Progression Of Microalbuminuria Research Articles

High-sensitivity C-reactive protein predicts microalbuminuria progression in essential hypertensive patients: a 3-year follow-up study.

To determine the independent effect of high-sensitivity C-reactive protein (hs-CRP) and the combined effects of hs-CRP and other traditional risk factors on microalbuminuria in hypertensive patients during the 3-year follow-up period. Baseline hs-CRP levels and other risk factors were measured in 280 adults in 2007. In the third year of examination, 199 patients (mean age 62.5 ± 9.5, men 59.3%) were approached for the measurement of microalbuminuria. The subjects were classified into two groups by the median of baseline hs-CRP. Compared to the patients with baseline hs-CRP below the median group ( n = 99, 50%), the group with baseline hs-CRP above the median ( n = 100, 50%) had higher urinary albumin-to-creatinine ratio (ACR) ( P = 0.007) at the end of follow-up period. ACR at the end of follow-up period was significantly correlated with baseline diabetes ( β = 0.342; P < 0.001), baseline SBP ( β = 0.148; P = 0.02), and baseline log-transformed hs-CRP ( β = 0.169; P = 0.01), while adversely correlated with baseline estimated glomerular filtration rate (eGFR) ( β = -0.163; P = 0.02) in multivariate stepwise linear analysis. In addition, ACR change during follow-up period was significantly correlated with baseline diabetes ( β = 0.359; P < 0.001) and baseline log-transformed hs-CRP ( β = 0.190; P = 0.004) in multivariate stepwise linear analysis. The combined effects of baseline hs-CRP and conventional risk factors, such as male sex, diabetes, smoking status, hyperlipidemia, hyperuricemia, and mildly reduced eGFR had a greater risk for microalbuminuria progression. There was no difference in eGFR changes during the follow-up period between two groups. Our findings offer a new piece of evidence on the predictive value of baseline hs-CRP for microalbuminuria progression in essential hypertensive patients, and highlight those who combined with traditional cardiovascular risk factors had a greater risk for developing microalbuminuria.

Association between Relative Thrombocytosis and Microalbuminuria in Adults with Mild Fasting Hyperglycemia.

An elevated platelet count may contribute to significant thrombotic events and pose a risk for diabetic microvascular complications. Albuminuria, one of the hallmarks of diabetes, is thought to be a risk factor for endothelial dysfunction. In this study, we investigated the association between relative thrombocytosis and an increased urine albumin-to-creatinine ratio in healthy adult participants. Using multivariate analyses on data from the Korea National Health and Nutrition Examination Survey V-VI, 12,525 eligible native Koreans aged ≥ 20 were categorized into platelet count quintiles by sex. The highest platelet count quintile included younger, more obese participants with elevated white blood cell counts, poor lipid profiles, and a better estimated glomerular filtration rate. Restricted cubic spline regression analysis revealed significant associations between platelet count and fasting blood glucose, glycated hemoglobin, and urine albumin-to-creatinine ratio. Adjusted logistic regression models indicated that heightened fasting blood glucose and platelet count were linked to risk of microalbuminuria (fasting blood glucose, odds ratio = 1.026, 95%CI = 1.011-1.042; platelet count, odds ratio = 1.004, 95%CI = 1.002-1.006). Particularly, an increased platelet count was notably associated with microalbuminuria progression in subjects with impaired fasting glucose. These findings suggest that an elevated platelet count, even below diagnostic thrombocytosis levels, independently correlates with an increased risk of vascular endothelial dysfunction in patients with impaired fasting glucose.

Intramyocellular Triglyceride Content During the Early Course of Type 1 and Type 2 Diabetes Mellitus.

Intramyocellular lipid content (IMCL) is elevated in insulin-resistant humans, but its changes over time and relationships with comorbidities remain unclear. We examined IMCL during the initial course of diabetes and its associations with complications. Participants of the German Diabetes Study (GDS) with recent-onset type 1 (n=132) or type 2 diabetes (n=139) and glucosetolerant controls (n=128) underwent 1H-magnetic resonance spectroscopy to measure IMCL and muscle volume, whole-body insulin sensitivity (hyperinsulinemic-euglycemic clamps; Mvalue) and cycling spiroergometry (VO2max). Subgroups underwent the same measurements after 5 years. At baseline, IMCL was ∼30% higher in type 2 diabetes than in other groups independently of age, sex, BMI and muscle volume. In type 2 diabetes, M-value was ∼36% and ∼62% lower compared to type 1 diabetes and controls, respectively. After 5 years, M-value decreased by ∼29% in type 1 and ∼13% in type 2 diabetes, whereas IMCL remained unchanged. The correlation of IMCL and M-value in type 2 diabetes at baseline was modulated by VO2max. IMCL also associated with microalbuminuria, Framingham risk score for cardiovascular disease and cardiac autonomic neuropathy. Changes in IMCL within 5 years after diagnosis do not mirror progression of insulin resistance in type 2 diabetes but associate with early diabetesrelated complications.

