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Transplantation with a diabetic donor kidney may have some benefits compared to remaining on the waitlist for selected patients. However, we found that some kidney transplant recipients have ongoing donor-transmitted diabetic kidney disease (DT-DKD) despite fair blood sugar control. This study aimed to survey the incidence and clinical pattern of DT-DKD in kidney transplant recipients.

We retrospectively reviewed the medical records of kidney transplantations in our hospital. We found 357 kidney transplantations from February 2006 to April 2018. Among these, 23 (6.4%) diabetic donor kidney transplantations were done in the study period.

Among the 23 recipients, 6 (26.1%) displayed biopsy-proven DKD. Recipients with biopsy-proven DKD had longer dialysis vintage, higher proteinuria amount, lower last estimated glomerular filtration rate (eGFR), and a more rapid decline in the eGFR. The median fasting blood sugar level in the biopsy-proven DKD group was unexpectedly lower than the non-DKD group. Most of th fair blood sugar control. The zero-time pre-transplant kidney biopsy may be an important examination before the allocation of diabetic donor kidneys. Further study is needed to elucidate the possible mechanism of ongoing DT-DKD in non-diabetic recipients with fair blood sugar control as well as the impaction of pre-implantation diabetic lesion on the graft outcome.

Fatty acid-binding protein 4 (FABP4), but not FABP1 (liver-type FABP), is ectopically induced in injured glomerular endothelial cells, and urinary FABP4 (U-FABP4) level is associated with proteinuria and renal dysfunction in a general population.

The clinical significance of U-FABP4 was investigated in 81 patients (male/female 43/38, age 57 ± 17 years) who underwent kidney biopsy.

U-FABP4 was negatively correlated with estimated glomerular filtration rate (eGFR) (r = - 0.56, P < 0.01) and was positively correlated with age, blood pressure, triglycerides, proteinuria (r =0.58, P < 0.01), plasma FABP4 and urinary FABP1 (U-FABP1) (r =0.52, P <0.01). Multivariable regression analysis showed that eGFR, proteinuria and U-FABP1 were independent predictors of U-FABP4. The level of U-FABP4, but not that of proteinuria, eGFR or U-FABP1, in minimal change nephrotic syndrome (MCNS) was significantly lower than the level in membranous nephropathy (MN) and that in diabetic nephropathy. Receiver operating chaS and MN, which are common causes of nephrotic syndrome.Diabetic Mellitus (DM) is a metabolic disorder that has attracted worldwide concern. DM is caused due to lack of insulin or ineffective production of insulin in the pancreas. A total of 463 million people have diabetes mellitus in 2019 and it was predictedto raise upto 578 million by 2030 and 700 million by 2045. High blood sugar gives rise to many complications like diabetic retinopathy, diabetic nephropathy, atherosclerosis, hypercoagulability, cardiovascular disease, coronary heart disease, abdominal obesity, hypertension, hyperlipidemia, cerebrovascular disease, coronary artery disease, foot damage, skin complications, Alzheimer's disease, hearing impairment, and depression. These life-threatening complications make diabetes more severe than other diseases. Many synthetic drugs are developed, but still cure is not provided by any of the molecules up to this date. Continuous use of some synthetic agents caused many severe side effects, and thus the demands for non-toxic, affordable drugs are still awaited.d voglibose are some of the examples of marketed drugs, which are obtained from the natural origin and used as antidiabetic drugs. The active principles derived from the plants work through many antidiabetic mechanisms, which include inhibition of α-glucosidase, α-amylase, and protein tyrosine phosphatase 1B activities. One of the major advantages of herbal drugs is the low level of side effects attributed to these medicines, and this attracted the various researchers to develop new molecules for treatment of diabetes. In this review, emphasis will be given on the recent advances in the field of herbal drugs to treat diabetes, to prevent the secondary complications arising due to diabetes, and various herbal molecules in different stages of clinical trials.

Painful Diabetic Neuropathy (PDN) is a devastating condition affecting one in three people with diabetes.

Keeping in mind the unceasingly escalating prevalence of diabetes mellitus worldwide, the number of PDN patients is also expected to rise with a reduced quality of life in patients and staggering increase in healthcare cost. Bemcentinib ic50 Despite relentless efforts and continuous research, the commercially available medication for relieving diabetic neuropathy pain are only partially effective with substantial side effects. This is, in part, due to our partial awareness of the underlying complexities causing PDN. The pathogenesis of PDN remains elusive because of the difficulty in obtaining damaged nerve samples and the absence of non-invasive methods to investigate the pathogenesis at different stages of disease progression. The purpose of this review is to describe the pathogenesis, the clinical manifestations and treatment options for PDN.

The keywords relevant to the scope of this paper were put in electronic attain maximum pain relief with minimum side effects.Glucolipotoxicity-induced oxidative stress and mitochondrial dysfunction of pancreatic β-cells are one of the mechanisms that have been related to the low insulin secretion and cell death during diabetes development. In early or non-chronic stages, the pancreatic β-cells respond to hyperglycemia or hyperlipidemia, stimulating insulin secretion. However, the chronic effect of both leads to the establishment of glucolipotoxicity which induces constant overstimulation of pancreatic β-cells, a condition that leads to cell death by apoptosis. The mechanism described, at this moment, is the accelerated mitochondrial dysfunction triggered by the high production of reactive oxygen species (ROS) due to excess nutrients. At first, mitochondria respond to over-nutrition accelerating oxygen consumption and consequently increasing the ATP synthesis. A permanent increase of ATP/ADP ratio leads to a constant inhibition of K+ ATP-channel and therefore a continuous insulin secretion accompanied by an increase in ROS. Finally, ROS accumulation compromises mitochondrial function due to the uncontrolled oxidation of proteins, lipids, and DNA generating functional alterations such as a drop of membrane potential, deregulation of mitochondrial dynamics, low rate of ATP synthesis and consequently the cell death.