Diabetic Renal Disease Research Articles

“A Case Report on T2dm With Systemic Amyloidosis Leading To Non Diabetic Renal Disease.”

“A Case Report on T2dm With Systemic Amyloidosis Leading To Non Diabetic Renal Disease.”

Cardiovascular disease biomarkers are associated with declining renal function in type 2 diabetes

Aims/hypothesisWe investigated whether biochemical cardiovascular risk factors and/or markers of subclinical cardiovascular disease were associated with the development of reduced renal function in people with type 2 diabetes.MethodsA cohort of 1066 Scottish men and women aged 60–74 years with type 2 diabetes from the Edinburgh Type 2 Diabetes Study were followed up for a median of 6.7 years. New-onset reduced renal function was defined as two eGFRs <60 ml−1 min−1 (1.73 m)−2 at least 3 months apart with a > 25% decline from baseline eGFR. Ankle brachial pressure index (ABI), N-terminal pro-B-type natriuretic peptide (NT-proBNP) and high-sensitivity troponin T (hsTnT) were measured at baseline. Pulse wave velocity (PWV) and carotid intima media thickness were measured 1 year into follow-up. Data were analysed using Cox proportional hazards models.ResultsA total of 119 participants developed reduced renal function during follow-up. ABI, PWV, NT-proBNP and hsTnT were all associated with onset of decline in renal function following adjustment for age and sex. These associations were attenuated after adjustment for additional diabetes renal disease risk factors (systolic BP, baseline eGFR, albumin:creatinine ratio and smoking pack-years), with the exception of hsTnT which remained independently associated (HR 1.51 [95% CI 1.22, 1.87]). Inclusion of hsTnT in a predictive model improved the continuous net reclassification index by 0.165 (0.008, 0.286).Conclusions/interpretationOur findings demonstrate an association between hsTnT, a marker of subclinical cardiac ischaemia, and subsequent renal function decline. Further research is required to establish the predictive value of hsTnT and response to intervention.

Melioidosis: Clinical impact and public health threat in the tropics.

This review briefly summarizes the geographical distribution and clinical impact of melioidosis, especially in the tropics. Burkholderia pseudomallei (a gram-negative bacterium) is the major causative agent for melioidosis, which is prevalent in Singapore, Malaysia, Thailand, Vietnam, and Northern Australia. Melioidosis patients are increasingly being recognized in other parts of the world. The bacteria are intrinsically resistant to many antimicrobial agents, but prolonged treatment, especially with combinations of antibiotics, may be effective. Despite therapy, the overall case fatality rate of septicemia in melioidosis remains significantly high. Intracellular survival of the bacteria within macrophages may progress to chronic infections, and about 10% of patients suffer relapses. In the coming decades, melioidosis will increasingly afflict travelers throughout many global regions. Clinicians managing travelers returning from the subtropics or tropics with severe pneumonia or septicemia should consider acute melioidosis as a differential diagnosis. Patients with open skin wounds, diabetes, or chronic renal disease are at higher risk for melioidosis and should avoid direct contact with soil and standing water in endemic regions. Furthermore, there are fears that B. pseudomallei may be used as a biological weapon. Technological advancements in molecular diagnostics and antibiotic therapy are improving the disease outcomes in endemic areas throughout Asia. Research and development efforts on vaccine candidates against melioidosis are ongoing.

Efficacy of Saxagliptin versus Mitiglinid in patients with type 2 diabetes and end-stage renal disease