Predictors of microalbuminuria in workers of locomotive crews: prospective observational study

BACKGROUND: Cardiorenal relationships are one of the key problems in cardiology and nephrology. Microalbuminuria is a symptom of kidney pathologies and cardiovascular diseases. Studying the causes of microalbuminuria will help in solving the issue of pathological cardiorenal relationships.&#x0D; AIM: To study the causes of the origin of microalbuminuria on the group of locomotive crews employees of the Trans-Baikal Railway.&#x0D; MATERIALS AND METHODS: Predictors of microalbuminuria were established using data from a 6-year prospective follow-up of 22 clinical and anamnestic items in a natural cohort group of initially healthy 7,959 men (workers of locomotive crews) aged 1866 years. A confusion matrix, multivariate regression model, and relative risk assessment were used for this purpose.&#x0D; RESULTS: Microalbuminuria was found to be caused by excessive alcohol consumption, arterial hypertension, dyslipidemia, family history of early cardiovascular disease, grade III retinopathy, and smoking. The established predictors of microalbuminuria showed statistical heterogeneity in different analyses, referring to the significance of their assessment in the models used.&#x0D; CONCLUSION: The statistical heterogeneity of microalbuminuria predictors of is probably determined by and related to their qualitative characteristics and the unique implementation of their damaging effect in the formation and progression of microalbuminuria at the cellular level. The results of the study showed the need to continue the examination of predictors of microalbuminuria using other statistical analysis tools until their unique specific characteristics are known and the effects of damage on the formation of this pathological symptom are clarified.

Effect of multifactorial intensive treatment in patients with diabetic kidney disease: a meta-analysis with trial sequential analysis.

This meta-analysis was performed to assess the efficacy and safety of multifactorial intensive treatment (MT) in patients with diabetic kidney disease (DKD). We systematically searched PubMed, Embase and Web of science from their inception to February 2023 to identify randomized control trials (RCTs) evaluating the effect and safety of MT in patients with DKD. The quality of included RCTs was assessed using the risk of bias tool. The outcomes were expressed as hazard ratios (HR), risk ratio (RR) or weight mean difference (WMD) with 95% confidence intervals (95% CI), with a meta-analysis of a fixed-effect or random-effect model. Five RCTs were included for data analysis. The pooled analysis showed that, MT was associated with significant reductions in all-cause mortality (HR=0.75, 95%CI: 0.60, 0.93; P=0.008) and cardiovascular event disease (CVD) rate (HR=0.55, 95%CI: 0.44, 0.68; P<0.001). MT significantly decreased the retinopathy progression (HR=0.79, 95%CI: 0.66, 0.95; P=0.011), progression of macroalbuminuria (HR=0.64, 95%CI: 0.43, 0.95; P=0.027) and progression of microalbuminuria (HR=0.69, 95%CI: 0.56, 0.86; P=0.001). In addition, MT was not associated with an increased risk of all adverse events (RR=1.00, 95%CI: 0.97, 1.03; P=0.830) and all severe adverse events (RR=0.92, 95%CI: 0.74, 1.15; P=0.478), and the statistical power was confirmed by trial sequential analysis. The present study suggested that MT had a remarkable benefit on the risk of all-cause mortality and CVD in patients with DKD. Our results were promising, but had certain limitations, which warrants additional large-scale RCTs to validate our findings. This article is protected by copyright. All rights reserved.

Short- and long-term treatment with angiotensin-converting enzyme inhibitors or calcium channel blockers for the prevention of diabetic nephropathy progression: A meta-analysis.

Treatments with angiotensin-converting enzyme (ACE) inhibitors or calcium channel blockers (CCBs) may delay the development of albuminuria in patients with early diabetic nephropathy. However, evidence in the literature has not been consistent. The present meta-analysis aimed to compare the short- and long-term therapeutic effects of ACE inhibitors and CCBs (when used separately) for preventing the progression of nephropathy in patients with diabetes mellitus. A comprehensive search of various databases was performed from inception until March 2015 for studies in the Chinese and English languages. Randomized controlled trials (RCTs) comparing the efficacy of ACE inhibitors with that of CCBs in patients with early diabetic nephropathy were considered. A total of 12 RCTs were included with a total of 947 patients. ACE inhibitors were indicated to be more effective in reducing the albumin excretion rate than CCBs after short-term treatments (<6 months) [mean difference (MD), 32.35; 95% confidence interval (CI), 31.62-33.07; P<0.00001]. There was no difference in serum creatinine values after treatment with either drug (MD, 8.7; 95% CI, -21.5-38.91; P=0.57). Data from six studies were used to compare long-term treatment effects (≥1 year). In terms of progression to normoalbuminuria, a marginal difference was obtained between the two drugs with better outcomes with ACE inhibitors [odds ratio (OR), 0.70; 95% CI, 0.49-1.00; P=0.05]. There was no statistically significant difference between ACE inhibitors and CCBs regarding the progression from microalbuminuria to macroalbuminuria (OR, 1.78; 95% CI, 0.82-3.87; P=0.15). In conclusion, the present study indicated that the antiproteinuric efficacy of CCBs may be less than that of ACE inhibitors after short-term treatment in patients with DN. However, both types of drugs are equally effective in reducing the progression of microalbuminuria to macroalbuminuria in the long term.

