Table 1.

Pyruvate-mediated protection against glycerol-mediated AKI assessed 4 hours postglycerol injection

Groups	BUN (mg/dl)	LDH/plasma (units/ml)	NGAL (mRNA)	MCP-1 (mRNA)	IL-10 (mRNA)	HO-1 (mRNA)	H2O2 (μmol/g)	ATP (μmol/g)
Controls	22±1	2.0±0.3	0.002±001	0.06±0.03	0.58±0.13	0.07±0.01	2.68±0.23	6.8±0.3
Glycerol	51±3	19.4±1.5	0.26±0.05	1.58±0.22	1.3±0.3	2.09±0.1	1.21±0.25	2.4±0.6
Glycerol+pyruvate	26±2 (<0.001)	18.9±1.3 (NS)	0.12±0.03 (<0.03)	0.40±0.06 (<0.001)	2.51±0.4 (<0.04)	2.45±0.1 (<0.02)	2.28±0.24 (<0.03)	3.5±0.7 (<0.01)a

Eighteen mice were injected with glycerol: one half with and one half without pyruvate therapy. Four hours later, plasma and renal cortical samples were obtained, and the values were contrasted with the values seen in six normal mice. Glycerol caused early ARF, which was denoted by BUN elevations. Pyruvate almost completely normalized postglycerol BUN concentrations (P<0.001 compared with glycerol alone; P<0.001), but it did not seem to alter the severity of muscle injury or hemolysis (based on comparable plasma LDH elevations with or without pyruvate therapy). Renal protection with pyruvate was also supported by a marked reduction in NGAL mRNA levels (factored by glyceraldehyde-3-phosphate dehydrogenase; P<0.03). Pyruvate-mediated protection was associated with a marked reduction in the inflammatory marker MCP-1 mRNA and significant increases in the mRNAs for IL-10 and HO-1 (P values given represent comparisons with glycerol treatment alone). Furthermore, pyruvate improved ATP levels. Finally, glycerol induced a paradoxical decrease in renal cortical H₂O₂ levels, which was largely normalized by pyruvate therapy (P<0.03 versus glycerol alone).

^aP<0.02 by nonparametric testing.