Renal Failure In Diabetic Patients Research Articles

Development of a LC–MS/MS analytical method of 15 compounds related to renal function for a prognostic method of progression risk in patients with diabetic kidney disease

Diabetic kidney disease (DKD) onset and progression is a major cause of end-stage renal failure in diabetic patients, however, no practical method has been reported to predict the progression rate of renal function decline. Nine serum compounds are reported to associate with prognosis in type 1 diabetes patients; however, quantitative analytical methods for these compounds lacks. Herein, we developed a simultaneous quantitative method for 15 compounds, including Niewczas’s nine biomarker candidates, associated with renal function and its prognosis in kidney disease patients to achieve a prognostic method of renal function decline in DKD patients. This report describes the development and validation of a LC–MS/MS analytical method for 15 compounds of biomarker candidates using human plasma, serum, and urine as sample matrices. The analytes are N-acetyl-L-alanine, N6-acetyl-L-lysine, N-acetyl-L-serine, N-acetyl-L-threonine, phenyl sulfate, pseudouridine, N6-threonylcarbamoyladenosine, tryptophan 2-C-mannoside, tyrosine O-sulfate, creatinine, p-cresol sulfate, 4-ethylphenyl sulfate, indoxyl sulfate, N1-methyladenosine, and trimethylamine N-oxide. The Capcell Pak ADME-HR column was compared to several general columns and selected as the most suitable column for the simultaneous analysis of all 15 compounds. The proposed method was validated for selectivity, accuracy, precision, stability, dilution integrity, and parallelism. This report describes the suitability of the calibration ranges established and the actual sample concentrations of serum and urine from type 2 diabetic patients, as well as new findings on the unknown analyte levels of several compounds in these samples. The proposed method can be used to aid the development of prognostic methods for renal function decline in patients with DKD.

Frequency Distribution of Oral Manifestations in Diabetic and Non-Diabetic Patients Undergoing Hemodialysis

Introduction: Chronic renal failure, as it affects different systems of the body, can cause major changes in the oral cavity. Therefore, the aim of this study was to compare oral manifestations in diabetic and non-diabetic patients undergoing hemodialysis. 60 patients under hemodialysis treatment referred to the dialysis departments of the teaching hospitals of Shahid Sadougi University of Medical Sciences, Yazd were examined.
 Methods: In this descriptive cross-sectional study, 60 patients undergoing hemodialysis in the dialysis wards of teaching hospitals of Shahid Sadoughi University of Medical Sciences were studied. Patients were divided into two groups of diabetic and non-diabetic (n=30). The oral cavity was examined with a mirror, explorer and flashlight. Gender, age, duration of hemodialysis, oral signs and symptoms were recorded in the patients' checklists. Data analysis was run by SPSS17 statistical software, T-tests, Fisher Exact and Chi-square.
 Results: 37 (61.7%) of the patients were male and 23 (38.3%) were female. The mean age of the patients was 57.17 ±16.15 years (age range 15-88 years). Dry mouth (76.7%) and dental erosion (50%) were the highest frequency in diabetic and non-diabetic patients, respectively. There was a statistically significant difference between the two groups in dry mouth and candidiasis (P <0.05).
 Conclusion: The combined effect of diabetes and renal failure in diabetic patients undergoing hemodialysis has increased oral complications in these individuals, so close collaboration between the patient and health care team to rapid diagnosis of oral lesions could lead to promotion of the patient’s oral health and quality of life and also a decrease in the burden of disease.

Solasonine alleviates high glucose-induced podocyte injury through increasing Nrf2-medicated inhibition of NLRP3 activation.

