Role of nitric oxide [NO], endothelin-1 [ET-1], interleukin-1 IIL-1], and tumor necrosis factor [TNF alpha] in hemodialysis induced hypotension

Serum levels of Nitrite and Nitrate [NO2 + NO3], ET-1, IL-1 and TNF alpha have been estimated in 20 patients with end stage renal failure [ESRF] undergoing regular hemodialysis [HD] treatment in a trial to explain the hypotension occurring in some of these patients. According to the incidence of hypotension, patients were divided into GI [n=10] hypotension prone patients and GII [n=10] hypotension resistant patient [normotensives]. Clinical examination with measurement of systolic and mean arterial blood pressure was done to all cases before and after hemodialysis session. After HD, GI showed significnat increase in serum levels of [NO2 + NO3], IL-1 and TNF; where as a significant increase in serum ET-1 level was noticed. GII showed no significant change in serum level of the 4 parameters mentioned above. In hypotensive patients there was a significant positive correlation between [NO2 + NO3] and the duration of dialysis, and a significant negative correlation between [NO2 + NO3] and post dialysis systolic blood pressure, also between IL-1 and ET-1. From the previous results it could be concluded that the cascular endothelial factors studied [NO and ET-1] together with the inflammatory cytokines IL-1 and TNF contribute in the development of HD induced hypotension in ESRF subjects which is evidenced by: - The coupling of decrease of BP and increase in NO2 + NO3 level after HD in group I. - ET-I level, which is a powerful vasoconstrictor, showed a significant decrease post dialysis. - Cytokines [IL-1 and TNF alpha] levels, which are potent NO inducers, were found to be significantly increased post dialysis in group I

Hypomagnesemia in type II diabetes mellitus: effect of magnesium replacement therapy on glycaemic control and microalbuminuria

To study the effect of magnesium administration on the glycaemic control and microalbuminuria in type II diabetic patients with hypomagnesemia, 46 patients were included in this randomized clinical study. Patients were randomly divided into 2 groups Group l and Group II. Group I 26 patients [17 males and 9 females, their ages ranging from 39 to 64 years] received magnesium, first by IV route [Mg[2+] sulfate] to restore serum Mg[2+] level to normal, then orally [Mg[2+] citrate] to maintain normal serum level for one month. Group II. 20 patients [12 males and 8 females, their ages ranging from 35 to 64 years] did not receive magnesium. Results showed a high baseline fasting blood glucose, HBAlc and a 24 h urinary albumin excretion in all studied patients with no significant statistical differences between the two groups, P>0.05. Magnesium supplementation to group I patients was associated with significant decrease in fasting blood glucose [from 182.46 +/- 29.42 to 138.84 +/- 23.06 mg/dl. P<0.001] and HbAlc [from 12.12 +/- 2.18 to 9.1 +/- 1.66%. P<0.001] and a non-significant decrease in fasting insulin level [from 28.31 +/- 5.32 to 25.03 +/- 4.21 unit/mL. P>0.05] and a 24 hour urinary albumin excretion [from 185.35 +/- 91.75 to 165.21 +/- 63.3 mg/day, p>0.05]. On the other hand, there was no significant difference in group II patients, before and after receiving placebo. Thus, short-term restoration of serum magnesium level to normal seems to have a beneficial effect on glycaemic control but have no significant effect on microalbuminuria in NIDDM patients with hypomagnesemia. Further studies, however, are needed to verify the benefit of long-term magnesium supplemented diets on diabetic control and possibly on the progression of microalbuminuria