BackgroundThere are very few oral antidiabetic drugs recommended for patients on dialysis. Saxagliptin is known for its potent effect and long duration of action. In this study, we compared the efficacy of Saxagliptin with Mitiglinid for diabetes control and renal anemia in hemodialysis patients with type 2 diabetes mellitus.MethodsWe performed a 6-month prospective, open-label, parallel group study of 41 patients with type 2 diabetes mellitus undergoing hemodialysis who took alpha-glucosidase inhibitors or meglitinides and did not use insulin. Saxagliptin and Mitiglinid were administered at 2.5 and 5 mg/day, respectively. The primary outcomes were changes in hemoglobin A1c (HbA1c) and glycated albumin (GA). Other efficacy assessments included changes in Hb, darbepoetin alpha (DA) dose, and erythropoietin responsiveness index (ERI).ResultsNo patient required an increase in Saxagliptin or Mitiglinid dose, and there were no cases of hypoglycemia with symptoms. HbA1c and GA values were not significantly different between both groups. For HbA1c, the gradient of the regression line of the Saxagliptin and Mitiglinid groups were Y = −7.144e-005*X + 6.023 and Y = −0.02604*X + 6.292, respectively, and no significant difference was found (p = 0.3281). However, for GA, the regression line of the Saxagliptin group significantly decreased (Y = −0.5036*X + 19.34 and Y = −0.2346*X + 18.79, p = 0.0371). Both groups did not have a significant change in the DA dose through the observation period. However, the DA dose of the Saxagliptin group significantly decreased when we compared the regression lines (Y = −0.8304*X + 21.06 and Y = 0.6286*X + 16.12, p = 0.0019) of both groups. Furthermore, ERI did not change significantly but showed a significant difference when regression lines were compared (Y = −0.2030*X + 6.654 and Y = 0.1116*X + 5.288, p = 0.0082).ConclusionsThe present study showed that Saxagliptin was not inferior to Mitiglinid in the glycemic control of ESRD patients with type 2 diabetes mellitus, and it is well tolerated and safe. Saxagliptin may also improve bioavailability of iron compared to Mitiglinid, but long-term follow-up in a large scale study with more precise ferrokinetic marker measurements are necessary to confirm these results.

Treatment choices for managing glucose control in impaired renal function: Interim Results

ABSTRACT&#x0D; ObjectivesPatients with chronic kidney disease (CKD ≥3) and diabetes mellitus comprise approximately 25% patients with diabetes. These patients are at a higher risk of cardiovascular morbidity and mortality and furthermore therapies targeting glucose control are limited. The management of glycaemic control in type 2 diabetes and chronic renal disease is difficult with limited therapeutic choices. This issue has been a matter of longstanding debate. Following a number of joint Diabetes-Renal meetings between the Diabetes and Renal teams based in Hywel Dda and ABM University Health Boards, a proposal was put forward to the SAIL team to examine the relationship between diabetes therapies in relation to eGFR, as this may influence further practice and guidance for patients with type 2 diabetes and renal impairment.&#x0D; ApproachLinkage and re-use of routinely collected anonymised clinical data held in the SAIL databank was employed, to identify a cohort of adult patients in Abertawe Bro Morgannwg Health Board (ABMU) having type 2 diabetes (excluding type 1 diabetes). Diagnosis of diabetes was achieved by use of National Health Service ‘Read’ codes. Creatinine, eGFR, age, gender, weight, height, cholesterol, LDL, HDL, TG, systolic blood pressure, diastolic blood pressure, diabetes medication prescriptions, the use of statins, ACEis, aspirin, CHD status, CVD status, duration of diabetes were identified in primary care GP and pathology datasets.&#x0D; Results42170 (6.0%) of adults in ABMU were identified as having type 2 (excluding type 1) diabetes , 13369 of which had good GP registration coverage. The gender split was male 56%, female 44%. Duration of diabetes (years) was (mean/median/SD/IQR) 9.96/8.97/6.78/8.10; weight (Kg) was 86.94/85.00/21.23/28.19; age (years) 65.49/66.74/13.75/19.03; BMI 31.57/30.70/6.62/7.99. Incidence of CKD as defined by GP coded data was 24%, renal replacement therapy 0.4%, Ischaemic Heart Disease 22%. Prevalence of prescriptions during 2014 was: Anti-diabetic medication 72%, statins 75%, aspirin 34%, ACEi/ARB 61%. The import of pathology laboratory data into SAIL is currently pending, and is anticipated before April 2016. This will allow the accurate stratification of CKD status and detailed description of use of anti-diabetic agents.&#x0D; ConclusionThe project methods and coding structure are well place to provide anticipated results as soon as pathology data arrives. The percentage of ABMU patients having type 2 diabetes is in line with other literature for adults in the UK.