Time-sequential correlations between diabetic kidney disease and diabetic retinopathy in type 2 diabetes - an 8-year prospective cohort study.

To investigate the time-sequential correlations between progression/remission of diabetic kidney disease (DKD) and development of diabetic retinopathy (DR) or diabetic macular oedema (DME) in type 2 diabetes (T2D). This was an 8-year prospective cohort study in which 576 patients with T2D and microalbuminuria from one medical centre in Taiwan were recruited. Progression of microalbuminuria was defined as shift of urinary albumin/creatinine ratio (ACR) into 300mg/g or more; remission of microalbuminuria was defined as having a urinary ACR less than 30mg/g in at least two of three tests over a period of 6months. Cox regression analysis was used to evaluate the hazard ratios (HRs) for progression or remission of microalbuminuria on development of any DR, proliferative DR (PDR) and DME. After adjusting for baseline characteristics , remission of microalbuminuria was a significant protecting factor for development of PDR (HR=0.290, 95% CI: 0.102-0.826, p=0.020) and DME (HR=0.404, 95% CI: 0.188-0.864, p=0.020). After further adjustment for the mean follow-up HbA1c and systolic blood pressure, remission of microalbuminuria was still a significant protecting factor for development of PDR (HR=0.348, 95% CI: 0.122-0.992, p=0.048). Remission of microalbuminuria was an independent protecting factor for development of PDR and DME. Aggressive treatment for DKD might help prevent the progression of DR.

Predictive Roles of Urinary Liver Type - Fatty Acid-Binding Protein and N-Acetyl-β-D-Glucosaminidase for Progression of Diabetic Nephropathy in Type 2 Diabetic Patients

Background: diabetes mellitus (DM) is a common metabolic disorder characterized by chronic hyperglycemia leading to significant morbidity and mortality as a result of the development of chronic macrovascular and microvascular complications. The onset of type 2 diabetes mellitus (T2DM) is often silent and insidious and this accounts for the relatively high prevalence of complications at initial presentation. Objective: The aim of the current study was to evaluate the urinary level of liver type-fatty acid binding protein (u-LFABP) as a proximal tubular damage biomarker in prediction or early detection of Diabetic nephropathy (DN) and whether its levels parallel the severity of kidney disease in type 2 diabetic patients, as assessed by the degree of albuminuria and other biochemical indices of renal dysfunction (e-GFR, serum creatinine and urea). Patients and Methods: the study was conducted on 69 diabetic patients and 20 age and sex- matched apparently healthy control subjects. All patients included in this study were recruited from the inpatient and outpatient Endocrinology Clinic, Al-Zahraa University Hospital, between October 2016 and April 2018. The enrolled patients included 37 women and 32 men with age ranged from 40 to 67. They were diagnosed as having type 2 diabetes mellitus (T2DM). Results: Statistical analysis of results presumed that u-L-FABP levels ˃37.2 and 92.2 ng/L were the optimum cutoff levels to discriminate micro- and macroalbuminuric diabetic patients from controls with 90% and 100% diagnostic specificity and 96% and 100% accuracy, respectively. In addition, u-L-FABP levels ˃ 28.5 and ˃386.1 ng/L, were the optimum cutoff values that predict the progression of microalbuminuria and macroalbuminuria with 100% diagnostic sensitivity and 87.9% and 99.7% accuracy, respectively. Conclusion: the use of u-L-FABP as a specific proximal tubular damage biomarker alone, or together with microalbumin, is beneficial for early diagnosis and monitoring of DN, compared to u- N-Acetyl-β-DGlucosaminidase (NAG) excretion.

