Neutrophil gelatinase-associated lipocalin: a novel biomarker for the early diagnosis of acute kidney injury in the emergency department.

Acute kidney injury (AKI) is a common medical problem among critical patients. In current clinical practice, AKI is diagnosed by measuring serum creatinine concentration, which is an unreliable and delayed marker of the deterioration of kidney function. Its rise occurs when a significant amount of renal function has been lost. Many are the factors able to modify physiological levels, such as age, gender, ethnicity, dietary protein intake, muscle mass or metabolism, hydration status and drugs. Definitely, creatinine, as well as blood urea nitrogen (BUN) or urine markers of kidney injury (fractional excretion of sodium, urinary concentrating ability, casts), do not directly reflect cell injury, but rather the delayed functional consequences of the damage. Due to the lack of sensitive and specific biomarkers, the identification of early stages of AKI has been impossible but, recently, neutrophil gelatinase-associated lipocalin (NGAL) is emerging as a novel biomarker of AKI from several etiologies, such as cardiac surgery, contrast nephropathy, kidney transplantation and sepsis. This protein, produced in a number of human tissues and particularly in the distal nephron, has siderophore-chelating property and acts as an iron-trasporting shuttle. NGAL increases in both serum and urine 48 hours before the rise of creatinine, and shows a strong correlation with change in creatinine concentrations. An early diagnosis of AKI allows the early institution of therapeutic measures for the protection of renal function and improves the prognosis. This possibility is particularly important in the Emergency Department for the treatment of critical patients with potential nefrotoxic therapies. Use of NGAL as early marker of AKI in the Emergency Department is discussed.

Hypokalemic rhabdomyolysis in a patient with a laparoscopic adjustable gastric banding.

Rhabdomyolysis is an acute skeletal muscle disorder characterized by altered integrity of the cell membranes of muscle fiber cells. It can be related to a variety of factors: muscular trauma, muscle enzyme deficiencies, infections, drugs, toxins, alcohol ingestion, endocrinopathies and electrolyte imbalances such as hypokalemia. We report the case of a 46-year-old woman admitted to the Emergency Department for frequent episodes of vomiting associated with food intake in the last two weeks, general muscular weakness and myalgia. Physical examination on admission was unremarkable, except for a symmetrical and dominantly proximal muscular weakness of all four extremities. Blood pressure was 116/70 mmHg with a sinus bradycardia (53 beats/min) on the electrocardiogram. Laboratory tests showed a metabolic alkalosis with marked hypokalemia (K+= 1.9 mEq/l) and elevation of muscular enzymes (myglobin= 993 ng/ml, troponin T= 0,10 ng/ml e CK= 1113 U/l). No symptoms of recurrent rhabdomyolysis were reported, patient denied alcohol consumption and there was not clinical evidence of hyperthyroidism. A iatrogenic etiology could not be excluded for certain because patient was in therapy with lansoprazole (Naranjo algorithm 3/13) but, revealing medical history that she underwent a laparoscopic adjustable gastric banding for the treatment of a severe obesity, we focused our attention on hypokalemia, due to persistent vomiting. Fasting, administration of metoclopramide and infusion of potassium chloride resulted in steady improvement of clinical conditions and normalization of electrolyte imbalance. At the clinical follow-up of three months, after partial deflation of the gastric banding, the patient was asymptomatic with muscular enzymes and potassium levels in the normal range. Authors discuss the pathophysiologic mechanisms of these alterations.

Giant paraesophageal hernia in an asymptomatic old man. The case for misdiagnosing.

We describe the case of an asymptomatic 66 year-old man with a giant paraesophageal hernia including colonic migration into the chest, responsible for the appearance of a bilateral anterior mediastinal mass on the chest radiograph. We would like to emphasise that this radiologic pattern could lead to misdiagnosing, due to the bilateral air-fluid level in the chest, close to the heart. Pericardial (effusion, cyst), bronchogenic (cyst), as well as esophageal (diverticula) diseases should be considered in the differential diagnosis, although the paucity of symptoms in our patient makes all of these syndromes unlikely to occur. It should also be emphasised that the esophagram can help differential diagnosis between mediastinic organs responsible for the pattern shown in the chest radiograph.

Modulation by adenosine of thromboxane A2 receptor-mediated constriction in the human umbilical artery.

The powerful vasoconstrictor autacoid thromboxane A2 (TxA2) has pathological roles in many diseases including pre-eclampsia or pregnancy induced hypertension (PIH). Adenosine and other purines are released by tissues during ischemia as occurs in the utero-placental circulation during PIH. These substances, particularly adenosine, may modulate TxA2 constrictor responses. We therefore characterized TxA2 receptors in the umbilical artery in vitro using the competitive antagonist GR32191. Also examined was the Ca2+ channels' involvement in adenosine-induced inhibition of TxA2 vasoconstriction. Results showed that TxA2 receptors on umbilical arteries are identical to those present in platelets, the placenta and umbilical vein. Adenosine was found to inhibit equally constriction involving either voltage or receptor operated Ca2+ channels.