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This AKI was intrinsic as showed by the Na/K urinary ratio increase and the decrease in urine concentration ability.
Another small trial applying RIC to DCD recipients (n=48), showed that RIC was associated with an increase in early estimated-GFR (eGFR) and a decrease in urine concentration of the renal injury marker neutrophil gelatinase-associated lipocalin (NGAL).
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PCE body burden, as assessed by both urine specimens and exhaled breath levels, decreased appreciably after two days away from the workplace; however, the decline in creatinine-adjusted TCA in urine concentration was not statistically significant.
Correcting for creatinine adjusts urine C-peptide concentration for variation in urine concentration and enables the use of 'spot' urine samples in place of 24-h urine collection.
Secondary outcomes included absolute increase in [Na+] at 24 h, absolute increase of [Na+] at 72 h, and absolute decrease in urine sodium concentration.
The main outcome was a serum sodium increase of ≥ 4 mmol/L in 24 h; secondary endpoints were the ability to maintain serum sodium at 24 and 72 h, a decrease in urine sodium concentration and an increase in sodium-free diuresis.
The decrease in urine [Na+] concentration was likely a dilutional effect of the increased urine water content, as total urine sodium output did not change significantly.
Rationale: As mentioned in the introduction, regardless of its severity, AKI is characterized by renal dysfunction expressed by an increased Scr concentration or a decrease in urine output.
All these patients also had a decrease in urine output.
This implicates IL-1β in sepsis-associated tubular dysfunction with decreased glomerular filtration rate, failure of urine concentration, decreased urine osmolality, increased fractional sodium excretion and glucosuria.
6-keto-PGF1α concentrations were also increased in blood vessels and the renal cortex but decreased in urine (P<0.05).
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