Predictive Roles of Urinary Liver Type - Fatty Acid-Binding Protein and N-Acetyl-β-D-Glucosaminidase for Progression of Diabetic Nephropathy in Type 2 Diabetic Patients

Background: diabetes mellitus (DM) is a common metabolic disorder characterized by chronic hyperglycemia leading to significant morbidity and mortality as a result of the development of chronic macrovascular and microvascular complications. The onset of type 2 diabetes mellitus (T2DM) is often silent and insidious and this accounts for the relatively high prevalence of complications at initial presentation. Objective: The aim of the current study was to evaluate the urinary level of liver type-fatty acid binding protein (u-LFABP) as a proximal tubular damage biomarker in prediction or early detection of Diabetic nephropathy (DN) and whether its levels parallel the severity of kidney disease in type 2 diabetic patients, as assessed by the degree of albuminuria and other biochemical indices of renal dysfunction (e-GFR, serum creatinine and urea). Patients and Methods: the study was conducted on 69 diabetic patients and 20 age and sex- matched apparently healthy control subjects. All patients included in this study were recruited from the inpatient and outpatient Endocrinology Clinic, Al-Zahraa University Hospital, between October 2016 and April 2018. The enrolled patients included 37 women and 32 men with age ranged from 40 to 67. They were diagnosed as having type 2 diabetes mellitus (T2DM). Results: Statistical analysis of results presumed that u-L-FABP levels ˃37.2 and 92.2 ng/L were the optimum cutoff levels to discriminate micro- and macroalbuminuric diabetic patients from controls with 90% and 100% diagnostic specificity and 96% and 100% accuracy, respectively. In addition, u-L-FABP levels ˃ 28.5 and ˃386.1 ng/L, were the optimum cutoff values that predict the progression of microalbuminuria and macroalbuminuria with 100% diagnostic sensitivity and 87.9% and 99.7% accuracy, respectively. Conclusion: the use of u-L-FABP as a specific proximal tubular damage biomarker alone, or together with microalbumin, is beneficial for early diagnosis and monitoring of DN, compared to u- N-Acetyl-β-DGlucosaminidase (NAG) excretion.

Relationship of chronic kidney disease of the with glycemic status, cardiovascular diseases and laboratory indicators in patients with type 2 diabetes mellitus

Aim. To study the relationship of chronic kidney disease parameters with glycemic control, subclinical and clinical signs of cardiovascular diseases and laboratory parameters.Material and methods. The study included 528 patients with type 2 diabetes mellitus (T2DM) aged 30-69 years. All respondents answered questions from the ARIC questionnaire about T2DM and cardiovascular diseases. We determined the ankle-brachial index, sonographic left ventricular hypertrophy, intima-media thickness and defined hypertensive, diabetic angiopathy and polyneuropathy. The levels of glycemia, lipid spectrum, creatinine, uric acid, glycohemoglobin were evaluted. Glomerular filtration rate (GFR) was calculated using the Cockroft-Gault method, and microalbuminuria (MAU) was determined using Micral tests.Results. Glycohemoglobin did not depend on MAU (p=0,564), a decrease in GFR was accompanied by an improvement in glycemic control (p=0,393). There was a direct association between MAU and the duration of diabetes (p=0,001), in patients with a longer course of the disease GFR was reduced (p=0,001). With increasing of systolic blood pressure, MAU progressed (p=0,016), while GFR decreased (p&lt;0,01). In patients with hypertensive angiopathy, MAU of 100 mg/dl (p=0,001) and stage 2 of chronic kidney disease (p=0,048) occurred with the highest incidence (1/4) (p=0,048). According to the survey, angina was found in patients with MAU of 100 mg/dl (p=0,006). Chronic heart failure led to the progression of albuminuria (p=0,007), in patients with clinical signs of atherosclerosis of the lower extremities, the frequency of MAU was 72-87,5% (p=0,032). The highest intima-media thickness of the right carotid artery in patients with GFR 89-60 ml/min and MAU 100 mg/dL (respectively, 1,77±0,41, 1,33±0,49) were determined. Sonographic signs of left ventricular hypertrophy were observed in 84,6% of patients with an MAU of 300 mg/dL (p=0,022), as the severity of albuminuria increased, the ejection fraction of the left ventricle decreased (p=0,003). Albuminuria increased the level of myocardial remodeling (p&lt;0,05) and this indicator showed a direct relationship with the severity of MAU. With an increase in albuminuria, the degree of triglyceridemia increased. An increase of MAU level and a decrease in GFR was accompanied by an increase in creatininemia (p&lt;0,001). A direct relationship was found between lithemia and MAU. Conversely, a decrease in GFR contributed to the progression of MAU (p&lt;0,001).Conclusion. Reduction of GFR and MAU are the major risk factors for cardiovascular diseases in the Azerbaijani population with T2DM. We suppose that periodic monitoring of these parameters for primary and secondary prevention of diabetic nephropathy plays an important role.

Progression of Renal Insufficiency in Patients with Essential Hypertension Treated with Renin Angiotensin Aldosterone System Blockers: An Electrocardiographic Correlation.

