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Caffeine, or 1, 3, 7-trimethylxanthine, is one of the most frequently consumed active drugs worldwide. Its main mechanisms of action include inhibiting the phosphodiesteratic enzyme and adenosine receptors and activating the ryanodine receptors with several actions on all organs. What effect does caffeine have on the kidney? Is caffeine beneficial or dangerous? A review of the current literature reveals conflicting opinions regarding the prolithiasic effect of this substance, whereas its diuretic action is least disputed and more easily observed. Caffeine may have a toxic or preventive effect in some physiologic or pathologic conditions. Some of these incongruences may depend on several factors, such as dosage, prior chronic exposure, genetic-enzymatic axes, and concomitant drug consumption. While awaiting further insight from forthcoming studies on the issue, we may reach a preliminary conclusion that, as yet, there is no evidence contraindicating the consumption of the equivalent of 3 to 4 cups of coffee per day in healthy or nephropathic subjects. However, particular attention should be paid to the elderly, children, and patients on concomitant treatment with analgesics or diuretics, whereas in subjects with a family or clinical history of calcium lithiasis a moderate caffeine consumption should be associated with an adequate fluid intake. Further in-depth studies are required to investigate whether this beverage is beneficial to patients on hemodialysis.

Unlike the more commonly used diuretics, aquaretic agents can induce an increase in urinary volume without incurring a loss of electrolytes. These molecules belong to a family of vasopressin receptor antagonists, V2 in particular, that regulate optional renal water re-absorption via the synthesis and expression of aquaporin-2. In view of their properties, they have become the agent of choice in the treatment of hyponatremic states with water retention, and different studies have demonstrated that they are more effective and practical to use than other traditional approaches in the treatment of diseases such as cirrhosis-related ascites, SIADH and, above all, heart failure. However, the future probably holds the promise of new and unexpected applications for this type of drug in the treatment of several conditions, including polycystic kidney and glomerular disease, glaucoma and Meniere's syndrome.

During haemodialysis (HD) the endothelium is the first organ to sense and to be impaired by mechanical and immunological stimuli. We hypothesized that a single HD session induces mobilization of endothelial progenitor cells (EPCs) and that cardiovascular risk factors may influence this process. We quantified EPCs at different maturational stages (CD34+, CD133+/VEGFR2+) in blood samples from 30 patients, during HD and on the interdialytic day, and in 10 healthy volunteers. Samples were drawn at the start of HD, 1, 2 and 3 h after, at the end of HD and at 24 h on the interdialytic day. Patients were divided into two groups based on a recent risk scoring system (SCORE project): low-risk (LR) and high-risk groups (HR). HD patients showed a significantly reduced basal number of EPCs with respect to healthy volunteers. In contrast, we observed increasing EPCs during HD whereas they diminished on the interdialytic day. The EPC number was directly correlated with HD time progression. The EPC number during HD was increased in the HR group with respect to the LR group. We had a direct correlation between risk score and number of EPCs. Cardiovascular risk factors influenced the mobilization of stem cells from the bone marrow. This feature could be the direct consequence of an augmented request of stem cells to respond to the most important endothelial impairment but could also show a defective capacity of EPCs to home in and repair the sites of vascular injury., (Copyright 2007 S. Karger AG, Basel.)

Background/aims: Patients with chronic renal failure show the presence of massive oxidative genome damage but the role played by dialysis is still a controversial issue. The aim of our study was to verify the genomic damage in B- and T-lymphocyte subpopulations of uremic patients after a single hemodiafiltration session., Methods: We enrolled 30 patients on maintenance acetate-free biofiltration and 25 age-matched healthy volunteers and studied chromosomal alterations., Results: Our data show that the basal levels of DNA damage, the number of sister chromatid exchanges and basal high-frequency cells levels are significantly higher in patients on hemodiafiltration than in controls and in T lymphocytes than in B cells., Conclusions: These findings suggest that hemodialytic treatment could represent a potential source of damage, maybe through the oxidative action of the extracorporeal circuit components, which might explain the well-known T-specific immunodeficiency correlated with uremia.

Patients undergoing renal graft failure and returning to dialysis are often regarded to like facing for the first time a substitutive treatment, without considering the technical complications, the economical impact, and the psychological implications. This review attempt, to give answers to various questions, concerning the management of vascular access, the immunosuppressive therapy, the transplantectomy, the emotional and neuropsychic aspects, and the quality of life of graft-failed patients.

Oxidative stress is a pathogenic element of great importance in uremic patients, with a great impact on their survival. The cause of oxidative stress in patients on hemodialysis is traditionally attributed to the recurrent activation of polymorphonucleate neutrophils and monocytes. The effects of oxidative stress are evident on all biochemical components of biological tissues: lipids, proteins, carbohydrates, and nucleic acids. This study briefly reviews the effects of different dialytic techniques and of kidney transplant on several parameters of oxidative stress. Many different modalities of pharmaceutical intervention are then analyzed, and the clinical evidences reported., (Copyright 2005 Wiley Periodicals, Inc.)

Aging is a physiological process that causes structural and functional changes in human body systems, sometimes leading to various organ failure. As far as the kidney is concerned, both genetic factors and environmental agents may influence the tissues damage in elderly people and the related loss of function. On the other hand, functional adaptations to structural changes appear to be compromised by co-morbid conditions that are frequently found in elderly people, such as atherosclerosis and hypertension. It is not yet known whether physiological aging is inevitably accompanied by a decline in renal function or how rapidly it might happen. The discovery of molecular mechanisms responsible for tissue damage in aging could offer new perspectives on interventions. The role of nitric oxide, oxidative stress, the renin-angiotensin system, changes in length of telomeres, and klotho gene expression are important subjects for further in-depth studies about aging. A better understanding of physiological renal aging could improve the clinical approach to this process and widen the therapeutic possibilities offered by transplantation.

Complications from atherosclerosis cause most deaths in western countries, and their incidence appears to be markedly increasing in developing countries, thus suggesting a correlation that is directly proportional to social progress. In recent years, the different branches of medical research, from studies on vascular disease to those on lipid and glucose metabolism, and also clinical research on coronary, carotid and peripheral artery diseases, epidemiologic and pharmacologic research, have concentrated on these diseases with the common aim of reducing the incidence of cardiovascular diseases, and mortality. Scientific progress has greatly improved our understanding of the pathogenic mechanisms underlying the progression of cardiovascular disease, and efforts in this discipline now appear more necessary than ever.