Abstract 30: Effect of Adipose Stromal Vascular Fraction on Random Pattern Flap Viability in Rats With Diabetes And Chronic Renal Disease: An Experimental Study

Corrected and republished with permission from the European Plastic Surgery Research Council Meeting 2016 supplement to the January 2017 compendium of PRS Global Open. Ozkan B, Çagri Uysal A, Terzi A, Özturan Özer E. Abstract: 11.10 Effect of adipose stromal vascular fraction on random pattern flap viability in rats with diabetes and chronic renal disease: an experimental study. Plast Reconstr Surg Glob Open 2017;5(1S):7. DOI: 10.1097/01.GOX.0000512409.03081.d3 Please refer to Correction Notice on page 127 of this supplement. INTRODUCTION: Diabetes (DM) and chronic renal disease (CRD) are epidemic diseases with increasing prevalence. Wounds due to microangiopathy and macroangiopathy tend to heal slowly which can lead to severe morbidites such as amputations. High flap failure rates reported in the reconstruction of these wounds. Studies have shown increased flap viability by adipose derived stromal vascular fraction (SVF). However; there is no study in the literature about the effect of adipose stromal vascular fraction on skin flap viability in chronic renal disease and diabetes with chronic renal disease. MATERIALS AND METHODS: 48 male Sprague Dawley rats were used. Diabetes was induced by 65mg/kg intraperitoneal streptozocin administiration. Chronic renal disease was induced by 5/6 nephrectomy. Four groups consisting of 12 rats were formed. 2 rats were used for obtaining adipose tissue from the inguinal regions for stromal vascular fraction preparation in each group. Group I (Control group): Two dorsal flaps were elevated, phosphate buffered saline (PBS) were injected to the flaps. Group II (DM), Group III(CRD), Group IV(DM+CRD): After disease induction and period;, two dorsal flaps were elevated, SVF were injected to the left flap, PBS were injected to the right flap. Flaps were harvested for macroscopic and histopathological assessments at postoperative 7th day. Percentage of flap viability measurement and microangiography were performed for macroscopic assessment. Capillary density assessment were evaluated in both hemotoxylin-eosin and CD31 stained specimens for microscopic assessment. Plasma levels of VEGF were studied in all rats at day 1 and day 7. RESULTS: SVF was improved flap viability significantly (p<0,05). New capillary formation found significantly more in SVF groups in capillary density assessment (p<0,05). This result was compatible with the scarcity of the vasculature in microangiography. When blood VEGF levels were compared, increase in day 1 and day 7 were significant according to control group (p<0,05). When groups were compared each other there were not significant difference except Group II(diabetes). CONCLUSIONS: The result of the study has shown that DM and CRD impaired flap viability. Diabetes with chronic renal disease deteriorated the flap viability much more. It has shown that SVF were increased flap viability via neovascularization by endothelial differentiation. Flap viability percentage was found lower in diabetic and uremic groups when compared with healthy control group. Blood VEGF levels were not elevated in uremic groups. This results were indicated that in vivo function of stem cells were possibly impaired by uremia dominantly and diabetes due to microenviromental changings.

Decreased incidence of end-stage renal disease in American Indians with diabetes: a model for other high-risk populations?

Indigenous populations in North America have very high rates of diabetes and diabetic complications, including end-stage renal disease. A promising new report demonstrates a substantial decline in the incidence of diabetic end-stage renal disease among American Indians and Alaska Natives, coinciding with a public health intervention targeting diabetes management in this population. This success may offer a model for interventions to improve kidney disease outcomes in other high-risk populations.

Association of rs 3807337 polymorphism of CALD1 gene with diabetic nephropathy occurrence in type 1 diabetes - preliminary results of a family-based study.

