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Few studies address alteration of sexual function in women with diabetes and chronic kidney disease (CKD). Quality of life surveys suggest that discussion of sexual function and other reproductive issues are of psychosocial assessment and that education on sexual function in the setting of chronic diseases such as diabetes and CKD is widely needed. Pharmacologic therapy with estrogen/progesterone and androgens along with glycemic control, correction of anemia, ensuring adequate dialysis delivery, and treatment of underlying depression are important. Changes in lifestyle such as smoking cessation, strength training, and aerobic exercises may decrease depression, enhance body image, and have positive impacts on sexuality. Many hormonal abnormalities which occur in women with diabetes and CKD who suffer from chronic anovulation and lack of progesterone secretion may be treated with oral progesterone at the end of each menstrual cycle to restore menstrual cycles. Hypoactive sexual desire disorder (HSDD) is the most common sexual problem reported by women with diabetes and CKD. Sexual function can be assessed in women, using the 9-item Female Sexual Function Index, questionnaire, or 19 items. It is important for nephrologists and physicians to incorporate assessment of sexual function into the routine evaluation protocols.

The aim of this study was to investigate the effects of apocynin, a NADPH (nicotinamide adenine dinucleotide phosphate)-oxidase inhibitor, in diabetic rats with nephropathy induced by contrast medium (CIN). Diabetes was induced in male Wistar rats by a single dose of streptozotocin (60 mg/kg i.v.). Animals were then divided into the following groups: 1) control group (diabetic rats treated i.v. with saline solution); 2) iomeprol group (iomeprol at 10 ml/kg was injected i.v. 30 min after saline administration); 3) apocynin group (identical to the iomeprol group, except for pre-treatment with apocynin 5mg/kg i.v., 30 min before iomeprol injection) and 4) N-acetylcysteine group (NAC) (same as iomeprol group, except for the treatment with NAC 20 mg/kg i.v. 30 min before iomeprol injection). CIN in animals were assessed 24h after administration of iomeprol. Apocynin significantly attenuates the impaired glomerular function, concentration of Na(+), K(+), alpha glutathione S-transferase levels in urine and neutrophil gelatinase-associated lipocalin levels in plasma caused by iomeprol. In kidney, immunohistochemical analysis of some inflammatory mediators, such as nitrotyrosine, poly-ADP-ribosyl polymerase, tumor necrosis factor-α, interleukin-1β as well as apoptosis (evaluated as terminal deoxynucleotidyltransferase-mediated UTP end labeling assay) revealed positive staining in tissue obtained from iomeprol group. These parameters were markedly reduced in animals treated with apocynin. Similarly, these parameters were also markedly modified by NAC pre-treatment. Here, we have shown that apocynin attenuates the degree of iomeprol-induced nephropathy in diabetic rats.

Intestinal ischemia/reperfusion causes tissue hypoxia and damage, leading to the pathophysiology of inflammation. The aim of this study was to investigate the effects of glutamine on the tissue injury caused by ischemia/reperfusion of the gut. Ischemia/reperfusion injury of the intestine was caused by clamping both the superior mesenteric artery and the celiac trunk for 30 min followed by the release of the clamp allowing reperfusion for 1h. This procedure results in splanchnic artery occlusion-injury. Based on our findings we propose that the amino acid glutamine, administered 15 min before reperfusion at the dose of 1.5mg/kg, i.v. may be useful in the treatment of various ischemia and reperfusion diseases. The present study was performed in order to determine the pharmacological effects of glutamine ischemia/reperfusion-induced intestinal injury in rats. In particular, to gain a better insight into the mechanism(s) of action of glutamine, we evaluated the following endpoints of the inflammatory response: (1) histological damage; (2) neutrophil infiltration of the reperfused intestine (MPO activity); (3) NF-kappaB activation and cytokines production; (4) expression of ICAM-1 and P-selectin during reperfusion; (5) nitrotyrosine and poly-ADP-ribose formation; (6) pro-inflammatory cytokine production; (7) inducible nitric oxide synthase expression; (8) apoptosis as shown by TUNEL staining and (9) Bax/Bcl-2 expression.