The worldwide high prevalence of diabetic nephropathy is one of the common causes of renal failure in diabetic patients. Hyperglycemia-caused podocyte injury is considered as a major contributor to diabetic kidney disease, accompanied by a chronic inflammatory condition. Pyroptosis, a characterized inflammatory form of programmed cell death, is believed to be involved in the pathogenesis of diabetic nephropathy. Solasonine (SS) is a natural alkaloid and received attention as a potential anticancer agent. However, its protective effect against hyperglycemia-caused podocyte injury remains to be determined. Our study found that SS alleviates cell apoptosis, and reduces pyroptosis and oxidative damage in high glucose (HG)-treated MPC5 podocytes. Pro-inflammatory cytokines, including interleukin (IL)-1β and IL-18, and caspase-1 activity were markedly suppressed by SS in HG-treated MPC5 podocytes. SS also reduced HG-induced oxidative damage in MPC5 podocytes. Nrf2 expression was activated by SS in vitro under a HG condition. In addition, Nrf2 silencing attenuated the protective effect of SS against apoptosis, pro-inflammatory cytokines release, caspase-1 activity, and oxidative damage in MPC5 podocytes under a HG condition. Taken together, our findings revealed for the first time that SS alleviated high glucose-induced podocyte apoptosis, pyroptosis, and oxidative damage via regulating the Nrf2/NLRP3 signaling pathway. Our results indicate that SS has the potential as a therapeutic agent for podocyte injury in diabetic nephropathy.

Glycated Hemoglobin is a Biomarker of Renal Failure in Diabetic Patients

Objective: In diabetic patients, this condition leads the cause the chronic kidney disease commonly known as diabetic nephropathy or diabetic kidney disease. Diabetic kidney disease patients were an exceptional cohort of the population that had a noticeable high glycated hemoglobin along with a low glomerular filtration rate. Methodology: The recent cross-sectional study was based on a 790 participants sample size, having both normal and diabetic patients with various complications and severities related to renal function. This research is based on diabetes mellitus type 2 patients under the treatment in Farwaniyah hospital, Kuwait from 2007 to 2010. The patients were divided into four groups based on Diabetic + Renal failure (Diab+RF), Diabetic + non-Renal failure (Diab+ NRF), Nondiabetic +Renal failure (NDiab +RF) compared with normal individuals. Correlations were evaluated between HbA1c with all groups and the estimated glomerular filtration rate. Results: In this study, we observed that higher HbA1c may the reason for the decline in glomerular filtration rate, irrespective of general characteristics like age, sex, and Blood Pressure. Our results showed that 37% of diabetic patients with renal failure. Conclusion: We report that in clinical exercise glycated hemoglobin acted as a biomarker to predict the renal disease stage. Control glucose restricts the decline in glomerular filtration rate this act shows the value of glycemic variability in glomerular filtration rate descent. endothelial damages cause by High glycated hemoglobin levels with low plasma glucose in fasting.

Interpretation of urine routine report of a diabetic patient: A review

Introduction: Diabetic patients are at an increased risk of multiple complications, among which one of the most dreaded complications is diabetic nephropathy. Early diagnosis and appropriate management will at least prolong the life of the kidney and prevent the development of end-stage renal failure. Materials and Methods: Simple urinalysis is a useful tool for early diagnosis of diabetic kidney disease and helps differentiate between diabetic and nondiabetic kidney diseases. In this review, we have discussed the usefulness of urinalysis for a diabetic patient. Results: Early detection of an abnormality can be an alarming sign, and we can diagnose treatable causes of renal failure in diabetic patients. Conclusions: History, examination, and urinalysis are sufficient in most of the cases for diagnosing diabetic kidney disease. Renal biopsy is indicated in special situations where diagnosis cannot be made even after appropriate non-invasive investigations. Few limitations of the study are resource settings and knowledge of this simple test to predict an alarming sign of the kidney disease.

Podocyte RNF166 deficiency alleviates diabetic nephropathy by mitigating mitochondria impairment and apoptosis via regulation of CYLD signal

Diabetic nephropathy (DN) is a major cause of renal failure in diabetic patients. RING-finger protein 166 (RNF166), composed of an N-terminal RING domain and C-terminal ubiquitin interaction motif, plays a critical role in mediating various cellular processes. However, its potential in DN has not been investigated. In the present study, we found that DN patients exhibited significantly increased expression of RNF166 in renal tissues compared with the normal individuals, and abundant RNF166 was detected in podocytes. We then showed that podocyte-conditional RNF166 knockout (RNF166cKO) markedly reduced blood glucose levels and ameliorated renal dysfunction in streptozotocin (STZ)-induced diabetic mice. Additionally, abnormal histological changes and podocyte injury were observed in STZ-induced diabetic mice, while being markedly ameliorated by RNF166cKO. Furthermore, podocyte-specific RNF166 deficiency considerably mitigated apoptosis and mitochondrial impairments in glomeruli podocytes of STZ-challenged mice through suppressing Caspase-3 cleavage and improving mitochondrial fission-associated molecules. In vitro studies further confirmed that high glucose (HG) induced mitochondrial dysfunction, along with enhanced releases of Cyto-c from mitochondria and elevated expression of cleaved Caspase-9, contributing to intrinsic apoptosis in podocytes. Intriguingly, these effects triggered by HG were dramatically ameliorated by RNF166 knockout. Mechanistically, we demonstrated that RNF166 directly interacted with cylindromatosis (CYLD), and negatively regulated CYLD expression. Notably, RNF166 knockout-attenuated mitochondrial damage and apoptosis were mainly through CYLD in podocytes upon HG stimulation. Together, all these findings provided new insights into the novel effects of RNF166 on maintaining mitochondrial function and apoptosis in podocytes during DN progression both in vivo and in vitro through interacting with CYLD, indicating that RNF166/CYLD may be an innovative therapeutic target for developing effective strategy against DN development.

