Hyperlipidemia is common in chronic renal failure (CRF), but the underlying mechanisms are not clearly defined. Certain data points toward a potential role for the state of secondary hyperparathyroidism of CRF in its pathogenesis. We examined the effects of parathyroid hormone (PTH) on lipid metabolism utilizing intravenous fat tolerance test (IVFTT) and post-heparin lipolytic activity in five normal dogs, in six animals with CRF and secondary hyperparathyroidism (NPX) and in six normocalcemic-thyroparathyroidectomized dogs (NPX-PTX) with comparable degree and duration of CRF. NPX dogs had fasting hypertriglyceridemia (82 + 6.0 mg/dl vs. 49 +/- 2.7 mg/dl in normal dogs, P less than 0.01), abnormal IVFTT, and reduced post-heparin plasma LPL activity (151 +/- 10 vs. 275 +/- 15 mumol fatty acids/ml/min in normal dogs, P less than 0.01). The NPX-PTX dogs had normal fasting levels of serum triglycerides (42 +/- 0.6 mg/dl), normal IVFTT, and normal post-heparin plasma LPL (317 +/- 19 mumol fatty acids/ml/min) despite CRF. Post-heparin HL activity in plasma was not different between NPX and NPX-TPX dogs. The results show that excess blood levels of PTH and not other consequences of CRF are mainly responsible for the abnormalities in lipid metabolism. The data are consistent with the notion that excess PTH reduces post-heparin LPL activity in plasma, which in turn results in impaired lipid removal from the circulation and consequently hyperlipidemia.

Background Coronavirus disease-19 (COVID-19) is an ongoing pandemic causing considerable fatalities worldwide. Vitamin D modulates the immune response through effects on various cells, such as: macrophages, B and T lymphocytes, neutrophils, and dendritic cells. Aim To explore whether supplementation of vitamin D, in the form of a single intramuscular cholecalciferol injection, to patients with diabetes, COVID-19, and low vitamin D levels could improve the prognosis of those patients. Methods This was a placebo-controlled randomized prospective study. The study has two arms as follows: the intervention arm (40 vitamin D deficient diabetes elderly patients that acquired SARS-CoV-2), compared to the control arm (16 elderly diabetes patients, with deficient vitamin D with SARS-CoV-2). Patients in the intervention arm were given vitamin D as a single intramuscular injection (200,000 IU); patients in the control arm were given placebo. The primary outcome was mortality within 6 weeks of the diagnosis of COVID-19. Clinical, laboratory, treatment, and outcome data were recorded after 6 weeks of follow-up. Results No significant difference in 6 weeks mortality was observed between patients who received vitamin D and patients who received placebo (17.5% vs 18.8%, p = 0.838). Age, presence of hypertension, and chronic obstructive pulmonary disease were independent predictors of mortality at 6 weeks. Conclusion Vitamin D supplementation did not reduce the severity or mortality of COVID-19 at 6 weeks. Further large scale studies are required to explore the effect of vitamin D therapy on survival in patients with diabetes mellitus who acquire COVID-19.

Background: End-stage renal disease (ESRD) has significantly increased in developing countries such as Egypt. Diabetes mellitus is still the leading cause of ESRD, while numbers of hypertensive patients among that population have significantly risen. Materials and Methods: The data presented in this article were obtained from various nephrology centers in response to the specific questionnaires distributed by the researchers. Results: Hemodialysis is available in most parts of the country. Continuous ambulatory peritoneal dialysis and renal transplantation programs have been performed in few nephrology centers. Costs for dialysis and renal transplantation are still unaffordable for most patients with ESRD. Since the cost burden has significantly increased, nephrology services should be changed from curative medicine to preventive medicine. Currently, the Egyptian Ministry of Health plans to have a detection and prevention program for chronic kidney disease. Conclusion: These data give the impression that both incidence and prevalence rates of ESRD in various areas of Egypt are increasing over time, although the rates presented here are far lower than expected.

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Insulin release from pancreatic islets is impaired in chronic renal failure (CRF), and this is due to the state of secondary hyperparathyroidism of CRF. This defect in association with resistance to the peripheral action of insulin-caused glucose intolerance in CRF. It has been suggested that the impaired insulin release induced by excess parathyroid hormone (PTH) is related to the ability of the hormone to augment calcium entry into the pancreatic islets, resulting in accumulation of calcium in the pancreas. Therefore, a calcium channel blocker may antagonize this effect of PTH, and hence normalize glucose tolerance in CRF. The present study examined this postulate by studying intravenous glucose tolerance and insulin release from pancreatic islets in normal and CRF rats and in CRF animals treated with the calcium channel blocker, verapamil. Rats with 42 days of CRF displayed impaired glucose tolerance, significant reduction (P less than 0.01) in insulin release by islets, and doubling of calcium content of the pancreas (P less than 0.01) as compared to normal rats. Simultaneous treatment of CRF rats with verapamil for 42 days resulted in normal glucose tolerance, higher blood insulin levels during glucose infusion, normal calcium content of the pancreas, and normal insulin secretion by the islets. Treatment of normal rats with verapamil for 42 days did not affect any of the parameters studied. The results show that the calcium channel blocker, verapamil, by preventing calcium accumulation in the pancreas, reversed the abnormalities in insulin release that occur in CRF. This effect allowed a greater rise in blood levels of insulin during glucose infusion in CRF rats.(ABSTRACT TRUNCATED AT 250 WORDS)

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Objectives: The aim of this study was to evaluate the effectiveness of sitagliptin, alone or in combination with metformin, in kidney transplant patients with newly diagnosed new-onset diabetes mellitus after transplant who had inadequate glycemic control, compared with a group of patients receiving insulin glargine with special emphasis on weight gain. Materials and Methods: Newly diagnosed renal transplant patients with new-onset diabetes mellitus after a transplant was defined by a blood glucose ≥ 11.1 mmol/L after an oral glucose tolerance test were examined. They were treated with standard immunosuppression composed of triple therapy with tacrolimus or cyclosporine, mycophenolate mofetil or azathioprine, and prednisone. They had stable graft function for more than 6 months after the transplant. Results: Patients with new-onset diabetes mellitus after transplant (n=28) whose glycemia was not controlled adequately with oral hypoglycemic agents (either alone or in combination) received oral sitagliptin 100 mg once daily in addition to existing therapy for 12 weeks. Patients who received insulin glargine as add-on therapy (n=17) served as the control group. Data analyses included glycated hemoglobin, fasting plasma glucose, lipid profile, body weight, and the occurrence of hypoglycemia. We found significant reductions in glycated hemoglobin and fasting plasma glucose values after 12 weeks of additional sitagliptin therapy that were comparable to those with insulin glargine. While the addition of stagliptin resulted in a small weight loss (0.4 kg), the addition of insulin glargine resulted in a weight gain (0.8 kg). The overall incidence of adverse experiences was low and generally mild in both groups. Conclusions: In a group of renal transplant recipients with new-onset diabetes mellitus after a transplant in whom glycemia was not controlled adequately by oral hypoglycemic agents, the addition of sitagliptin helped to achieve glycemic control similar to insulin glargine but with a marginal weight advantage.