Background: There is a frequent association between renal insufficiency and cardiovascular disease in patients with essential hypertension (HTN). The aim of this study was to analyze the relationship between ECG parameters and the progress of renal damage in patients with treated HTN. Methods: 109 patients with HTN had their microalbuminuria monitored over a 3-year time frame. During the last 3 months of follow-up, an ECG was recorded. Patients were divided into 3 groups according to the deterioration of their renal function: normoalbuminuria during the study period (normo–normo; n = 51); normoalbuminuria developing microalbuminuria (normo–micro; n = 29); and microalbuminuria at baseline (micro–micro; n = 29). Results: There were no differences in presence of left ventricular hypertrophy between the 3 groups. RV6/RV5 >1 was observed more frequently as renal function declined (p = 0.025). The 12-lead QRS-complex voltage-duration product was significantly increased in patients without microalbuminuria at baseline who went on to develop microalbuminuria (p = 0.006). Patients who developed microalbuminuria during follow-up, with positive Cornell voltage criteria, showed a lesser degree of progression of microalbuminuria when compared with the rest of the subgroups (p = 0.044). Furthermore, patients with microalbuminuria at baseline treated with angiotensin receptor blockers and diuretics, and positive Cornell voltage criteria, showed a higher degree of microalbuminuria compared to those with negative Cornell voltage criteria (p = 0.016). Conclusions: In patients with HTN, we identified some ECG parameters, which predict renal disease progression in patients with HTN, which may permit the identification of patients who are at risk of renal disease progression, despite optimal antihypertensive pharmacotherapy.

Plasma Leucine-Rich α-2-Glycoprotein 1 Predicts Rapid eGFR Decline and Albuminuria Progression in Type 2 Diabetes Mellitus.

Abnormal angiogenesis plays an important role in pathogenesis of diabetic kidney disease (DKD). Leucine-rich α-2 glycoprotein 1 (LRG1) is a newly identified angiogenic factor. To study whether plasma LRG1 may independently predict progression of DKD in individuals with type 2 diabetes mellitus (T2DM). Prospective cohort study in a regional hospital. In total, 1226 T2DM participants were followed for a mean ± standard deviation (SD) of 3.1 ± 0.4 years. Albuminuria progression was defined as elevation in albuminuria level to a higher category. Chronic kidney disease (CKD) progression [rapid estimated glomerular filtration rate (eGFR) decline] was defined as a 40% or greater deterioration in eGFR in 3 years. Both participants with albuminuria progression and those with CKD progression had higher plasma LRG1 levels at baseline. LRG1 independently predicted albuminuria progression above traditional risk factors, including baseline eGFR and urine albumin to creatinine ratio. A 1-SD increment in LRG1 was associated with a 1.26-fold [95% confidence interval (CI), 1.04 to 1.53, P = 0.018] higher adjusted risk for albuminuria progression. The association of LRG1 with microalbuminuria to macroalbuminuria progression was stronger than its association with normoalbuminuria to microalbuminuria progression [odds ratio (OR), 1.51; 95% CI, 1.04 to 2.18, P = 0.029 vs OR, 1.09; 95% CI, 0.86 to 1.37, P = 0.486, per 1-SD LRG1 increment]. Also, LRG1 independently predicted CKD progression above traditional risk factors. A 1-SD increment in LRG1 was associated with a 1.48-fold (95% CI, 1.04 to 2.11, P = 0.032) higher adjusted risk for CKD progression. Plasma LRG1 predicts both albuminuria and CKD progression beyond traditional risk factors. It may play a role in the pathologic pathway leading to progression of DKD in T2DM.

Glucose targets for preventing diabetic kidney disease and its progression.