Serum lncRNA HAND2-AS1 is downregulated in diabetic patients with chronic renal failure and ameliorates cell apoptosis

BackgroundLncRNA HAND2-AS1 has been reported to be a tumor suppressor in several types of malignancy, while its involvement in other human diseases is unclear. Our preliminary RNA-seq analysis revealed the downregulation of lncRNA HAND2-AS1 in diabetic patients with chronic renal failure, indicating the involvement of lncRNA HAND2-AS1 in this disease. This study was therefore carried out to explore the role of lncRNA HAND2-AS1 in the development of chronic renal failure in diabetic patients.MethodsMouse podocyte cells and plasma samples of diabetic patients (46 diabetic patients with chronic renal failure, 38 diabetic patients without obvious complications and 42 healthy volunteers) were used in this study. Cell apoptosis assay and PCR were performed.ResultsLncRNA HAND2-AS1 was downregulated in diabetic patients with chronic renal failure but not in diabetic patients without obvious complications. Downregulation of lncRNA HAND2-AS1 distinguished diabetic patients with chronic renal failure from diabetic patients and healthy controls. High glucose environment did not affect the expression of lncRNA HAND2-AS1 in mouse podocyte cells. Overexpression of lncRNA HAND2-AS1 inhibited the apoptosis of mouse podocyte cells under high glucose treatment.ConclusionsWe therefore conclude that lncRNA HAND2-AS1 may participate in the development of chronic renal failure in diabetic patients by regulating cell apoptosis.

Inflammation, Left Ventricular Mass Index and Chronic Renal Failure in Diabetic Patients

Inflammation, Left Ventricular Mass Index and Chronic Renal Failure in Diabetic Patients

Correlation between oxidative stress and hematological profile abnormalities in diabetic nephropathy

AimsDiabetes patients with renal impairment commonly have a degree of hematological abnormalities than those non-diabetics with chronic kidney disease. The present study aimed to clarify the association between oxidative stress and hematological abnormalities with the progression of diabetic nephropathy. MethodsA total of 20 healthy subjects and 100 patients were enrolled in the study. Eligible renal dysfunction patients were classified according to biochemical markers into five groups (20 patients); diabetic patients, pre-renal failure patients, diabetic pre-renal failure patients, renal failure patients, and diabetic renal failure patients. ResultsErythrocytes and platelets count, hemoglobin and hematocrit levels revealed a significant decrease in all renal dysfunction groups, while leukocytes count, red cell distribution width, platelet distribution width, and mean platelet volume showed significant increases in diabetic and renal dysfunction groups as compared to the healthy control. Nitric oxide level increased significantly, while reduced glutathione showed a marked decrease in diabetic and all renal dysfunction groups compared to the healthy control. ConclusionNitric oxide and reduced glutathione were associated with the inflammatory status in diabetic renal dysfunction patients which reflected by elevation in leukocytes and neutrophils count, red cell distribution width as well as the reduction in values of erythrocytes, platelets count, hemoglobin and hematocrit. Therefore, hematological indices can play a role in predict the progression of diabetic nephropathy.

