Introduction: Any vascular access is of limited duration with many factors which influence survival in patients on chronic hemodialysis (HD). Hypoproteinemia as a marker of chronic illness is common among chronic HD patients. Our aim was to analyze the survival of the primary arteriovenous fistula (AVFs) and the risk factors which influence their patency and to test the hypothesis that patients with normal values of serum proteins have lower risk of AVF failure compared to patients with hypoproteinemia.Methods: Seven hundred thirty-four consecutive patients were included who underwent creation of an AVF. The patients were prospectively followed-up for 2 years. Only patients with AVF function after a month from its creation were analyzed. The patients were divided into two subgroups, with normal and low serum protein levels (<65 g/L).Findings: At follow-up 497 (67.7%) AVFs were still functional while 237 (32.3%) AVFs failed due to thrombosis or stenosis. Serum proteins and AVFs created on the forearm were positive predictors while diabetes was a negative predictor of longer AVF survival (P < 0.001; P 5 0.003; P 5 0.043). When comparing patients with normal and low serum protein levels (<65 g/L), mean survival time was significantly longer in patients with normal serum levels (P < 0.001).Discussion: In this study, hypoproteinemia was an independent prognostic marker for AVF failure at 2 years. Hypoproteinemia, based on our results, is an independent, more sensitive and prognostic marker of possible vascular access failure than the presence of other common factors which influence shorter AVF survival.

SUMMARY – The aim of the review is to establish sexual and reproductive functions in men with spinal cord lesion (SCL). Many sexual and reproductive dysfunctions may be found in these patients including individual’s low self-esteem, delay of orgasm, erectile or ejaculatory disorder and abnormalities of semen, which are characterized by lower sperm motility or viability. Owing to improvements in physical medicine and rehabilitation, the focus has been shifted from keeping patients alive towards ensuring the quality of life and improvements of sexual dysfunctions and later reproduction. Erectile dysfunction can be treated by using phosphodiesterase-5 inhibitors, intracavernosal injections, vacuum devices and penile prostheses. Semen can be retrieved from anejaculatory patients by medically assisted methods utilizing penile vibratory stimulation, electroejaculation, prostate massage, or surgically. Although there is low chance for pregnancy in natural way in most of SCL patients, fatherhood is possible through the introduction of assisted medical management. By use of various medical, technical and surgical procedures for sperm retrieval combined with assisted reproductive methods, high pregnancy rates have been reported comparable to those in able-bodied subfertile patients. Nevertheless, future studies are needed to improve semen quality and methods of assisted ejaculation in patients with SCL.

Background: Non-obstructive azoospermia (NOA) is a form of male infertility caused by disorders of the testicular parenchyma and impaired spermatogenesis. This study aimed to investigate the nature of Leydig cell changes in patients with NOA, especially whether their actual proliferation occurred. Methods: 48 testicular biopsies from infertile patients with NOA and 24 testicular biopsies originating from azoospermic patients suffering from obstructive azoospermia (OA) were included in the study. Leydig cells and their possible proliferative activity were analysed by immunohistochemistry and morphometry (stereology). Results: Unlike in the OA group, Leydig cells in NOA patients were sometimes organised into larger clusters and displayed an abundant cytoplasm/hypertrophy. Moreover, significant fibrosis of the interstitial compartment was demonstrated in some NOA samples, often accompanied by inflammatory cells. Stereological analysis showed no increase/proliferation of Leydig cells; on the contrary, these cells decreased in number in the NOA group. Conclusions: The decrease in the number of Leydig cells can be explained by previous inflammatory changes within the testicular interstitium and consequent interstitial fibrosis. The interstitial fibrosis might have a deteriorating effect on Leydig cells.