https://www.kidney-international.org/article/S0085-2538(15)58302-6/pdf

The impact of hepatitis C virus infection on renal allograft recipients

Current therapies for type 2 diabetes are frequently associated with inadequate control of postprandial hyperglycemia, weight gain, and, in the case of oral agents, loss of efficacy over time. A better understanding of physiological responses to meals is leading to the development of new agents whose therapeutic action is based on the enhancement of gastrointestinal hormone action. These therapies are associated with slowing of gastric emptying, stimulation of insulin and inhibition of glucagon secretion, improved control of postprandial hyperglycemia, and control of body weight. This review summarizes several limitations in the treatment of type 2 diabetes and describes the mechanisms of action and clinical data obtained with amylin and glucagon-like peptide 1 (GLP-1) receptor agonists and dipeptidyl peptidase IV (DPP-IV) inhibitors for the treatment of diabetes.

Despite considerable effort by patients and physicians, the results of treating type 2 diabetes are often disappointing. This review examines the limitations of current antihyperglycemic therapies and assesses the potential of the emerging class of agents that mimic or enhance the actions of amylin and GLP-1, which are both gastrointestinal peptide hormones that in concert with insulin and glucagon regulate fuel homeostasis and eating behavior (1–4). Several agents from this class have been recently approved for clinical use or are in the advanced stages of development. Their mechanisms of action and therapeutic effects, as described in peer-reviewed publications, will be discussed.

The evidence-based target for glycemic control is an HbA1c (A1C) ≤7% (5), although several groups have proposed an A1C target of 6.5% based on epidemiological analyses (6,7). In clinical trials, patients have achieved A1C values near 7% using basal-bolus insulin treatment in type 1 (8) or type 2 (9) diabetes or combinations of oral treatments and insulin for type 2 diabetes (10). However, routinely maintaining glycemic control at …

https://care.diabetesjournals.org/content/diacare/29/2/435.full.pdf

Emerging therapies mimicking the effects of amylin and glucagon-like peptide 1.

https://www.ajkd.org/article/0272-6386(95)90617-7/pdf

Hepatitis C virus : the nephrologist's view

https://www.ajkd.org/article/S0272-6386(01)02061-3/pdf

Hepatitis C virus infection and renal transplantation

Hepatitis C virus (HCV) is the predominant cause of posttransplant non-A, non-B hepatitis among renal allograft recipients. Prior studies evaluating the impact of HCV in kidney transplantation have been retrospective in design and based largely on changes in serum transaminases. We studied a group of HCV-infected end-stage renal disease patients prospectively with pretransplant liver biopsies and close virologic and biochemical follow-up posttransplant. Fourteen patients have been followed a mean of 11.6 +/- 5.6 months posttransplant (range, 5-21 months). Six had changes of chronic hepatitis on pretransplant liver biopsy while 8 showed only mild histologic abnormalities. Circulating viral titers increased several-fold over baseline levels during posttransplant follow-up. Viral replication was particularly enhanced immediately following a course of antilymphocyte therapy. Although all patients showed a 2-3 fold increase in alanine aminotransferase (ALT) following transplantation, there were no association noted between pretransplant liver histology, the use of FK506 and/or cyclosporine-based immunosuppression, and the magnitude of ALT change posttransplant. The only clinical outcome found to differ significantly was a higher incidence of cytomegalovirus infection among patients with chronic hepatitis. All patients are alive with functioning grafts. There have been no episodes of fulmiinant or subfulminant liver failure. We conclude that HCV-infected patients can be safely transplanted with excellent short-term follow-up. Continued monitoring with sequential liver biopsies will be needed to define the long-term course of HCV infection in an immuno-suppressed population.

A prospective study of hepatitis C virus infection in renal allograft recipients.

Hepatitis C antibody in renal transplant patients.

The aim of this study was to compare total cholesterol and triglyceride levels in 281 kidney graft recipients with stable graft function and different immunosuppressive regimens. All patients had low‐dose prednisolone (mean daily dose 7.7 mg ± 4.8). In 57 patients immunosuppression consisted of prednisolone and azathioprine (Group A), 141 had prednisolone and cyclosporin A (Group B) and 83 were treated with prednisolone, azathioprine and cyclosporin A (Group C). There was no significant difference in daily prednisolone dose, sex, age, mean graft survival and proteinuria between the three groups. Cholesterol values for Groups A, B and C were 257 mg/dl, ± 69.6, 261 mg/dl, ± 70.2 and 247 mg/dl, ± 65.9, respectively. The triglyceride values for the groups A, B and C were 201 mg/dl, ± 199, 211 mg/dl, ± 139, and 220 mg/dl, ± 154. All values are the group means with their standard deviations. Comparison of the cholesterol and triglyceride values between the three treatment groups showed no significant differences. Importantly, no difference could be observed between patients receiving cyclosporin A and conventional therapy. We conclude that immunosuppression with cyclosporin A need not cause hyperlipidemia in the face of low‐dose prednisolone administration.

Cyclosporin A does not cause hyperlipidemia in kidney graft recipients

Amylin, a 37 amino acid polypeptide, has been suggested to play a prominent role in the pathogenesis of insulin resistance in type II diabetes mellitus. Various studies have demonstrated most recently that amylin is cosecreted with insulin. No data are available on the elimination of amylin from the circulation. We therefore tested plasma levels of amylin, insulin and C-peptide in 49 non-obese, non-diabetic patients (27 male/22 female) with various degree of renal impairment (Group A: CCr less than 20 ml/min, n = 20; Group B: CCr 20-89 ml/min, n = 18; and Group C: CCr greater than 80 ml/min, n = 9). We found a significant increase of plasma amylin when kidney function, expressed by creatinine clearance fell below 20 ml/min (17.9 +/- 1.7 vs. 12.2 +/- 0.8 vs. 8.8 +/- 1.2 pg/ml; p = 0.0005). Plasma amylin correlated closely with serum C-peptide (r = .764; p = 0.0001), and to a lesser extent with insulin (r = .595; p = 0.0001) underlining its postulated cosecretion with these peptides. The data indicate that amylin might be eliminated by renal mechanisms. Our data show that besides type II diabetes mellitus, advanced renal failure is another clinical situation with enhanced plasma amylin levels. Whether amylin plays any pathogenetic role in renal patients remains to be elucidated.

Increased levels of plasma amylin in advanced renal failure.

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Hepatitis C antibody in renal transplant patients.

Cyclosporin A does not cause hyperlipidemia in kidney graft recipients

Increased levels of plasma amylin in advanced renal failure.