Examining the effect of prescription sequence on developing adverse drug reactions: The case of renal failure in diabetic patients

ObjectivesWhile the effect of medications in development of Adverse Drug Reactions (ADRs) have been widely studied in the past, the literature lacks sufficient coverage in investigating whether the sequence in which [ADR-prone] drugs are prescribed (and administered) can increase the chances of ADR development. The present study investigates this potential effect by applying emergent sequential pattern mining techniques to electronic health records. Materials and methodsUsing longitudinal medication and diagnosis records from more than 377,000 diabetic patients, in this study, we assessed the possible effect of prescription sequences in developing acute renal failure as a prevalent ADR among this group of patients. Relying on emergent sequential pattern mining, two statistical case-control approaches were designed and employed for this purpose. ResultsThe results taken from the two employed approaches (i.e. 76.7% total agreement and 68.4% agreement on the existence of some significant effect) provide evidence for the potential effect of prescription sequence on ADRs development evidenced by the discovery that certain sequential patterns occurred more frequently in one group of patients than the other. ConclusionGiven the significant effects shown by our data analyses, we believe that design and implementation of automated clinical decision support systems to constantly monitor patients’ medication transactions (and the sequence in which they are administered) and make appropriate alerts to prevent certain possible ADRs, may decrease ADR occurrences and save lives and money.

Tolvaptan alleviates excessive fluid retention of nephrotic diabetic renal failure unresponsive to furosemide.

Patients with diabetic nephropathy develop nephrotic syndrome and may show limited response to conventional therapy. They often require earlier initiation of renal replacement therapy because they become refractory to diuretics, and experience excessive fluid retention. We aimed to investigate the efficacy of tolvaptan, an oral arginine vasopressin type 2 receptor antagonist, in a case series of 14 severe diabetic renal failure patients who were severely refractory to maximal doses of furosemide and had excessive fluid retention despite preserved cardiac function and residual renal function. All 14 patients experienced immediate and sustained water diuretic effects, resulting in alleviation of congestive heart failure. None required initiation of renal replacement therapy. Tolvaptan promptly increased urine volume and free water clearance, reversed progressive fluid retention, and alleviated congestive heart failure. Thus, tolvaptan could serve as a potential adjunct therapy for severe diabetic renal failure patients with excessive fluid retention and congestive heart failure.

Urinary Vitamin-D Binding Protein as an Early Predictor of Diabetic Nephropathyin Type 1 and Type 2 Diabetes

Diabetic nephropathy (DN) is the most common microvascular complication that may lead to chronic renal failure in diabetic patients. Till now microalbuminuria, with its restrictions, is the early marker of DN, appeared after the disease exacerbation. Thus, new biomarkers are required to predict the early onset of DN before the appearance of microalbuminuria. The aim of this study is to investigate the possible use of uVDBP in the early prediction of DN. Fifty diabetic patients with DN and 40 diabetic patients without DN for both types of diabetes were enrolled in this study. All patients were tested for uACR, uVDBP (measured by ELISA), and blood HbA1c. The results demonstrated a highly significant elevation of uACR, HbA1c and uVDBP in diabetic patients with DN compared to those without DN. uVDBP exhibited a strong positive correlation with HbA1c and uACR in DN patients. ROC curve analysis showed a greater AUC (0.93), and cutoff value was >152 ng/ml with 94% sensitivity and 82% specificity for early detection of DN. These findings suggesting the sensitive and potential role of uVDBP in the early prediction and diagnosis of DN in type 1 and type 2 diabetes.

Role of phytotherapy in diabetic neuropathy and neurodegeneration: from pathogenesis to treatment

Diabetes mellitus is a metabolic disorder associated with structural and functional alterations of various organ systems. The tissue injury is attributed primarily to chronic hyperglycemia. Diabetic complications are associated with microvascular and macrovascular damage to the major organs of the body, here in this topic role of herbals for complications of Nervous system in diabetes is discussed as a new therapeutic horizon. Peripheral neuropathy along with the small and large blood vessel disease can explain most of the diabetesrelated organ failure, over the last two decades that the deleterious effects of chronic hyperglycemia extend beyond neuropathy and angiopathy. Examples of such diabetic complications include opacification of the lens and central nervous system [CNS] dysfunction. In contrast to the high prevalence rate of renal failure in diabetic patients, except for retinal disease, the chronic diabetic complications of the CNS are subtle and often unrecognized. Whereas the CNS effects of acute alterations in blood glucose level are well known, the effect of chronic hyperglycemia on brain metabolism and cognitive function is not widely appreciated. All the conventional therapies for the diabetic neuropathy with neurodegeneration do have disadvantage from the point of view of efficacy and side effects. Since last few decades Herbals getting more attraction towards neuroprotection in CNS complications of diabetes, further more studies are going on herbals for neuroprotection in diabetes. In the treatment of diabetic neuropathy [DN] herbals and phytoconstituents were proved better option, because excellent efficacy and cost effectiveness compared to conventional treatment.

