Fructose-1,6 diphosphate as a protective agent for experimental ischemic acute renal failure.

Cold ischemia time is a risk factor for the development of acute renal failure in the immediate post-transplant period. In this study, we aimed to determine if intravenous fructose-1,6-diphosphate (FDP), given before nephrectomy, attenuates renal cell injury in a cold ischemia model. Male adult Wistar rats were subjected to infusion of either FDP 350 mg/kg (group F, n=6), an equal volume of 0.9% NaCl (group S, n=6), an equal volume/osmolality of mannitol (group M, n=6) or no infusion (group C, n=7). Kidneys were then perfused in situ with Collins solution and nephrectomy was performed. Other kidney slices were stored in Collins solution at 4 degrees C. Adenosine triphosphate (ATP) levels and lactate dehydrogenase (LDH) release were examined at 0, 24, 48 and 72 h. Other slices, obtained after 50 min immersion in Collins solution at 37 degrees C, were frozen for characterization of cytoskeletal preservation using phalloidin-FITC staining. Apical fluorescence intensity of proximal tubule cells, indicative of the F-actin concentration, was measured in a fluorescence microscope interfaced with computer image analysis system. Adenosine triphosphate levels, after up to 72 h of tissue incubation, were higher (P<0.05) in the FDP group when compared to other groups. In addition, LDH release was smaller (P<0.0001) in the FDP group. The F-actin concentration of proximal tubule cells cells was greater in the FDP group (P<0.0001). Results indicate that FDP is a useful tool to increase tissue viability in a rat kidney subjected to cold ischemia, by maintaining ATP cell content, decreasing LDH release and preventing microfilament disruption of proximal tubule cells.

Carnitine supplementation in diphtheria.

We studied the effect of carnitine supplementation in patients with diphtheria. Six hundred and twenty five children of diphtheria received either DL-carnitine (100 mg/kg/day in two divided doses orally for four days), or no carnitine, in addition to the routine treatment for diphtheria. The patients receiving carnitine (n = 327) and controls (n = 298) were matched for age, sex, duration of symptoms, grade of toxemia and immunization status. Patients receiving carnitine showed a significant reduction in incidence of myocarditis as compared to controls (p = 0.001). Cases with myocarditis receiving carnitine therapy showed a significant reduction in mortality as compared to controls (p < 0.001). In view of a significant decline in incidence and mortality of myocarditis in cases of diphtheria, we recommended that all cases with diphtheria should receive carnitine supplementation.

The protective effect of carnitine in human diphtheric myocarditis.

Carnitine, an important cofactor in the transport of fatty acids to the interior of cell mitochondria, is depleted in myocardial tissue of guinea pigs submitted to diphtheric toxin administration. Mortality rates were reduced in these animals by supplying exogenous amounts of carnitine. The accumulation of fatty acids in the cytoplasm of human heart cells reported in cases of diphtheria suggests that carnitine might possibly be depleted in human myocardium as well. For the purpose of studying the effect of carnitine administration, 132 diphtheric patients were randomly divided into two groups, one of them (carnitine-treated group, n = 73) receiving DL-carnitine, 100 mg/kg/day during 4 days after admission, in addition to routine treatment, which was prescribed for this and the control group (n = 59). The presence of myocardial damage was evaluated by clinical, electrocardiographic, radiological, and enzymatic criteria. Carnitine administration resulted in decreased incidence of heart failure (P = 0.0475), of pacemaker implants (P = 0.0256), and of lethality indexes due to myocarditis (P = 0.013). We suggest that carnitine can play an important role in the treatment of diphtheric patients.