Diabetes is the leading cause of end-stage kidney disease (ESKD) around the world. Blood pressure lowering and glucose control are used to reduce diabetes-associated disability including kidney failure. However there is a lack of an overall evidence summary of the optimal target range for blood glucose control to prevent kidney failure. To evaluate the benefits and harms of intensive (HbA1c < 7% or fasting glucose levels < 120 mg/dL versus standard glycaemic control (HbA1c ≥ 7% or fasting glucose levels ≥ 120 mg/dL for preventing the onset and progression of kidney disease among adults with diabetes. We searched the Cochrane Kidney and Transplant Specialised Register up to 31 March 2017 through contact with the Information Specialist using search terms relevant to this review. Studies contained in the Specialised Register are identified through search strategies specifically designed for CENTRAL, MEDLINE, and EMBASE; handsearching conference proceedings; and searching the International Clinical Trials Register (ICTRP) Search Portal and ClinicalTrials.gov. Randomised controlled trials evaluating glucose-lowering interventions in which people (aged 14 year or older) with type 1 or 2 diabetes with and without kidney disease were randomly allocated to tight glucose control or less stringent blood glucose targets. Two authors independently assessed studies for eligibility and risks of bias, extracted data and checked the processes for accuracy. Outcomes were mortality, cardiovascular complications, doubling of serum creatinine (SCr), ESKD and proteinuria. Confidence in the evidence was assessing using GRADE. Summary estimates of effect were obtained using a random-effects model, and results were expressed as risk ratios (RR) and their 95% confidence intervals (CI) for dichotomous outcomes, and mean difference (MD) and 95% CI for continuous outcomes. Fourteen studies involving 29,319 people with diabetes were included and 11 studies involving 29,141 people were included in our meta-analyses. Treatment duration was 56.7 months on average (range 6 months to 10 years). Studies included people with a range of kidney function. Incomplete reporting of key methodological details resulted in uncertain risks of bias in many studies. Using GRADE assessment, we had moderate confidence in the effects of glucose lowering strategies on ESKD, all-cause mortality, myocardial infarction, and progressive protein leakage by kidney disease and low or very low confidence in effects of treatment on death related to cardiovascular complications and doubling of serum creatinine (SCr).For the primary outcomes, tight glycaemic control may make little or no difference to doubling of SCr compared with standard control (4 studies, 26,874 participants: RR 0.84, 95% CI 0.64 to 1.11; I2= 73%, low certainty evidence), development of ESKD (4 studies, 23,332 participants: RR 0.62, 95% CI 0.34 to 1.12; I2= 52%; low certainty evidence), all-cause mortality (9 studies, 29,094 participants: RR 0.99, 95% CI 0.86 to 1.13; I2= 50%; moderate certainty evidence), cardiovascular mortality (6 studies, 23,673 participants: RR 1.19, 95% CI 0.73 to 1.92; I2= 85%; low certainty evidence), or sudden death (4 studies, 5913 participants: RR 0.82, 95% CI 0.26 to 2.57; I2= 85%; very low certainty evidence). People who received treatment to achieve tighter glycaemic control probably experienced lower risks of non-fatal myocardial infarction (5 studies, 25,596 participants: RR 0.82, 95% CI 0.67 to 0.99; I2= 46%, moderate certainty evidence), onset of microalbuminuria (4 studies, 19,846 participants: RR 0.82, 95% CI 0.71 to 0.93; I2= 61%, moderate certainty evidence), and progression of microalbuminuria (5 studies, 13,266 participants: RR 0.59, 95% CI 0.38 to 0.93; I2= 75%, moderate certainty evidence). In absolute terms, tight versus standard glucose control treatment in 1,000 adults would lead to between zero and two people avoiding non-fatal myocardial infarction, while seven adults would avoid experiencing new-onset albuminuria and two would avoid worsening albuminuria. This review suggests that people who receive intensive glycaemic control for treatment of diabetes had comparable risks of kidney failure, death and major cardiovascular events as people who received less stringent blood glucose control, while experiencing small clinical benefits on the onset and progression of microalbuminuria and myocardial infarction. The adverse effects of glycaemic management are uncertain. Based on absolute treatment effects, the clinical impact of targeting an HbA1c < 7% or blood glucose < 6.6 mmol/L is unclear and the potential harms of this treatment approach are largely unmeasured.

Cigarette Smoking and Its Hazards in Kidney Transplantation.

Cigarette smoking affects many organs. It causes vasoconstriction through activation of sympathetic nervous system which leads to elevation of blood pressure and reduction in glomerular filtration rate and filtration pressure. It also causes thickening of renal arterioles. Cigarette smoking increases the risk of microalbuminuria and accelerates progression of microalbuminuria to macroalbuminuria. Furthermore, it causes rapid loss of glomerular filtration rate in chronic kidney disease patients. After kidney donation, these factors may be injurious to the solitary kidney. Kidney donors with history of cigarette smoking are prone to develop perioperative complications, pneumonia, and wound infection. Postkidney transplantation various stressors including warm and cold ischemia time, delayed graft function, and exposure to calcineurin inhibitors may result in poor graft function. Continuation of cigarette smoking in kidney transplant recipients will add further risk. In this review, we will specifically discuss the effects of cigarette smoking on normal kidneys, live kidney donors, and kidney transplant recipients. This will include adverse effects of cigarette smoking on graft and patient survival, cardiovascular events, rejection, infections, and cancers in kidney transplant recipients. Lastly, the impact of kidney transplantation on behavior and smoking cessation will also be discussed.

Nocturnal blood pressure is associated with the progression of microvascular complications and hypertension in patients with type 1 diabetes mellitus

