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Objectives. Systemic lupus erythematosus is occasionally accompanied with bacterial infection. Lipopolysaccharide (LPS) from bacteria can accelerate and exacerbate lupus nephritis (LN) in animal models, but some mechanisms underlying the LPS-induced acceleration are still unclear. First, it is not known whether LPS can stimulate mesangial cells (MCs) to secrete the pro-inflammatory cytokine, interleukin (IL)-18. Second, it is also unclear whether LPS and/or IL-18 can induce MC apoptosis. Here, we attempted to clarify the cause-and-effect relationships between LPS stimulation, IL-18 production and MC apoptosis to address the above questions. [ABSTRACT FROM PUBLISHER]

BACKGROUND: Heat stroke is the clinical syndrome produced when the body overheats. It can develop in the army and in healthy civilian populations who physically exert themselves in a hot and humid environment during the summer, and may result in a significant number of heat-related deaths. Since strenuous exercise is one of the major exacerbating and precipitating factors, the incidence of exertional heat stroke (ExHS) is high among military personnel undergoing military training. Furthermore, acute renal failure (ARF) may occur in 25% of patients with ExHS and it can cause metabolic alterations that affect amino acid, carbohydrate, and lipid metabolism. Adequate nutritional support is essential for the treatment of ARF. The most important determinant of nutrient requirement in ARF is the degree of hypercatabolism caused by disease associated with renal function impairment. Indirect calorimetry (IDCM) is the method by which metabolic rate is estimated from measurements of oxygen consumption and carbon dioxide production. It can also provide information about the type and rate of substrate utilization in vivo (protein, carbohydrate, and fat). METHOD: The present clinical study is a comprehensive analysis of metabolic changes which includes energy expenditure (EE) and substrate utilization in 10 patients with ExHS with ARF and 10 patients with exertional heat exhaustion (ExHE) by the use of IDCM. RESULTS: Serum urea nitrogen, creatinine, peak creatine phosphokinase levels and heart rate were significantly increased in ExHS patients during ARF stage. Serum albumin levels were significantly decreased in ExHS patients with ARF. Resting energy expenditure (REE) was increased in patients with ExHS induced ARF and was not correlated with body temperature (r = 0.421). The average increase in EE during ARF stage was about 24%. The respiratory quotient in patients with ExHS induced ARF was lower than that in normal subjects and also in patients with ExHE. Urea nitrogen appearance rate increased in patients with ExHS induced ARF and in patients with ExHE without ARF. The percentage of total REE derived from fat in ExHS induced ARF and ExHE increased, while in patients with ExHS induced ARF and ExHE, the percentages of total REE derived from carbohydrate and protein were lower than those in control subjects. CONCLUSIONS: The present results suggest that patients with exertional heat injury (both ExHS and ExHE) have hypermetabolism during the acute stage. Furthermore, patients with exertional heat-induced rhabdomyolysis and ARF have a moderately higher hypermetabolism than those without ARF during the acute stage. We believe that this mainly reflects a more pronounced reduction of the vital cell mass (muscle) in relation to body weight, and/or a compromised substrate oxidation in ExHS with ARF. Whether or not this subgroup of patients will require a higher energy/caloric support merits further investigation. [ABSTRACT FROM PUBLISHER]