scholarly journals Diabetes mellitus in dialysis and renal transplantation

2021 ◽  
Vol 12 ◽  
pp. 204201882110486
Author(s):  
Eyal Ben-David ◽  
Richard Hull ◽  
Debasish Banerjee

Diabetes mellitus is the commonest cause of end-stage kidney failure worldwide and is a proven and significant risk factor for the development of cardiovascular disease. Renal impairment has a significant impact on the physiology of glucose homeostasis as it reduces tissue sensitivity to insulin and reduces insulin clearance. Renal replacement therapy itself affects glucose control: peritoneal dialysis may induce hyperglycaemia due to glucose-rich dialysate and haemodialysis often causes hypoglycaemia due to the relatively low concentration of glucose in the dialysate. Autonomic neuropathy which is common in chronic kidney disease (CKD) and diabetes increases the risk for asymptomatic hypoglycaemia. Pharmacological options for improving glycaemic control are limited due to alterations to drug metabolism. Impaired glucose tolerance and diabetes are also common in the post-kidney-transplant setting and increase the risk of graft failure and mortality. This review seeks to summarise the literature and tackle the intricacies of glycaemic management in patients with CKD who are either on maintenance haemodialysis or have received a kidney transplant. It outlines changes to glycaemic targets, monitoring of glycaemic control, the use of oral hypoglycaemic agents, the management of severe hyperglycaemia in dialysis and kidney transplantation patients.

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 2293-PUB ◽  
Author(s):  
VEERANNA KARADI ◽  
DILIP PAWAR ◽  
SARAH JABEEN ◽  
SANDEEP S. ◽  
SAPTARSHI BOSE ◽  
...  

2018 ◽  
Vol 314 (4) ◽  
pp. F517-F530 ◽  
Author(s):  
Victoria L. Halperin Kuhns ◽  
Jennifer L. Pluznick

Obesity is a significant risk factor for both chronic kidney disease and end-stage renal disease. To better understand disease development, we sought to identify novel genes differentially expressed early in disease progression. We first confirmed that mice fed a high-fat (HF) diet exhibit early signs of renal injury including hyperfiltration. We then performed RNA-Seq using renal cortex RNA from C57BL6/J male mice fed either HF or control (Ctrl) diet. We identified 1,134 genes differentially expressed in the cortex on HF vs. Ctrl, of which 31 genes were selected for follow-up analysis. This included the 9 most upregulated, the 11 most downregulated, and 11 genes of interest (primarily sensory receptors and G proteins). Quantitative (q)RT-PCR for these 31 genes was performed on additional male renal cortex and medulla samples, and 11 genes (including all 9 upregulated genes) were selected for further study based on qRT-PCR. We then examined expression of these 11 genes in Ctrl and HF male heart and liver samples, which demonstrated that these changes are relatively specific to the renal cortex. These 11 genes were also examined in female renal cortex, where we found that the expression changes seen in males on a HF diet are not replicated in females, even when the females are started on the diet sooner to match weight gain of the males. In sum, these data demonstrate that in a HF-diet model of early disease, novel transcriptional changes occur that are both sex specific and specific to the renal cortex.


2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Toyofumi Abe ◽  
Taniguchi Ayumu ◽  
Kawamura Masataka ◽  
Kato Taigo ◽  
Tomoko Namba-Hamano ◽  
...  

Abstract Background and Aims This study aimed to evaluate whether the experience of pregnancy and delivery would be associated with poor maternal outcome among kidney transplant recipients. Method A total of 401 female transplant recipients from the Osaka University Transplantation Group Database were included in this study. 73 women who underwent renal transplantation between 1970 and 2017 and became pregnant and delivered at Osaka University Kidney Transplant Group Hospitals. Multivariable logistic regression analysis was used to assess the impact of pregnancy and delivery on renal transplant recipient outcome after one-to-one propensity score (PS) matching for 12 variables including serum creatinine at one year post-transplant between the parous group and the nulliparous group. The outcomes were kidney graft survival and patient survival. Results In all patients before PS matching, 75 (18.7%) of the 401 patients died and 137 (34.2%) of the 401 patients lost their kidney grafts during the follow-up period. In the multivariate analysis, pregnancy and delivery was not a significant risk factor for death (adjusted HR 0.662 [95%CI, 0.265-1.656], p-value 0.378) and for death-censored graft survival (adjusted HR 1.224 [95%CI, 0.683-2.196], p-value 0.497). In the PS matched population, 14 (17.5%) of the 80 patients died and 31 (38.8%) of the 80 patients lost their grafts. In the multivariate analysis, pregnancy and delivery was not a significant risk factor for death (adjusted HR 0.611 [95%CI, 0.180-2.072], p-value 0.430) and for death-censored graft survival (adjusted HR 1.308 [95%CI, 0.501-3.416], p-value 0.584). Conclusion Pregnancy and delivery after kidney transplantation was not associated with poor kidney transplant outcome in recipients with adequate and stable graft function.