The worldwide growing burden of diabetes and end-stage renal disease due to diabetic nephropathy has become the reason for research looking for a single marker of chronic kidney disease development and progression that can be found in the early stages of the disease, when preventive action delaying the destructive process could be performed. The aim of the study was to investigate the influence of rs3807337 polymorphism of the caldesmon 1 (CALD1) gene located on the long arm of chromosome 7 encoding for protein that is connected with physiological kidney function on development of diabetic nephropathy. There was an association study of rs3807337 polymorphism of the CALD1 gene in parent-offspring trios by PCRRFLP method. Ninety-nine subjects: 33 patients with diabetic nephropathy due to type 1 diabetes and 66 of their biological parents, were examined. The mode of alleles transmission from heterozygous parents to affected offspring was determined using the transmission disequilibrium test. The allele G of rs3807337 polymorphism of the CALD1 gene was transmitted to affected offspring significantly more often than expected for no association. The obtained results suggest that the genetic variability of the CALD1 gene may influence the development of diabetic nephropathy in type 1 diabetes, but further studies involving larger studied groups of patients are needed. (Endokrynol Pol 2017; 68 (1): 13-17).

SGLT2 Protein Expression Is Increased in Human Diabetic Nephropathy: SGLT2 PROTEIN INHIBITION DECREASES RENAL LIPID ACCUMULATION, INFLAMMATION, AND THE DEVELOPMENT OF NEPHROPATHY IN DIABETIC MICE

There is very limited human renal sodium gradient-dependent glucose transporter protein (SGLT2) mRNA and protein expression data reported in the literature. The first aim of this study was to determine SGLT2 mRNA and protein levels in human and animal models of diabetic nephropathy. We have found that the expression of SGLT2 mRNA and protein is increased in renal biopsies from human subjects with diabetic nephropathy. This is in contrast to db-db mice that had no changes in renal SGLT2 protein expression. Furthermore, the effect of SGLT2 inhibition on renal lipid content and inflammation is not known. The second aim of this study was to determine the potential mechanisms of beneficial effects of SGLT2 inhibition in the progression of diabetic renal disease. We treated db/db mice with a selective SGLT2 inhibitor JNJ 39933673. We found that SGLT2 inhibition caused marked decreases in systolic blood pressure, kidney weight/body weight ratio, urinary albumin, and urinary thiobarbituric acid-reacting substances. SGLT2 inhibition prevented renal lipid accumulation via inhibition of carbohydrate-responsive element-binding protein-β, pyruvate kinase L, SCD-1, and DGAT1, key transcriptional factors and enzymes that mediate fatty acid and triglyceride synthesis. SGLT2 inhibition also prevented inflammation via inhibition of CD68 macrophage accumulation and expression of p65, TLR4, MCP-1, and osteopontin. These effects were associated with reduced mesangial expansion, accumulation of the extracellular matrix proteins fibronectin and type IV collagen, and loss of podocyte markers WT1 and synaptopodin, as determined by immunofluorescence microscopy. In summary, our study showed that SGLT2 inhibition modulates renal lipid metabolism and inflammation and prevents the development of nephropathy in db/db mice.

Quality of life in Japanese patients with type 1 diabetes and end-stage renal disease undergoing simultaneous pancreas and kidney transplantation.

We conducted this cross-sectional study to assess quality of life (QOL) in Japanese patients with type 1 diabetes mellitus (T1DM) and end-stage renal disease (ESRD) undergoing simultaneous pancreas and kidney transplantation (SPK). Japanese patients with T1DM without diabetic nephropathy (N=10), and those undergoing chronic dialysis (N=52), kidney transplantation alone (KTA, N=25), and SPK (N=16) were studied. Comprehensive health-related QOL was assessed using the Short Form 36 version 2 (SF-36v2). Emotional functioning in diabetes was measured by the Problem Area In Diabetes (PAID) scale. Severity of impaired hypoglycemic awareness was assessed using the Clarke hypoglycemic score. SPK patients had significantly higher (or tended to have higher) subscale and summary SF-36 scores than dialysis patients and KTA patients. PAID scores were significantly lower in SPK patients than in dialysis patients and KTA patients. Clarke hypoglycemic scores were also significantly lower in SPK patients than dialysis patients. In KTA and dialysis patients, there were no significant differences in the SF-36 subscale/summary scores, PAID scores, or Clarke hypoglycemic scores. In conclusion, QOL for Japanese patients receiving SPK may be superior to that of dialysis patients and KTA patients. Whether SPK actually improves QOL needs to be clarified in longitudinal studies.

Enhanced expression of two discrete isoforms of matrix metalloproteinase-2 in experimental and human diabetic nephropathy.

