More than 100 trillion microbial cells that reside in the human gut heavily influence nutrition, metabolism and immune function of the host. Gut dysbiosis, seen commonly in patients with Chronic Kidney Disease (CKD), results from qualitative and quantitative changes in host microbiome profile and disruption of gut barrier function. Alterations in gut microbiota and a myriad of host responses have been implicated in progression of CKD, increased cardiovascular risk, uremic toxicity and inflammation. We present a discussion of dysbiosis, various uremic toxins produced from dysbiotic gut microbiome, and their roles in CKD progression and complications. We also review the gut microbiome in renal transplant, highlighting the role of commensal microbes in alteration of immune responses to transplantation, and conclude with therapeutic interventions that aim to restore intestinal dysbiosis.

Allopurinol lowers uric acid and improves insulin resistance and systemic inflammation in asymptomatic hyperuricemia. Larger clinical trials are recommended to determine if lowering uric acid can help prevent type 2 diabetes.

IntroductionType 2 diabetes mellitus is a chronic disorder characterized by chronic hyperglycemia, with long term macrovascular and microvascular complications. The treatment is lifestyle management, exercise, weight control, and antihyperglycemic drugs such as sulfonylureas, biguanides, alpha-glucosidase inhibitors, thiazolidinediones, and meglitinide. Recently, a direct association between high levels of C-reactive protein and serum adenosine deaminase levels in patients with uncontrolled diabetes with long-term complications has been seen. This study was conducted to assess the antihyperglycemic, lipid-lowering, anti-inflammatory, and improving glycemic control of garlic in type 2 diabetes patients with obesity.Materials and methodsThis was an open-label, prospective, comparative study, conducted on 60 patients having type 2 diabetes mellitus and obesity. The patients were divided into two groups of 30 each, of either sex. Group 1 was given metformin tablets, 500 mg twice a day (BD)/three times a day (TDS), after meals, and group 2 was given metformin tablets, 500 mg BD/TDS, after meals, along with garlic (Allium sativum) capsules, 250 mg BD. Patients were routinely investigated for fasting and postprandial blood glucose, glycosylated hemoglobin (HbA1c), serum adenosine deaminase levels and lipid profile (serum cholesterol, high-density lipoprotein cholesterol, triglycerides and low-density lipoprotein cholesterol) at the start of the study. Patients were followed up for 12 weeks, with monitoring of fasting and postprandial blood glucose at 2 week intervals, and monitoring of the other parameters at the end of study. Data obtained at the end of the study was statistically analyzed using Student’s t test.ResultsIt was observed that both metformin alone and metformin with garlic reduced fasting blood glucose and postprandial blood glucose significantly, with a greater percentage reduction with metformin plus garlic; however, change in HbA1c levels was not significant. A fall in total cholesterol, triglyceride, and low-density lipoprotein and an increase in high-density lipoprotein were more pronounced in patients treated with metformin plus garlic. Similarly, a fall in C-reactive protein and adenosine deaminase levels was greater in patients taking metformin with garlic than in patients taking only metformin.ConclusionGarlic has been shown to have antihyperglycemic and lipid-lowering properties. The additional lowering of C-reactive protein and serum adenosine deaminase levels with garlic suggests that garlic can be a valuable agent in providing good glycemic control and the prevention of long-term complications.

Hyponatraemia--the most common serum electrolyte disorder--has also emerged as an important marker of the severity and prognosis of important diseases such as heart failure and cirrhosis. Acute hyponatraemia can cause severe encephalopathy, but the rapid correction of chronic hyponatraemia can also profoundly impair brain function and even cause death. With the expanding elderly population and the increased prevalence of hyponatraemia in this segment of society, prospective studies are needed to examine whether correcting hyponatraemia in the elderly will diminish cognitive impairment, improve balance and reduce the incidence of falls and fractures. Given that polypharmacy is also common in the elderly population, the various medications that may stimulate arginine vasopressin release and/or enhance the hormone's action to increase water absorption must also be taken into consideration. Whether hyponatraemia in a patient with cancer is merely a marker of poor prognosis or whether its presence may alter the patient's quality of life remains to be examined. In any case, hyponatraemia can no longer be considered as just a biochemical bystander in the ill patient. A systematic diagnostic approach is necessary to determine the specific aetiology of a patient's hyponatraemia. Therapy must then be dictated not only by recognized reversible causes such as advanced hypothyroidism, adrenal insufficiency, diuretics or other medicines, but also by whether the hyponatraemia occurred acutely or chronically. Information is emerging that the vast majority of cases of hyponatraemia are caused by the nonosmotic release of arginine vasopressin. Now that vasopressin V2-receptor blockers are available, a new era of clinical investigation is necessary to examine whether hyponatraemia is just a marker of severe disease or whether correction of hyponatraemia could improve a patient's quality of life. Such an approach must involve prospective randomized studies in different groups of patients with hyponatraemia, including those with advanced heart failure, those with cirrhosis, patients with cancer, and the elderly.

C ardiovascular disease underlies the majority of deaths in patients with dialysis-dependent end-stage renal disease (ESRD). 1 Standard cardiovascular therapies have rarely been tested in this population and with disappointing results. For example, 3 trials of HMG-CoA reductase inhibitors found that neither overall nor cardiovascular mortality was reduced in hemodialysis (HD) patients treated with statins compared with placebo. 2-4 These and other findings highlight the need to evaluate therapies to reduce cardiovascular morbidity and mortality specifically in patients receiving maintenance dialysis. 5 Several lines of evidence suggest that in ESRD, the heart undergoes progressive fibrosis and rarefaction of the microvasculature, 6-8 structural changes that predispose to arrhythmias and contribute to heart failure by reducing