Presentation and outcome of acute renal failure in diabetic patients

Presentation and outcome of acute renal failure in diabetic patients

Association of Serum Prolactin Concentrations with Renal Failure in Diabetic Patients

Abstract Background and aims: Diabetes is one of the causes of end-stage renal disease, so that about 70% of all diabetic patients have nephropathy. Prolactin is a hormone that is affected by diabetes but the interaction between diabetes and prolactin has not been understood properly. This study aimed to evaluate the relationship between changes in serum prolactin levels in diabetic patients with renal failure. Material and methods: In this study 223 individuals were participated and after assessment of inclusion/exclusion criteria 189 individuals were evaluated. Finally, the individuals were divided into three groups: Control (C), Diabetic (D), and Diabetic Nephropathy (DN). Blood samples were collected between 8.00 a.m. and 12.00 a.m. for measurement of prolactin levels and biochemical analysis. Results: The results showed that sodium, potassium, urea, creatinine and prolactin significantly increased in DN group compared to control individuals (P< 0.001). The prolactin levels were significantly decreased in the group of patients with diabetes (P< 0.001). Conclusion: The results of the current study indicated that serum prolactin level decreased in diabetes while it increased in diabetic nephropathy.

The superoxide dismutase mimetic tempol blunts diabetes-induced upregulation of NADPH oxidase and endoplasmic reticulum stress in a rat model of diabetic nephropathy

Endoplasmic reticulum (ER) stress contributes to progression of diabetic nephropathy, which promotes end-stage renal failure in diabetic patients. This study was undertaken to investigate the actions of tempol and ramipril, pharmacological agents that target the consequences of NADPH oxidase, on diabetic nephropathy in a rat model of type 1 diabetes, with an emphasis on markers of ER stress. Male Sprague-Dawley rats were injected intravenously with a single bolus of streptozotocin (55mg/kg) to induce type 1 diabetes. An additional age-matched group of rats was administered with citrate vehicle as controls. After 4 weeks of untreated diabetes, rats received tempol (1.5mM/kg/day subcutaneously, n=8), ramipril (1mg/kg/day in drinking water, n=8) or remained untreated for an additional 4 weeks (n=7). After 8 weeks of diabetes in total, kidneys were collected for histological analysis, gene expression and protein abundance. Tempol and ramipril blunted diabetes-induced upregulation of NADPH oxidase isoforms (Nox4, Nox2, p47phox), accompanied by an amelioration of diabetes-induced glomerular injury (podocin, nephrin, Kim-1), tubulo-interstitial fibrosis (TGFβ1, TGFβ-R2, pSMAD3, α-SMA) and pro-inflammatory cytokines (TNFα, MCP-1, ANX-A1, FPR2) expression. In addition, the diabetes-induced renal ER stress, evidenced by increased expression of GRP-78 chaperone and stress-associated markers ATF4, TRB3, as well as XBP1s, phospho-p38 mitogen-activated protein kinase (MAPK) and 3-nitrotyrosination, were all attenuated by tempol and ramipril. These observations suggest that antioxidant approaches that blunt NADPH upregulation may attenuate diabetic nephropathy, at least in part by negatively regulating ER stress and inflammation, and hence ameliorating kidney damage.

Study of Serum urea and Creatinine in Diabetic and non-diabetic patients in in a tertiary teaching hospital