BackgroundWe recently reported on the enhanced expression of two isoforms of matrix metalloproteinase-2 (MMP-2) in human renal transplantation delayed graft function. These consist of the conventional secreted, full length MMP-2 isoform (FL-MMP-2) and a novel intracellular N-Terminal Truncated isoform (NTT-MMP-2) generated by oxidative stress-mediated activation of an alternate promoter in the MMP-2 first intron. Here we evaluated the effect of hyperglycemia and diabetes mellitus on the in vitro and in vivo expression of the two MMP-2 isoforms.MethodsWe quantified the abundance of the FL-MMP-2 and NTT-MMP-2 transcripts by qPCR in HK2 cells cultured in high glucose or 4-hydroxy-2-hexenal (HHE) and tested the effects of the NF-κB inhibitor pyrrolidine dithiocarbamate (PDTC). The streptozotocin (STZ) murine model of Type I diabetes mellitus and renal biopsies of human diabetic nephropathy were used in this study.ResultsBoth isoforms of MMP-2 in HK2 cells were upregulated by culture in high glucose or with HHE. PDTC treatment did not suppress high glucose-mediated FL-MMP-2 expression but potently inhibited NTT-MMP-2 expression. With STZ-treated mice, renal cortical expression of both isoforms was increased (FL-MMP-2, 1.8-fold; NTT-MMP-2, greater than 7-fold). Isoform-specific immunohistochemical staining revealed low, but detectable levels of the FL-MMP-2 isoform in controls, while NTT-MMP-2 was not detected. While there was a modest increase in tubular epithelial cell staining for FL-MMP-2 in STZ-treated mice, NTT-MMP-2 was intensely expressed in a basolateral pattern. FL-MMP-2 and NTT-MMP-2 isoform expression as quantified by qPCR were both significantly elevated in renal biopsies of human diabetic nephropathy (12-fold and 3-fold, respectively).ConclusionsThe expression of both isoforms of MMP-2 was enhanced in an experimental model of diabetic nephropathy and in human diabetic nephropathy. Selective MMP-2 isoform inhibition could offer a novel approach for the treatment of diabetic renal disease.

Etiology of End-Stage Renal Disease and Arterial Stiffness among Hemodialysis Patients.

Background. Prior studies have demonstrated that conventional and emerging CV risk factors are associated with worsening arterial stiffness among end-stage renal disease (ESRD) patients on hemodialysis. The present cross-sectional study evaluates the association between the etiology of ESRD and arterial stiffness among a cohort of hemodialysis patients. Methods. Etiology of ESRD was identified from patients' medical records and classified as either vascular renal disease, diabetic nephropathy, nondiabetic glomerulopathy, tubular interstitial nephropathy, hereditary nephropathy, or ESRD of unconfirmed etiology. Results. A total of 82 subjects were enrolled. cfPWV was independently associated with the composite of either diabetic nephropathy or vascular renal disease (p = 0.022), pulse pressure (p = 0.001), and a history of CV events (p = 0.025), but not history of hypertension or diabetes mellitus alone. The median cfPWVs in diabetic nephropathy and vascular renal disease were comparable and significantly higher than median cfPWVs in other etiologies of ESRD. Conclusion. The study suggests that the etiology of ESRD is independently associated with arterial stiffness among hemodialysis patients. Furthermore, arterial stiffness was higher among patients who developed renal sequelae of either diabetes mellitus or hypertension as compared with those who have a history of either diabetes mellitus or hypertension alone.

Curcumin Ameliorates Diabetic Nephropathy by Suppressing NLRP3 Inflammasome Signaling.

