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D Musone

Publications and source records attributed to D Musone.

2 recordsLinked to original sources

[Erectile dysfunction in kidney transplanted patients].

BACKGROUND: Erectile dysfunction (ED) is the inability to achieve and/or maintain an erection for satisfactory sexual performance or intercourse. ED profoundly affects the quality of life. While the effects of dialysis on ED are documented, the benefits of renal transplantation are unknown. METHODS: This study evaluates the prevalence of ED and the effects of transplantation on ED in kidney transplanted patients. Erectile function was assessed using the self-administered International Index of Erectile Function (IIEF). The domains investigated by IIEF are: (1) erectile function, (2) orgasmic function, (3) sexual desire, (4) intercourse satisfaction, (5) overall satisfaction. At the entry patients underwent clinical examination by urologist and neurologist; blood was collected for biochemical analysis. One-hundred-fifteen (89%) patients filled in the questionnaire. RESULTS: Fifty-two (45%) patients did not complain about ED, which was reported by sixty-three patients (55%). No clinical and/or biochemical difference was found between patients with and without ED. Hypertension was equally present among patients; administration of beta-blockers was significantly more frequent among patients without ED. ED was already present during dialysis in 40 patients. After transplantation ED disappeared in 8 (20%), ameliorated in 13 (32,5%), worsened in 2 (5%), remained unchanged in 17 (42,5%) and appeared "ex novo" in 27 (43%) patients. ED is significantly correlated (p<0.01) to the age of subjects. CONCLUSIONS: The data of the present study indicate that: 1) ED is still present in many transplanted men; 2) renal transplantation cures ED in only few cases; 3) ED may appear "ex novo" after transplantation.

Adult↗

Sodium retention in preascitic stage of cirrhosis.

Renal Na+ handling abnormalities have been shown in preascitic cirrhosis. To investigate the underlying pathophysiology, the effects of different sodium intakes on Na(+) balance and renal hemodynamics were assessed at 100 mEq Na+/day (low-sodium diet [LSD]) and after 6 days of 250 mEq Na+/day (high-sodium diet [HSD]). Eight asymptomatic patients with cirrhosis (Pugh-Child A class) (PAC) and 10 healthy controls (CON) were studied. At HSD, although CON readjusted Na+ excretion within the fourth day, PAC did not reach the new balance and developed a final greater Na+ retention (+437 mEq in PAC v +228 mEq in CON, P<.001). In PAC, fractional Na+ excretion (FENa) was significantly lower than in CON at LSD (P<.05), and, after HSD, increased in both groups (P<.05). In PAC, renal vascular resistances (RVR) at LSD resulted lower than in CON (P<.05) and failed to decrease after HSD. As a consequence, after HSD, glomerular filtration rate and renal plasma flow failed to increase in PAC. PRA and plasma aldosterone were significantly lower in PAC, than in CON at LSD (P<.05), and decreased in both groups after HSD (P<.05). Proximal Na+ reabsorption (RProx) [as indicated by fractional free water clearance measured in a state of maximal water diuresis] at LSD was lower in PAC than in CON (P<.05) and decreased in both groups after HSD (P<.05). In summary, early stages of cirrhosis are characterized by: (1) a reduction of RVR, probably associated with splanchnic vasodilation; (2) a Na+ retention already at LSD, as indicated by the lower FENa observed in PAC, that produces extracellular volume (ECV) expansion, with a consequent RProx and renin-angiotensin-aldosterone axis (RAS) suppression; (3) a greater Na+ retention after HSD, associated with an abnormal adaptation of renal hemodynamic, a greater ECV expansion and a consequent Rprox and RAS suppression. These data show the presence of early renal hemodynamic dysfunction in PAC. Our findings also show in this phase of the disease a preserved adaptation of RProx and RAS, thus suggesting that the observed tubular Na+ reabsorption derangement is probably related to abnormal ANP behavior.

Aldosterone↗