AimsTo evaluate relationships between early alterations in blood pressure and the progression of microvascular complications of diabetes in clinically-normotensive patients with type 1 diabetes (T1DM). MethodsIn a prospective observational study of 85 normotensive T1DM patients without microalbuminuria, blood pressure (BP) was monitored over 24h using the ambulatory blood pressure monitoring (ABPM) system at baseline and 7years later. Development or progression of microalbuminuria, retinopathy and hypertension was evaluated. ResultsInitially, 20 patients (24%) were diagnosed with masked hypertension and 31 (37%) with non-dipper pattern as the only pathological findings. At 7years: 1) twenty-seven patients (32%) had progression of retinopathy related to the nocturnal diastolic blood pressure (BPD) (OR:1.122; p=0.034) and final non-dipper pattern (OR:5.857; p=0.005); 2) seven patients (10%) developed microalbuminuria for which nocturnal systolic blood pressure (BPS) was a risk factor (OR:1.129; p=0.007); 3) five of the normotensive patients (9%) progressed to hypertension; historic HbA1c (OR:2.767; p=0.046) and nocturnal BPD (OR:1.243; p=0.046) being the related risk factors. BPD level ≥65mmHg was associated with an increase in progression of retinopathy and hypertension. ConclusionsIn T1DM patients there is an elevated prevalence of BP alterations, detected using ABPM. Alterations in nocturnal BP predispose to development/progression of microvascular complications and overt hypertension.

Association of serum uric acid levels with the risk of development or progression of albuminuria among Japanese patients with type 2 diabetes: a prospective cohort study [Diabetes Distress and Care Registry at Tenri (DDCRT 10)

To assess the prospective association between baseline serum uric acid level and subsequent risk of development or progression in albuminuria. Longitudinal data were obtained from 2518 patients with type 2 diabetes in the development cohort and registered in a Japanese diabetes registry. To assess the independent correlations between baseline serum uric acid quartiles and either the development or progression of diabetic nephropathy for 2years, the Cox proportional hazards model was used and adjusted for potential confounders. The mean patient age, body mass index, and glycated hemoglobin (HbA1c) level were 66.1years, 24.6kg/m(2), and 7.5% (57.6mmol/mol), respectively. The baseline serum uric acid levels, with mean values of 3.6, 4.9, 5.8, and 7.3mg/dL from the first to fourth quartiles, were significantly associated with the urinary albumin/creatinine ratio at baseline (p<0.001). Baseline uric acid levels were not significantly associated with the development of nephropathy, but they were with the progression of nephropathy. The multivariable-adjusted hazards ratios for the progression from microalbuminuria to macroalbuminuria were 2.17 [95% confidence interval (CI) 1.15-4.08; p=0.016], 3.04 (95% CI 1.67-5.53; p<0.001), and 3.56 (95% CI 1.83-6.93; p<0.0011) for the first, third, and fourth quartiles of serum uric acid levels, respectively, as compared to that for the second quartile. We did not observe significant association between uric acid levels and change in estimated glomerular filtration rate. Low and high serum uric levels, independent of possible confounders, were associated with a subsequent risk of progression, not development, in albuminuria in type 2 diabetes patients. Therefore, serum uric acid levels may be useful for predicting the future risk of progression of microalbuminuria.

Abstract 15530: Omega-3 Fatty acids Supplementation Attenuates the Progression of Microalbuminuria in Diabetics With Coronary Artery Disease

Introduction: Microalbuminuria is a marker of generalized endothelial dysfunction, a key step in the pathogenesis of coronary artery disease (CAD). It is also an independent predictor of cardiovascular morbidity and mortality. Angiotensin converting enzyme inhibitor (ACEI) or angiotensin receptor blocker (ARB) therapy is considered a standard of care to attenuate progression of albuminuria in diabetic patients. Hypothesis: Omega-3 fatty acids (FAs) supplementation will attenuate progression of microalbuminuria in diabetic subjects with stable CAD. Method: In our study, 262 subjects with stable CAD were randomized to 3.6 g of omega-3 FAs (1.86 g of eicosapentaenoic acid + 1.5 g of docosahexaenoic acid) per day or no omega-3 FA (control) for one year. Urine microalbumin to creatinine ratio (urine MCR mg/g) was calculated as a measure of microalbuminuria at baseline and one year follow-up. Results: Mean age was 63.3 ± 7.6 yrs, 17% were women, 30% had diabetes, and 74% were on ACEI or ARB therapy. At one year follow-up in non-diabetics, there was no significant difference in the % change in urine MCR between the omega-3 FAs and control groups (see table). In contrast in diabetics, those not receiving omega-3 FAs had a significant 72.3% increase in urine MCR whereas those receiving omega-3 FAs had no change (table). In subgroup analysis, diabetics on an ACEI or ARB receiving omega-3 FAs had no change in urine MCR whereas those not receiving omega-3 FAs had a 64.2% increase at one year follow-up. Conclusions: Omega-3 FAs attenuated worsening of urine MCR in diabetics with CAD compared to diabetics not receiving omega-3 FAs over a one year period. Our results suggest that a combination of omega-3 FAs and ACEI or ARB is better in attenuating the progression of microalbuminuria than ACEI or ARB alone in diabetics with CAD. This suggests that omega-3 FAs may provide additional benefit when added to ACEI/ARB in diabetics with CAD.