Diabetic nephropathy (DN) is the leading cause of end-stage renal disease, partly because of the lack of effective treatments for DN. Curcumin has been shown to exert strong antifibrotic effects in DN, but the underlying mechanisms are not well characterized. In this study, we sought to determine the effects of curcumin on diabetic renal disease in db/db mice and characterize the underlying mechanism of action. We administered curcumin to db/db mice for 16 weeks. In comparison to mock-treated db/db mice, curcumin-treated mice showed diminished renal hypertrophy, reduced mesangial matrix expansion, and a lower level of albuminuria. Furthermore, the upregulated protein and mRNA expressions of collagen IV and fibronectin in the renal cortices of the db/db mice were inhibited by curcumin treatment. Additionally, curcumin treatment was associated with significant reductions in mature interleukin-1β, cleaved caspase-1, and NLRP3 protein levels in the renal cortices of db/db mice as well as in HK-2 cells exposed to high glucose concentration. In summary, curcumin, a potent antifibrotic agent, is a promising treatment for DN, and its renoprotective effects appear to be mediated by the inhibition of NLRP3 inflammasome activity.

Morbidity, Mortality and Costs Associated with Venous Thromboembolism in Hospitalized Patients with Cancer

Background: Venous thromboembolism (VTE) represents a leading cause of morbidity and mortality among hospitalized patients with cancer. Methods: Hospitalization data reported on adult cancer patients at US academic medical centers and affiliated hospitals between 1995 and 2012 were analyzed. Cancer diagnosis, presence of VTE, comorbidities and complications were based on ICD-9-CM codes. Major comorbidities considered were diabetes, and cerebrovascular, peripheral-vascular, heart, liver, and lung renal disease. In patients with multiple hospitalizations during the time period, a randomly selected hospitalization was utilized in the analysis. Hospitalization cost estimates were inflation adjusted to 2015 US dollars. Results: Nearly 6 million hospitalizations of 3,146,388 individual patients with cancer from more than 200 institutions were evaluated. VTE was reported in 8.4% of patients when all admissions are considered during the time period. When a single selected hospitalization is considered for each patient, VTE was reported in 166,547 (5.3%) of individual patients including 56,125 (1.8%) with pulmonary embolism (PE). The annual rate of VTE increased progressively from 3.5% in 1995 to over 6.5% in 2012 with the rate of PE nearly tripling from 0.8% in 1995 to 2.3% in 2012. For hospitalized patients receiving cancer chemotherapy, the annual rate of VTE more than doubled from 3.6% in 1995 to 8.3% in 2012. VTE was reported in 5.2%, 5.8% and 5.4% of patients with solid tumors, lymphoma, and leukemia, respectively (Table). Rates of VTE were greatest among patients with pancreatic (10.2%), gastric (7.1%) or other abdominal malignancies except colorectal cancer (9.2%) as well as those with ovarian (7.1%), lung (6.8%) and esophageal cancers (6.3%). The risk of VTE increased progressively from 2.3% in those with no comorbidities to over 11% for patients with 4 or more comorbid conditions. The strongest risk factors for VTE were infectious complications including sepsis (14%), invasive candidiasis (16%), pneumonia (11%) and IV line infections (14%).During this same time period, imaging related to VTE actually decreased with significantly lower rates of CT, vascular ultrasound and ventilation perfusion lung scans reported. In-hospital mortality was reported in 5.5% of cancer patients without VTE and in 15.0% of those with VTE including 19.4% of those with pulmonary embolism. In-hospital mortality during this time period decreased by approximately one-third in cancer patients both with and without VTE. While reported rates of VTE increased, the length of hospital stay shortened for patients with as well as without VTE during this period. Average costs per hospitalization adjusted to 2015 dollars for patients with and without VTE were $37,352 and $19,994, respectively. The estimated average inflation adjusted daily cost of hospitalization for patients with cancer and VTE increased nearly 50% between 1995 ($2,256) and 2012 ($3,297). Conclusions: VTE reported among hospitalized patients with cancer has increased significantly during the period of observation along with the cost of hospitalization while in-hospital mortality and imaging rates have decreased. However, patients with additional major medical comorbidities are at exceptionally high risk of serious complications including in-hospital mortality. Disclosures Lyman: Amgen: Research Funding. Kuderer:Janssen Scientific Affairs, LLC: Consultancy, Honoraria.

Clinical determinants of the severity of Middle East respiratory syndrome (MERS): a systematic review and meta-analysis.

