We analyzed the medical records of patients with an established diagnosis of acute renal infarction to identify predictive parameters of this rare disease. Seventeen patients (8 male) who were admitted to our emergency department between May 1994 and January 1998 were diagnosed by contrast-enhanced computed tomography (CT) as having acute renal infarction (0.007% of all patients). We screened the records of the 17 patients for a history with increased risk for thromboembolism, clinical symptoms, and urine and blood laboratory results known to be associated with acute renal infarction. A history with increased risk for thromboembolism with 1 or more risk factors was found in 14 of 17 patients (82%); risk factors were atrial fibrillation (n = 11), previous embolism (n = 6), mitral stenosis (n = 6), hypertension (n = 9), and ischemic cardiac disease (n = 7). All patients reported persisting pain predominantly from the flank (n = 11), abdomen (n = 4), and lower back (n = 2). On admission, elevated serum lactate dehydrogenase was found in 16 (94%) patients, and hematuria was found in 12 (71%) of 17 patients. After 24 hours all patients showed an elevated serum lactate dehydrogenase, and 14 (82%) had a positive test for hematuria. Our findings suggest that in all patients presenting with the triad--high risk of a thromboembolic event, persisting flank/abdominal/lower back pain, elevated serum levels of lactate dehydrogenase and/or hematuria within 24 hours after pain onset--contrast-enhanced CT should be performed as soon as possible to rule out or to prove acute renal infarction.

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Background-Platelet activation is a hallmark of acute coronary syndromes. Numerous lines of evidence suggest a mechanistic link between von Willebrand factor or platelet hyperfunction and myocardial damage in patients with acute coronary syndromes. Thus, we assessed whether platelet function under high shear rates (collagen adenosine diphosphate closure times [CADP-CTs]) measured with the platelet function analyzer (PFA-100) may be enhanced in patients with myocardial infarction (MI) and whether it may predict the extent of myocardial damage as measured by creatine kinase (CK-MB) or troponin T (TnT) levels. Methods and Results-Patients with acute chest pain or symptoms suggestive of acute coronary syndromes (nϭ216) were prospectively examined at an emergency department. CADP-CT was significantly shorter in patients with MI, particularly in those with an ST-segment-elevation MI (STEMI) compared with the other patient groups (unstable angina, stable coronary artery disease, or controls). Furthermore, CADP-CT and collagen epinephrine-CT at presentation were independent predictors of myocardial damage as measured by CK-MB or TnT. Patients with MI whose CADP-CT values fell in the first quartile had 3-fold higher CK-MB and TnT levels than those in the fourth quartile. Conclusions-Patients with STEMI have significantly enhanced platelet function when measured under high shear rates.CADP-CT is an independent predictor of the severity of MI, as measured by markers of cardiac necrosis. Measurement of platelet function with the PFA-100 may help in the risk stratification of patients presenting with MI. (Circulation.

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Recently we identified a novel EF-hand Ca-binding protein termed secretagogin, which is expressed in neuroendocrine cells. Immunohistochemical investigations, using a murine monoclonal and an affinity purified rabbit polyclonal anti-secretagogin antibody as well as Northern-blot and Western-blot analysis revealed a neuron-specific cerebral expression pattern. Secretagogin was detected in high quantity in basket and stellate cells of the cerebellar cortex, in secretory neurons of the anterior part of the pituitary gland and in singular neurons of the frontal and parietal neocortex. Remarkable staining intensity was observed in hypothalamic and in hippocampal neurons. Using a newly developed sandwich capture ELISA we show presence of secretagogin in serum of patients suffering from hypoxic neuronal damage. In sera obtained from 32 patients with different forms of neurological symptoms due to focal cerebral ischemia, secretagogin levels ranged from 3 to 236 pg/ml, with highest levels observed on days 2 and 3 after infarction. Three patients exhibiting minor, reversible neurological deficits had nondetectable serum secretagogin levels at time points of testing. In 50 control sera, secretagogin was below the detection limit of our ELISA. Parallel analysis of secretagogin and the established neurobiochemical marker S-100B in 14 representative patients revealed comparable results. However, S-100B levels were higher and exhibited different kinetics than secretagogin. Our data present the cerebral expression pattern of secretagogin and give evidence that this protein might represent a clinically relevant serum marker indicative for neuronal damage.

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Elevated admission CRP values in patients with symptomatic aortic aneurysm/dissection were independently associated with poor prognosis. CRP levels higher than 6.3 mg/dl indicate a high risk for short-term mortality.

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