A new therapy for kidney injury: regeneration.

Because of progressive population ageing and epidemic diffusion of type 2 diabetes mellitus in industrialized Countries, we are attending a growing incidence of end stage renal disease. This phenomenon has induced researchers to study potential alternative methods of renal function replacement. Actually, only dialytic methodics and renal transplant make possible survival of patients with terminal uremia, but both these therapeutic approaches show important limitations. The ideal solution would be represented by the possibility to "regenerate" the injured organ. This is the purpose of Regenerative Nephrology, a new medical domain which tries to develop new therapies through stimulation and induction in humans of regenerative processes already observed in other species, like reptiles and fishes. Such an ambitious and fascinating purpose requires a deep knowledge of the intricate networks which regulate the production of the hormones and mediators involved in the tissue regenerative processes. In this field the kidney embryonic development phases can represent a fundamental study model to acquire information about the reparative mechanisms of the structure and function of this excretory organ.

[Therapy with vasopressin receptor antagonists: the aquaretics]. / La terapia con gli antagonisti della vasopressina: gli acquaretici.

Aquaretic drugs, by definition, can induce an increase in urinary volume and urinary free water associated with a decreased urinary osmolarity with a consequent increase in plasma sodium. This enhanced diuresis is not accompanied by an increased loss of electrolytes, whereas traditional diuretics have the opposite, so-called saluretic effect. Aquaretics belong to a family of vasopressin receptor antagonists, V2 in particular, that regulate tubular water reabsorption. Several studies have confirmed their utility in the treatment of hyponatremic states associated with water retention such as heart failure, cirrhosis related ascites and SIADH. Furthermore, new applications may include the treatment of arterial hypertension, polycystic kidney disease, glaucoma and Meniere's syndrome.

Pulmonary hypertension and erythropoietin.

Numerous uremic patients on hemodialysis have pulmonary hypertension attributable to the presence of arteriovenous fistulas, vascular calcification, and endothelial dysfunction due to alterations in the balance between vasoconstrictive and vasodilatory substances. For these reasons, the effects of recombinant human erythropoietin, a drug widely used in patients on dialysis, on the pulmonary circulation were studied. Some authors maintain that recombinant human erythropoietin has an antihypertensive effect, while others have observed that this hormone induces a reduction in pulmonary arterial pressure due to its vasoactive and stimulatory effects on endothelial and smooth muscle cell precursors.

[A brief "update" on renal effects of caffeine]. / Rene e caffeina: un breve "update"

Caffeine is one of the most frequently consumed substances worldwide. It is present in some common beverages such as tea and coffee and in a variety of drugs, particularly analgesics. Its main mechanisms of action include inhibition of phosphodiesterase enzyme and adenosine receptors; its effects involve the whole body. In recent years there has been a debate in the scientific literature over the relationship between caffeine and the kidney and its possible toxicity. Several experimental studies have demonstrated that caffeine may exacerbate some pathological conditions such as polycystic disease and proteinuria, while others have underlined its protective effects in specific situations. While awaiting new, in-depth studies that will help to solve the debate, we can conclude that there is currently no evidence contraindicating the consumption of moderate quantities of caffeine by healthy subjects or kidney patients.

Dialysis-related genotoxicity: sister chromatid exchanges and DNA lesions in T and B lymphocytes of uremic patients. Genomic damage in patients on hemodiafiltration.

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.