BackgroundWhile the risk of severe complications of Middle East respiratory syndrome (MERS) and its determinants have been explored in previous studies, a systematic analysis of published articles with different designs and populations has yet to be conducted. The present study aimed to systematically review the risk of death associated with MERS as well as risk factors for associated complications.MethodsPubMed and Web of Science databases were searched for clinical and epidemiological studies on confirmed cases of MERS. Eligible articles reported clinical outcomes, especially severe complications or death associated with MERS. Risks of admission to intensive care unit (ICU), mechanical ventilation and death were estimated. Subsequently, potential associations between MERS-associated death and age, sex, underlying medical conditions and study design were explored.ResultsA total of 25 eligible articles were identified. The case fatality risk ranged from 14.5 to 100%, with the pooled estimate at 39.1%. The risks of ICU admission and mechanical ventilation ranged from 44.4 to 100% and from 25.0 to 100%, with pooled estimates at 78.2 and 73.0%, respectively. These risks showed a substantial heterogeneity among the identified studies, and appeared to be the highest in case studies focusing on ICU cases. We identified older age, male sex and underlying medical conditions, including diabetes mellitus, renal disease, respiratory disease, heart disease and hypertension, as clinical predictors of death associated with MERS. In ICU case studies, the expected odds ratios (OR) of death among patients with underlying heart disease or renal disease to patients without such comorbidities were 0.6 (95% Confidence Interval (CI): 0.1, 4.3) and 0.6 (95% CI: 0.0, 2.1), respectively, while the ORs were 3.8 (95% CI: 3.4, 4.2) and 2.4 (95% CI: 2.0, 2.9), respectively, in studies with other types of designs.ConclusionsThe heterogeneity for the risk of death and severe manifestations was substantially high among the studies, and varying study designs was one of the underlying reasons for this heterogeneity. A statistical estimation of the risk of MERS death and identification of risk factors must be conducted, particularly considering the study design and potential biases associated with case detection and diagnosis.Electronic supplementary materialThe online version of this article (doi:10.1186/s12889-016-3881-4) contains supplementary material, which is available to authorized users.

Influence of Donor and Recipient Ages in Survival of Simultaneous Pancreas-Kidney Transplantation

IntroductionSimultaneous pancreas-kidney transplantation (SPKT) is a well treatment for patients with insulin-dependent diabetes and end-stage renal disease. Donor age is a barrier to the acceptance of organs. Age matching has been extensively studied in kidney transplantation; however, there are no studies in graft survival after SPKT. We aimed to study the combined influence of the ages of the donors and recipients in graft survival after SPKT. Material and MethodsDonors and recipients are classified as younger (age <40 years) or older (age ≥40 years). There were four study groups (young-young, young-old, old-young, and old-old). They were evaluated retrospectively for demographic and clinical characteristics of donors and recipients and the long-term survival between 2001 and 2012 of kidney pancreas transplantation patients at our center. ResultsA total of 115 transplantations were performed. The four groups had 55 young-young, 40 young-old, 10 old-young, and 10 old-old patients. Serious complications occurred in 32%, 42%, 30%, and 40%, respectively, and deaths were 2%, 5%, 0%, and 20%, respectively, in the groups. Pancreas graft survival at 3 years for each group was 80%, 87, 5%, 90%, and 60%, respectively, and kidney graft survival was 92.7%, 90%, 90%, and 70%, respectively. Panel-reactive antibodies (PRAs) >30% were associated with poor graft survival, and serious postoperative complications associated with poor pancreas-kidney graft survival. ConclusionsIn conclusion, both younger and older recipients show excellent long-term graft and patient survival after SPKTs from younger donors. We recommended that older-recipient SPKT be transplanted from younger donors because older recipients who have been transplanted from older donors had decreased survival.