Gender-Related Differences in HDL Structure with the Progression of Microalbuminuria in Patients with Type 2 Diabetes

Background: The effect of gender on HDL molecules in patients with type2 diabetes and albuminuria has not been studied sufficiently. We questioned whether HDL-C, Apo A-I and their ratio in the early stages of diabetic nephropathy differs between men and women. Methods: We designed a matched case-control study of 38 microalbuminuric patients with type2 diabetes (cases) and 38 age and body mass index matched normoalbuminuric patients with type2 diabetes (controls). In this study, we investigated HDL-C/Apo A-I ratio as an index of HDL structure and function in clinic. We used diabetic nephropathy as a known model of dyslipidemia and investigated HDL-C, Apo A-I and HDL-C/Apo A-I levels in diabetic patients with microalbuminuria. Because of gender difference in HDL-C levels and cardiovascular risk, gender was considered as an interactive factor. Results: Apo A-I/HDL-C ratio in female microalbuminuric cases was higher than in the normoalbuminuric controls (P-value < 0.001), while there was no significant difference in HDL-C or Apo A-I between the two groups. No significant difference in; HDL-C, Apo A-I or Apo A-I/HDL-C ratio, was observed between microalbuminuric and normoalbuminuric males. In a conditional logistic regression model the Apo A-I/HDL-C ratio was significantly (P-value =0.04) associated with microalbuminuria. Apo A-I/HDL-C ratio and sex interaction also showed a borderline association (P-Value = 0.05). Conclusion: In patients with type 2 diabetes, measurement of HDL-C and Apo A-I has not conclusively represented the HDL role in albuminuria progression. This is partly due to structural or functional impairment of the HDL particles without any effect on their serum levels, and partly because of different alterations found in males and females. We suggest that such impairments happen faster and more progressively in females.

Circulating Progenitor Cell Count Predicts Microvascular Outcomes in Type 2 Diabetic Patients.

Diabetes reduces the levels of circulating progenitor cells (CPCs) and endothelial progenitor cells (EPCs), which promote vascular repair and are inversely correlated with cardiovascular risk. The objective of the study was to test whether CPC/EPC levels predict onset/progression of microangiopathy in a cohort of type 2 diabetic (T2D) patients. This was a pseudoprospective study with a 3.9-year follow-up. The study was conducted at a tertial referral diabetes outpatient clinic. A total of 187 T2D patients having a baseline determination of CPCs/EPCs participated in the study. Baseline data on demographics, anthropometrics, concomitant risk factors, diabetic complications, and medications were collected. Onset or progression of microangiopathy was assessed at follow-up compared with baseline. New onset or progression of microalbuminuria, chronic kidney disease, retinopathy, and neuropathy occurred in 70 patients (9.5%/y). After controlling the false discovery rate, baseline CD34(+) CPCs and EPCs were significantly lower in patients with onset/progression of microalbuminuria and any microangiopathy. Patients with baseline CD34(+) CPC or CD133(+)/kinase insert domain-containing receptor(+)/EPC levels below the median were more likely to experience worsening microangiopathy than those with high cell levels. Independently from confounders, including age, sex, glycated hemoglobin, and diabetes duration, CD34(+) cells predicted onset/progression of microalbuminuria, retinopathy, and any microangiopathy in false discovery rate-adjusted analyses. A low CD34(+) cell count limited the beneficial effects of renin-angiotensin system blockers on microalbuminuria progression. Levels of circulating (endothelial) progenitor cells predict microvascular outcomes in T2D. Together with previous studies showing an association with cardiovascular events, these data indicate that CPCs/EPCs represent biomarkers of the global complication burden in diabetes.

Screening and Correlation Between Nephropathy and Risk Factors of DM II Among Army Members Older than 45 in the City of Tehran

Considering the importance of military forces health and high prevalence of diabetes in Iran in addition to the the high burden (more than 50% of the whole disease’s burden on the health system) of controlling and treating the complications of DM II, make investigating factors that cause these complications in military forces significant. The aim of this study is to evaluate the relation between DM II risk factors (including metabolic syndrome) and MicroAlbuminuria among military members older than 45 in the city of Tehran. A cross-sectional study is designed using the outputs of a study down in 2010 in Iranian Army which revealed DM II prevalence and it’s relation with career and non-career dependent risk factors.36 diabetic patients were entered to the study and the subjective of the study was evaluated among them in three different sessions having 3 months intervals.The results were put into analysis using SPSS17 software. Among all factors studied only LDL(p-value<0.01) and age(p-value<0.05) had a meaning-full correlation with Micro-Albuminuria. Comparing the results of this study and the others we could dedicate that except LDL (which it’s rule in Micro-Albuminuria progression is controversial in other studies) and Age(which is mostly known as an etiologic factor for DM II itself), diabetic nephropathy is not mainly under effect of factors causing DM II. In the other words these factors have an etiologic impact on the disease rather than it’s progression and prognosis.