Diabetic Nephropathy and Management

Chronic kidney disease affects people worldwide. Approximately 1 out of 3 adults with diabetes have kidney disease. Among several etiological factors for CKD, diabetes mellitus (DM) and hypertension are the main factors. These factors not only cause CKD but are also responsible for several complications related to CKD. In this article, we have reviewed Diabetic Nephropathy (DN) in terms of etiology, pathophysiology, diagnosis, management, current guidelines for diabetic nephropathy management, and some of the research study findings. Diabetic nephropathy (DN) is the chief factor for end-stage renal disease (ESRD) development across the globe. The primary cause of DN is Diabetes Mellitus, which is an autoimmune lifestyle disorder having several etiological factors. Checking for urine albuminuria, estimated GFR (eGFR), and blood glucose are unswerving tests for DN diagnosis and subsequent monitoring. Controlling hyperglycemia, blood pressure, and proteinuria are critical in stopping the progression of DKD. Clinical practice and evidence-based medicine demonstrated that early diagnosis followed by treatment can prevent or halt DKD progression.

High sensitive C-reactive protein, adiponectin, and urine albumin excretion rate in Chinese coronary artery disease patients with different glucose tolerance status

Background Serum high sensitive C-reactive protein （hs-CRP）, adiponectin levels and urine albumin excretion rate （UAER） are probably associated with inflammation and atherosclerosis. The aim of this study was to determine the three markers in coronary artery disease （CAD） subjects with different glucose tolerance status in a Chinese population and further explore the levels of the three markers in these subjects and the possible association of these markers with CAD risk factors and the severity of CAD as well. Methods A total of 242 subjects with angiographically documented CAD were recruited, and then assigned to three groups： the normal glucose tolerance （NGT） ＋ CAD group, including 100 CAD patients with NGT; the impaired glucose tolerance （IGT） ＋ CAD group, 40 CAD patients with IGT; the type 2 diabetes mellitus （T2DM） ＋ CAD group, 102 CAD patients with T2DM. Serum hs-CRP, adiponectin levels as well as UAER were measured in all subjects. Results Serum hs-CRP levels were increased in the T2DM ＋ CAD group compared with the NGT ＋ CAD group （4.71±2.59） vs （3.60±2.46） mg/L, P=0.037. Serum adiponectin levels were gradually decreased from the NGT ＋ CAD to IGT ＋ CAD to T2DM ＋ CAD groups, （5.99±1.84）, （5.82±1.72） and （4.65±1.71） mg/L, P=0.002 and 0.040 for NGT ＋ CAD and IGT ＋ CAD groups vs T2DM ＋ CAD group, respectively. While the UAER was gradually increased from the NGT ＋ CAD to IGT ＋ CAD to T2DM ＋ CAD groups, （6.42±2.51）, （6.89±2.94） and （15.03±4.22） μg/min （P 〈0.001） for NGT ＋ CAD and IGT ＋ CAD groups vs T2DM ＋ CAD group. Multiple linear stepwise regression analysis showed that waist-hip ratio （WHR） and low density lipoprotein cholesterol （LDL-C） were the significant determinants of serum hs-CRP levels; triglyceride （TG）, high density lipoprotein cholesterol （HDL-C）, age, WHR, T2DM, 2-hour serum insulin （2hINS）, sex, and apolipoprotein B were the significant determinants of serum adiponectin levels; and systolic blood pressure （SBP）, T2DM and hemoglobin A1c （HbA1c） were the significant determinants of UAER in all subjects （R^2= 0.070, 0.352, and 0.214, respectively）. However, no significant correlation was seen for hs-CRP, adiponectin and UAER with the severity of CAD. Hs-CRP levels were significantly correlated with UAER. Conclusions There was a trend of increased serum hs-CRP levels from the NGT ＋ CAD to IGT ＋ CAD to T2DM ＋ CAD groups, though it only showed significance in the T2DM ＋ CAD group compared with the NGT ＋ CAD group. Serum adiponectin levels were decreased and UAER was increased from the NGT ＋ CAD to IGT ＋ CAD to T2DM ＋ CAD groups Increased UAER and serum hs-CRP, and decreased adiponectin levels were associated with traditional CAD risk factors but failed to be correlated with the severity of CAD. Hs-CRP levels were significantly correlated with UAER.

Mesenchymal stem cells transplantation mildly ameliorates experimental diabetic nephropathy in rats

Background Diabetic nephropathy is a common complication of diabetes mellitus. This study aimed to explore whether mesenchymal stem cells （MSCs） transplantation could attenuate diabetic nephropathy in experimental diabetic rats. Methods Sprague-Dawley rats received a single intraperitoneal injection of streptozotocin （STZ） （60 mg/kg）. Diabetic rats were randomized to four groups： diabetes control group （DC）, ciclosporin A group （CsA）, MSC group, and MSC＋CsA group （MSCA）. Bone marrow mesenchymal stem cells were cultured, identified and labeled by 5-bromo-2＇-deoxyuridine （BrdU） in vitro. Then they were transplanted to diabetic rats via introcardiac infusion. Ciclosporin A was administered daily at 5 mg/kg. At 1,2, 4, 8 weeks after transplantation, random blood glucose, urine albumin/creatinine ratio （AIb/Cr）, endogenous creatinine clearance rate and renal mass index were tested. Renal morphology and labeled cells were examined. Results Cultured MSCs expressed mesenchymal cell phenotype, and could be multidifferentiated to osteogenic and adipogenic cells. Labeled MSCs could be detected in the kidney of nephropathic rats, mainly in renal interstitium, but they did not propagate after engrafting in kidney. Over the course of the experiment, MSCA group showed a significant decrease in blood glucose compared with MSC group, CsA group and DC group （P 〈0.05, respectively）. The AIb/Cr in MSCA group and MSC group were significantly lower than CsA group and DC group （P〈0.05）. And the AIb/Cr in MSCA group showed a significant decrease compared with MSC group （0.74 vs 0.84, P 〈0.05）. There was a significant difference in renal mass index between the MSCA group and DC group （5.66 vs 6.37, P 〈0.05）. No significant difference was found in creatinine clearance rate among 4 groups （P 〉0.05）. Treatment with MSC＋CsA significantly ameliorated the morphology of diabetic kidney. Conclusion MSC could mildly ameliorate diabetic nephropathy by decreasing blood glucose, AIb/Cr ratio and renal mass index.