of related factors of uACR3.1The influence of history of hypertension, family history of diabetes,diabetic retinopathy, diabetic neuropathy, smoking history, use of RAAS inhibitor and gender on the decreasing amplitude of uACR was notstatistically significant (P>0.05). While the patients with chronic alcoholdrinking showed a more obvious decrease of eGFR and uACR than thosewithout drinking (P＜0.05), but there was no statistically significantdifference of FBG and ABG between drinkers and non-drinkers(P＞0.05).3.2There was no statistically significant linear correlation between age,duration of DM, HbA1c, interval time of uACR detection，25-(OH)VitD,LDL-C, BMI and the decreasing amplitude of uACR (P＞0.05).4In the patients without history of drinking, totally42, a multiple linearregression analysis was made with uACR2(Y) as the dependent variable,FBG1(X1)and uACR1(X2) as the the variables. The regression equation was:Y=69.487-6.787*FBG1(mmol/L)+0.652*uACR1(ug/mg). The multiplecorrelation coefficient (R)=0.925, indicating that the correlativity of actualuACR2value and the regression equation estimated uACR2value was0.925.The determination coefficient (R2)=0.855, indicating that uACR2could beexplained by FBG1and uACR1with a percentage of85.5%. This equationhad similar multiple correlation coefficient and determination coefficient withthe regression equation computed with uACR2as the dependent variable,ABG1and uACR1as the the variables (Y=29.086-2.437*ABG1+0.677*uACR1, R=0.939, R2=0.881).Conclusions:1Type2diabetic patients with poor glycaemic control and microalbunminuriawill show a significantly decrease of uACR after short-term glycaemiccontrol.2The decrease of uACR after short-term glycaemic control may beattributed to the remission of glomerular hyperfiltration state，but not theimprovement of renal structure.3Type2diabetic patients with chronic alcohol drinking will show a moreobvious decrease of eGFR and uACR after short-term glycaemic control,compared with patients without alcohol drinking.4For type2diabetic patients with poor glycaemic control, microalbunminuria and non chronic alcohol drinking, the correction equations for uACR beforeglycaemic control are: Y=69.487-6.787*FBG (mmol/L)+0.652uACR (ug/mg)or Y=29.086-2.437*ABG (mmol/L)+0.677*uACR (ug/mg). These equationsprovide correction parameters for the evaluation of early diabetic nephropathyin type2diabetic patients with poor glycaemic control. Considering theconvenience of clinical applications, I recommend the correction parameterwith FBG and uACR for DN evaluation.5This study suggests that marked hyperglycemia may elevate uACR overbaseline values, as a result, DN should be ebaluated after glycaemic control.While if DN evaluation is needed under high blood glucose, these correctionparameters can be used. But further studies are needed to define whether thesecorrection parameters are suitable for patients with type1diabetes, history ofdrinking or macroalbuminuria. |
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