Impact of kidney transplant on hypertension in diabetic end-stage renal disease (ESRD) patients

Impact of kidney transplant on hypertension in diabetic end-stage renal disease (ESRD) patients

Determinant Effects of Average Fasting Plasma Glucose on Mortality in Diabetic End-Stage Renal Disease Patients on Maintenance Hemodialysis

IntroductionDiabetic kidney disease is an increasingly frequent cause of end-stage renal disease. However, mixed results were shown between glycated hemoglobin and mortality.MethodsWe used the average fasting plasma glucose (FPG) levels to predict mortality rates in long-term hemodialysis patients. We enrolled 46,332 hemodialysis patients with diabetes mellitus, who were registered in the Taiwan Renal Registry Data System between January 2005 and December 2012. The patients were stratified based on the quartiles of average FPG levels measured for the first (1-year FPG) and third years (3-year FPG) of hemodialysis. Survival analysis was conducted via multivariable Cox regression.ResultsAfter the first year of hemodialysis, the mean FPG levels were 103.5 ± 14.5, 144.7 ± 11.5, 189.6 ± 15.2, and 280.8 ± 1.2 mg/dl for the first, second, third, and fourth quartile, respectively. The Kaplan-Meier curve showed an incremental reduction in the survival as FPG levels increased (P < 0.0001). In the Cox regression model, the adjusted hazard ratios were 1.15 (95% CI: 1.10–1.20), 1.30 (95% CI: 1.25–1.36), and 1.45 (95% CI: 1.39–1.51) for the pairwise comparisons between the first quartile and the second, third, and fourth quartile, respectively. Similar trends were observed by 3-year FPG. Patients whose FPG levels increased had a 22% increased risk (95% CI: 1.16–1.29) for all-cause mortality compared with patients whose FPG levels decreased.DiscussionOur results suggest that the average FPG levels are useful predictors of all-cause mortality in dialysis patients. In addition, an increasing trend in average FPG levels indicates poor survival.

PP.05.14] PREVALENCE OF HYPERKALEMIA IN MATCHED DIABETIC AND NON-DIABETIC PATIENTS WITH CHRONIC KIDNEY DISEASE

Objective: Hyperkalemia is a frequent and potentially life-threatening electrolyte disorder, usually complicating chronic kidney disease (CKD). Factors superimposed to reduced renal function, are further elevating the risk for hyperkalemia development, but their contribution is not fully elucidated in relevant literature. This study aimed to compare the prevalence of hyperkalemia in matched diabetic and non-diabetic patients with CKD and to evaluate factors associated with hyperkalemia occurrence. Design and method: This is a nested case-control study from a cohort of patients followed in a Nephrology outpatient clinic. A total of 180 type-2 diabetic and 180 non-diabetic patients with CKD matched for gender, age and eGFR, were included. Patients with type-1 diabetes or end-stage renal disease were excluded. Prevalence of hyperkalemia was defined as serum potassium > 5 mEq/L and/or use of sodium polystyrene sulfonate, and further by serum potassium levels >5 and greater or equal to 5.2 and 5.5 mEq/L. Prevalence was compared between the two study groups in total population and in CKD Stages separately. Univariate and multivariate logistic regression analysis were conducted to identify factors associated with hyperkalemia occurrence. Results: The prevalence of hyperkalemia was higher in diabetic CKD patients (27.2% vs 20%, p = 0.107) and remained around 30% higher with all secondary definitions used, but never reached statistical significance. In Stage 2 no difference was noted (8.7% vs 17.4%, p = 0.665), in Stage 3 prevalence was significantly higher in diabetics (28.6% vs 17.5%, p = 0.036) and in Stage 4 equally high in both groups (35.5% vs 32.3%, p = 0.788). In multivariate analysis, Stage 4 CKD (OR: 4.535, 95% CI: 1.561–13.173), use of angiotensine-converting enzyme inhibitors (OR: 2.228, 95%CI: 1.254–3.958), and smoking (OR: 2.254, 95%CI: 1.218–4.171) were independently associated with hyperkalemia. Conclusions: Diabetes mellitus is elevating the prevalence of hyperkalemia only in CKD Stage 3 patients (moderately impaired renal function) and this difference is attenuating in CKD Stage 4. Advanced CKD at Stage 4 and ACEIs are major determinants of hyperkalemia occurrence. As the vast majority of patients with CKD belong to Stage 3, the presence of diabetes must be appreciated regarding hyperkalemia risk and relevant therapeutic decisions.

WIfI Scores Predict Outcomes After Tibial Intervention in Patients With Diabetes and End-Stage Renal Disease

WIfI Scores Predict Outcomes After Tibial Intervention in Patients With Diabetes and End-Stage Renal Disease