2007 ◽  
Vol 293 (5) ◽  
pp. F1649-F1656 ◽  
Author(s):  
Susan Sheehan ◽  
Shirng-Wern Tsaih ◽  
Benjamin L. King ◽  
Caitlin Stanton ◽  
Gary A. Churchill ◽  
...  

Chronic kidney disease (CKD) is a growing medical problem and a significant risk factor for the development of end-stage renal disease, cardiovascular disease, and cardiovascular mortality. The genetic basis of CKD is recognized, but knowledge of the specific genes that contribute to the onset and progression of kidney disease is limited, mainly because of the difficulty and expense of identifying genes underlying CKD in humans. Results from genetic studies of CKD in rodents often correspond to findings in humans; therefore, we used quantitative trait locus (QTL) analysis to detect genomic regions affecting albuminuria in a cross between C57BL/6J and DBA/2J mice, strains resistant and susceptible to CKD, respectively. We identified several independent and interacting loci affecting albuminuria, including one QTL on mouse chromosome (Chr) 2 that is concordant with QTL influencing urinary albumin excretion on rat Chr 3 and diabetic nephropathy on human Chr 20p. Because this QTL was identified in multiple mouse crosses, as well as in rats and in humans, we used comparative genomics, haplotype analysis, and expression profiling to narrow the initial QTL interval from 386 genes to 10 genes with known coding sequence polymorphisms or expression differences between the strains. These results support the continued use of multiple cross-mapping and cross-species comparisons to further our understanding of the genetic basis of kidney disease.


2013 ◽  
Vol 16 (3) ◽  
pp. 276-283 ◽  
Author(s):  
G. E. C. Sun ◽  
B. J. Wells ◽  
K. Yip ◽  
R. Zimmerman ◽  
D. Raghavan ◽  
...  

2020 ◽  
Vol 4 (1) ◽  
pp. 119-125
Author(s):  
Sugeng Eko Irianto ◽  
Yudhinanto Yudhinanto

The trend of prevalence of Non-Communicable Diseases (NCD) such as hypertension, cardiovascular diseases, diabetes mellitus, and cancer has increased for the last few decades among low and midle income-countries including Indonesia. Based on the results of Basic Health Resarch performed in Indonesia in 2013, the prevalence of hypertension was 25.8 %, diabetes mellitus was 6.9 %, central obesity was 26.6 %, and stroke was 1.2 %. The cause of NCD is multi-factorial and the main risk factors are high consumption of sugar, salt, and fat, low consumption of vegetables and fruit, overweight, lack of physical activity, and smoking habit. Lower income countries such as Indonesia are beginning to experience disease patterns like high-income countries, as more processed foods are incorporated into diets in a nutrition transition, with less of the necessary healthcare resources to cope with increased disease burden. Globally, obesity or Body Mass Index (BMI) greater than 30 kg/m2 was estimated to have been the cause of 3.4 million deaths in 2010. Excess sugar consumption, particularly consumption of sugar-sweetened beverages (SSBs) is a well- documented, significant causal factor for weight gain. Several studies have found increases in BMI per additional daily serve of SSB and decreases in BMI when SSB consumption is reduced. Excess body mass is a significant risk factor for many NCDs such as ischemic heart disease (IHD), stroke, type 2 diabetes mellitus (T2DM) and various cancers, with the associated morbidity and mortality contributing to rising healthcare costs and reduced productivity. Excess sugar consumption directly increases   the risk of T2DM, mediated through both the risk due to higher weight and directly through inflammatory mechanisms triggered by elevated blood sugars.


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