Peritoneal dialysis is an alternative treatment of patients with end-stage renal disease. Sclerosing encapsulating peritonitis is a life-threatening complication of continuous ambulatory peritoneal dialysis. The aim of the present study was to evaluate the effect of thalidomide, which is used for the treatment of various inflammatory and autoimmune diseases, on the development of sclerosing encapsulating peritonitis induced by chlorhexidine gluconate (CG). A peritoneal fibrosis model was established using rats treated intraperitoneally with injections of CG. Thalidomide was administered orally at a dose of 100 mg/kg three times per week. When compared with CG-treated rats, thalidomide (100 mg/kg orally)-treated mice subjected to CG-induced peritoneal fibrosis experienced a significantly lower rate in the extent and severity of histological signs of peritoneal injury. Thalidomide also caused a substantial reduction of 1) the rise in myeloperoxidase activity (mucosa); 2) the expression in the tissue of TNF-alpha, IL-1beta, transforming growth factor-beta, and vascular endothelial growth factor; 3) the increase in staining (immunohistochemistry) for nitrotyrosine and for poly(ADP ribose), as well as 4) the nuclear factor-kappaB activation caused by CG in the peritoneum. Thus, thalidomide treatment reduces the degree of peritoneal fibrosis caused by CG. We propose that this evidence may help clarify the potential therapeutic actions of thalidomide in patients with peritoneal fibrosis.

Peritoneal dialysis (PD) is an alternative treatment of patients with end-stage renal disease. Unfortunately, long term peritoneal dialysis causes injury of the peritoneum associated with ultra filtration failure. Erythropoietin (EPO) is a potent stimulator of elytroid progenitor cells and its expression is enhanced by hypoxia. The aim of the present study was to evaluate the effect of EPO on the development of experimental peritoneal fibrosis induced by chlorhexidine gluconate (CG). A peritoneal fibrosis model was established using rats treated intraperitoneally with injection of CG. EPO was administered at the dose of 5000 U/kg i.p. three time per week for three weeks. When compared to CG-treated rats, EPO (5000 U/kg i.p. three time per week for three weeks) treated rats subjected to GC-induced peritoneal fibrosis experienced a significantly lower rate in the extent and severity of the histological signs of peritoneal injury. EPO also caused a substantial reduction of (i) the rise in myeloperoxidase activity (mucosa), (ii) the expression in the tissue of TNF-alpha, TGFbeta and VEGF (iii) the increase in staining (immunohistochemistry) for nitrotyrosine and for PAR, as well as (iv) the NF-kappaB activation caused by CG in the peritoneum. Thus, EPO treatment reduces the degree of peritoneal fibrosis caused by CG. We propose that this evidence may help to clarify the potential therapeutic actions of EPO in patients with peritoneal fibrosis.

To ascertain the effect of acetate-free biofiltration (AFB), performed with polyacrilonitrile filters, on serum concentrations of osteoprotegerin (OPG) and other bone-acting cytokines (interleukin (IL) IL-1, IL-6, tumor necrosis factor alpha (TNF-alpha) and transforming growth factor beta (TGF-beta)) in end-stage renal disease (ESRD) patients, we evaluated these parameters during an AFB session and 24 hr after it ended. In second time we verified the existence of eventual correlations among serum levels of all these cytokines at different times. We investigated 48 subjects: 24 healthy volunteers (controls) (12 females, 12 males, mean age 55 +/- 9 yrs) and 24 ESRD patients (12 females, 12 males, mean age 58 +/- 6.7 yrs, mean dialytic age 2.7 +/- 1.6 yrs, residual glomerular filtration rate (GFR) 2.3 +/- 0.6 ml/min). All dialyzed patients received regular AFB with polyacrilonitrile filters for 4 hr thrice-weekly. Statistical analysis showed significant increase in basal serum OPG, IL-6 and TNF-alpha concentrations in dialyzed patients compared to controls, while it did not show significant variations for the other cytokines. During the dialytic session, OPG and TGF-beta concentrations did not show significant variations, while serum TNF-alpha, IL-6 and IL-1 levels significantly decreased from the 1st hour of AFB. None of the cytokines showed significant differences between basal and interdialytic values. We did not find correlations between OPG, IL-1, IL-6, TNF-alpha and TGF-beta concentrations during hemodialytic sessions and during the interdialytic interval. It is our opinion that the lack of correlation between serum concentrations, observed in our study, could not exclude the presence of local interferences between OPG and the other cytokines.