Importance of blood cultures to aid the diagnosis of Lemierre's syndrome.

This is a case report of Lemierre's syndrome, a septic thrombophlebitis of the internal jugular vein (IJV) usually preceded by pharyngitis and bacteraemia with an anaerobic organism. Fusobacterium necrophorum is ananaerobic Gram-negative bacillus and is the most common organism reported to cause Lemierre's syndrome which usually occurs one to three weeks post pharyngitis or oropharyngeal surgery. A 21-year-old patient presented with signs of sepsis and a history of sore throat, fever, and tender cervical lymph nodes.

Some biomarkers of acute kidney injury are increased in pre-renal acute injury.

Pre-renal acute kidney injury (AKI) is assumed to represent a physiological response to underperfusion. Its diagnosis is retrospective after a transient rise in plasma creatinine, usually associated with evidence of altered tubular transport, particularly that of sodium. In order to test whether pre-renal AKI is reversible because injury is less severe than that of sustained AKI, we measured urinary biomarkers of injury (cystatin C, neutrophil gelatinase-associated lipocalin (NGAL), γ-glutamyl transpeptidase, IL-18, and kidney injury molecule-1 (KIM-1)) at 0, 12, and 24 h following ICU admission.

Albuminuria increases cystatin C excretion: implications for urinary biomarkers.

Background: Low-molecular weight (LMW) proteins, including albumin and novel urinary biomarkers of acute kidney injury (AKI) such as cystatin C and neutrophil gelatinase-associated lipocalin (NGAL), are normally absorbed from the glomerular filtrate by receptor-mediated transport. We evaluated the effect of albuminuria on urinary excretion of novel biomarkers.

Methods: Sprague-Dawley rats given four injections over 2 days of 5 mg/g body wt/day bovine serum albumin (BSA) in saline were compared with controls given saline alone.

Improved performance of urinary biomarkers of acute kidney injury in the critically ill by stratification for injury duration and baseline renal function.

To better understand the diagnostic and predictive performance of urinary biomarkers of kidney injury, we evaluated γ-glutamyltranspeptidase (GGT), alkaline phosphatase (AP), neutrophil-gelatinase-associated lipocalin (NGAL), cystatin C (CysC), kidney injury molecule-1 (KIM-1), and interleukin-18 (IL-18) in a prospective observational study of 529 patients in 2 general intensive care units (ICUs). Comparisons were made using the area under the receiver operator characteristic curve (AUC) for diagnosis or prediction of acute kidney injury (AKI), dialysis, or death, and reassessed after patient stratification by baseline renal function (estimated glomerular filtration rate, eGFR) and time after renal insult. On ICU entry, no biomarker had an AUC above 0.

Urinary cystatin C is diagnostic of acute kidney injury and sepsis, and predicts mortality in the intensive care unit.

Introduction: To evaluate the utility of urinary cystatin C (uCysC) as a diagnostic marker of acute kidney injury (AKI) and sepsis, and predictor of mortality in critically ill patients.

Methods: This was a two-center, prospective AKI observational study and post hoc sepsis subgroup analysis of 444 general intensive care unit (ICU) patients. uCysC and plasma creatinine were measured at entry to the ICU.

Rapid detection of acute kidney injury by plasma cystatin C in the intensive care unit.

Background: Plasma cystatin C (pCysC) has been proposed as an alternative to plasma creatinine (pCr) as a measure of renal function. We compared the detection of functional change by both biomarkers in critically ill patients.

Methods: pCysC and pCr were measured on admission to one of two intensive care units (ICU) and then daily over 7 days.