Prophylactic N-acetylcysteine decreases serum CRP but not PCT levels and microalbuminuria following major abdominal surgery. A prospective, randomised, double-blinded, placebo-controlled clinical trial

Abstract

In this study, short-term NAC treatment decreased CRP levels, but failed to attenuate any other inflammatory response, as monitored by serum PCT and microalbuminuria. Overall, our results do not support the routine prophylactic use of NAC as a free radical scavenger in abdominal surgery.

Monitoring Urinary Orosomucoid in Acute Inflammation: Observations on Urinary Excretion of Orosomucoid, Albumin, α1-Microglobulin, and IgG

“…The second group of patients (n ϭ 6), representing cases with an expected inflammatory response to surgery (10 ), were studied from the day before the surgical intervention for up to 23 days after surgery to monitor changes in urinary protein excretion from the beginning to the end of an inflammatory event. Data from catheter urine samples obtained within the first 4 h after surgery were used for comparison with results from catheter urine obtained from the sepsis patients.…”

“…Gosling and coworkers (2,8 ) have presented findings indicating that proteinuria occurring 2-4 days after trauma coincides with an increase in plasma C-reactive protein (CRP), and that albuminuria present within 15 min of admission to the intensive care unit (ICU) shows promise as a predictor of outcome. These authors stated that microalbuminuria is a marker of systemic capillary permeability, a view that has been rejected by Molnar and coworkers (9,10 ), who argued that microalbuminuria in the critically ill is an acute marker of an inflammatory insult rather than a marker of generalized capillary leakage.…”

Contrast-induced acute kidney injury and renal support for acute kidney injury: a KDIGO summary (Part 2)

“…In addition, NAC is inexpensive and appears to be safe, although it may have some detrimental effects on myocardial and coagulation function [36-38]. The safety of NAC should further be amended, particularly when high intravenous doses are used, as in some of the RCTs in CI-AKI.…”

Supplemental N-acetylcysteine and other measures that boost intracellular glutathione can downregulate interleukin-1β signalling: a potential strategy for preventing cardiovascular events?

“…Indeed, several studies evaluating intravenous or oral NAC administration in various proinflammatory conditions have demonstrated precisely this. [50][51][52][53] The other key determinant of the rate of glutathione synthesis is the expression of gamma-glutamylcysteine synthetase, a phase 2 enzyme whose transcription is stimulated by activation of the nuclear factor (erythroid-derived 2)-like 2 (nrf2) transcription factor. 54 55 A wide range of nutraceuticals and drugs, characterised as 'phase 2 inducers', are known to activate nrf2, leading to induction of a range of antioxidant enzymes, as well as gamma-glutamylcysteine synthetase.…”