Introduction: Diabetes is on the rise worldwide and India has more number of diabetics with more than 60 million people diagnosed to suffer from the disease in 2013. Approximately 20% to 30% of all diabetics will develop evidence of nephropathy, although a higher percentage of type 1 patients progress to end stage renal disease. Diabetic nephropathy (DN) is characterised by macro albuminuria and abnormal renal function as represented by a reduction in glomerular filtration and rise in serum urea and creatinine. Aim & Objectives: The aim of this study was to study the relationship between blood levels of urea and creatinine with blood glucose levels in diabetic and non-diabetic subjects for their utility in diagnosis of diabetic nephropathy and their comparison with glycemic status. Material and Methods: Diabetic and non-diabetic subjects; 100 in each group; attending out- patient department during 15 May to 15 September 2015 were studied. Patients with known kidney disease were excluded. Blood samples were analysed for blood sugar (glucose), serum urea and creatinine to determine presence of kidney disease and hyperglycemia on basis of reference laboratory standards in the institute. Results: Out of 100 diabetes samples, 18 had high urea level whereas 15 had increased creatinine level. In control group of 100 sample, there was no one with high urea value and 2 had high creatinine level. There was statistically significant increase in urea level with increased blood sugar level (p<0.05, 95%CI). Conclusion: Serum urea and creatinine are useful, simple biomarkers as predictor and prognostic tests of renal failure in diabetic patients, despite some limitations.

Usefulness of the BAST-24 smell and taste test in the study of diabetic patients: a new approach to the determination of renal function

Conclusion: A reduction in the percentage of correct responses in the olfactory test indirectly indicated increased albuminuria and worse glomerular filtration rate (GFR) in diabetic patients. The olfactory function test is an indirect indicator of early microvascular complications in diabetic patients. Objectives: Diabetes mellitus is a highly prevalent disease that causes numerous complications. The aim of this study was to determine whether olfactory and taste sensations are related to renal failure in diabetic patients. Methods: We studied 61 patients diagnosed with diabetes mellitus, mean age = 65.9 years (SD = 16.8), 54.1% male. We evaluated olfactory and taste sensations by determining the capacity of detection, identification and percentage of correct responses of the 29 components of the Barcelona Smell-taste Test-24 (BAST-24). We determined the relationship between these results and glycosylated haemoglobin (HbA1c), creatinine, albumin/creatinine, albuminuria and GFR (normal = GFR ≥ 60 ml/min/1.73 m2; impaired renal function = GFR < 60 ml/min/1.73 m2). Results: There was no significant relationship between HbA1c and olfactory and taste sensations. There was a significant relationship between the percentage of correct responses and albuminuria (p = 0.03) and between identification of odours through the olfactory nerve and GFR (p = 0.029), and the percentage of correct responses and GFR (p = 0.03). There was no significant relationship between taste and renal failure.

Serum uric acid and diabetic nephropathy.

Implication for health policy/practice/research/medical education:Diabetic nephropathy is the most common cause of end-stage renal disease worldwide. Recently, some prospective randomized controlled trials suggested that lowering of uric acid with allopurinol could decrease the severity of proteinuria and probably slow the progression of renal failure in diabetic patients. Mechanism of beneficial effect of xanthine oxidase inhibitor may related to preventing uric acid-induced renal inflammation.

Chronic renal failure in diabetic patients increases lipid risk factors for atherosclerosis

Diabetic patients are at high risk of cardiovascular disease and the risk is amplified in the presence of nephropathy, which may be partially attributed to modifications in lipoproteins. Moreover, lipoprotein profile may be affected by incipient nephropathy, glomerulopathy, and mild or severe renal failure. The aim of our study was to evaluate whether chronic renal failure (CRF) changes lipoprotein profile and apo A-I urinary excretion in diabetic subjects with glomerulopathy in comparison with non-diabetic subjects with glomerulopathy and CRF. Diabetic ( n = 25) and non-diabetic ( n = 10) patients with glomerulopathy and CRF showed significantly higher LDL-cholesterol, non-HDL-cholesterol and HDL-triglyceride levels than diabetic individuals without CRF ( n = 10). Arylesterase and paraoxonase activities did not show any difference between groups. Apo A-I could not be detected in urine samples from diabetic patients without CRF. All diabetic subjects with glomerulopathy and CRF who presented proteinuria above 6.5 g/24 h showed detectable urinary apo A-I (range = 13.1–61.0 mg/24 h). Similarly, all non-diabetic patients with glomerulopathy and CRF who had proteinuria above 8.0 g/24 h also evidenced detectable apo A-I in urine (range = 25.6–557.3 mg/24 h). Urinary apo A-I showed positive and significant correlations with urea ( r = 0.73, p < 0.05) and proteinuria ( r = 0.97, p < 0.0001), and a negative correlation with albumin plasma levels ( r = −0.68, p < 0.05). In conclusion, the presence of CRF in diabetic patients was associated with a more atherogenic lipoprotein profile.