Trends and outcomes of the use of percutaneous native kidney biopsy in the United States: 5-year data analysis of the Nationwide Inpatient Sample.

BACKGROUND: Despite an inordinate share of health care resources being utilized by patients with kidney disease, morbidity and mortality in these patients remain high. Although renal biopsy is an intervention to identify potential treatment-modifiable causes of disease, large-scale data studying the safety and outcomes of percutaneous native kidney biopsy in hospitalized patients are lacking. METHODS: We queried the Nationwide Inpatient Sample database from 2008 to 2012 and identified all hospital admissions during which a percutaneous renal biopsy was performed. Patients <18 years of age or with a transplanted kidney were excluded. Data regarding associated renal pathology and procedure-related complications were collected and analyzed. Outcomes studied were length of stay, mortality and cost adjusted for inflation. RESULTS: A total of 118 064 hospital admissions were included in our analysis. The most common complications reported after percutaneous kidney biopsy were packed red blood cell transfusion (261/1000 cases), hematuria (129/1000 cases) and bleeding (78/1000 cases). Patients had an overall mortality of 1.8%. The mean length of stay for each hospitalization was 10.65 days, with a significant difference between elective and nonelective admissions (6.3 versus 11.7; P < 0.01). The average cost per hospitalization was US$22 917 after adjusting for inflation, again with a significant difference between elective and nonelective admissions (15 168 versus 24 780; P < 0.01). CONCLUSION: Overall, percutaneous renal biopsy is considered a safe procedure; however, our study based on a national database demonstrates a relatively higher complication rate as compared with the limited prior available studies.

Decreased expression of Klotho in cardiac atria biopsy samples from patients at higher risk of atherosclerotic cardiovascular disease.

BACKGROUND: Klotho proteins (α- and ß) are membrane-based circulating proteins that regulate cell metabolism, as well as the lifespan modulating activity of Fibroblast Growth Factors (FGFs). Recent data has shown that higher plasma circulating Klotho levels reduce cardiovascular risk, suggesting Klotho has a protective role in cardiovascular diseases. However, although so far it has been identified in various organs, it is unknown whether cardiomyocytes express Klotho and FGFs, and whether high cardiovascular risk could affect cardiac expression of Klotho, FGFs and other molecules. METHODS: We selected 20 patients with an estimated 10-year high atherosclerotic cardiovascular disease and 10 age-matched control subjects with an estimated 10-year low risk undergone cardiac surgery for reasons other than coronary artery by-pass. In myocardial biopsies, we evaluated by immuno-histochemistry whether Klotho and FGFs were expressed in cardiomyocytes, and whether higher cardiovascular risk influenced the expression of other molecules involved in endoplasmic reticulum stress, oxidative stress, inflammation and fibrosis. RESULTS: Only cardiomyocytes of patients with a higher cardiovascular risk showed lower expression of Klotho, but higher expressions of FGFs. Furthermore, higher cardiovascular risk was associated with increased expression of oxidative and endoplasmic reticular stress, inflammation and fibrosis. CONCLUSIONS: This study showed for the first time that Klotho proteins are expressed in human cardiomyocytes and that cardiac expression of Klotho is down-regulated in higher cardiovascular risk patients, while expression of stress-related molecules were significantly increased.

Diagnostic Approach to Myocarditis Mimicking Myocardial Infarction at Initial Presentation.

We present a case of a 35-year-old male patient with a 12-hour history of sudden-onset, crushing chest pain and associated complaints of profuse diaphoresis, nausea and vomiting. The patient was transferred to our institution from an outside hospital for evaluation and possible emergent catheterization. Left heart catheterization was conclusive for normal coronary arteries and a ventriculogram revealed a left ventricular ejection fraction of approximately 45%. Due to a suspicion of myocarditis based on clinical history, pertinent serology tests were ordered, which were found to be negative. Cardiac magnetic resonance on delayed enhancement imaging showed typical sub-epicardial enhancement in a pattern most consistent with myocarditis. The patient was eventually diagnosed with myocarditis and discharged home later, without needing a myocardial biopsy. We present and discuss here the indications of myocardial biopsy and compare the relative utility of cardiac magnetic resonance imaging in formulating the diagnosis of myocarditis.

Current strategies in the evaluation and management of cocaine-induced chest pain.

With each successive year, the number of Emergency Department (ED) visits related to illicit drug abuse has progressively increased. Cocaine is the most common illegal drug to cause a visit to the ED. Cocaine use results in a variety of pathophysiological changes with regards to the cardiovascular system, such as constriction of coronary vessels, dysfunction of vascular endothelium, decreased aortic elasticity, hemodynamic disruptions, a hypercoagulable state, and direct toxicity to myocardial and vascular tissue. The clinical course of patients with cocaine-induced chest pain (CCP) is often challenging, and electrocardiographic findings can be potentially misleading in terms of diagnosing a myocardial infarction. In addition, there is no current satisfactory study regarding outcomes of use of various pharmacological drug therapies to manage CCP. At present, calcium-channel blockers and nitroglycerin are two pharmacological agents that are advocated as first-line drugs for CCP management, although the role of labetalol has been controversial and warrants further investigation. We performed an extensive search of available literature through a large number of scholarly articles previously published and listed on Index Medicus. In this review, we put forward a concise summary of the current approach to a patient presenting to the ED with CCP and management of the clinical scenario. The purpose of this review is to summarize the understanding of cocaine's cardiovascular pathophysiology and to examine the current approach for proper evaluation and management of CCP.

Mechanisms of myocardial ischemia-reperfusion injury and the cytoprotective role of minocycline: scope and limitations.

Deep insight into the complex mechanisms of myocardial ischemia-reperfusion injury has been attained in the past years. Minocycline is a second-generation tetracycline with US FDA approval for clinical use in various infections. Lately, several noninfectious cytoprotective activities of minocycline have been discovered as well. There now exists encouraging evidence of its protective role in cardiovascular pathology and its activity against myocardial ischemia-reperfusion injury. In this article, an overview of the major mechanisms involved in myocardial ischemia-reperfusion injury is presented. This is followed by an analysis of the mechanisms by which minocycline exerts its cytoprotective role and of studies that have been conducted in order to analyze minocycline, along with a review of the scope and limitations of its role as a cytoprotective agent.

The role and modulation of autophagy in experimental models of myocardial ischemia-reperfusion injury.

A physiological sequence called autophagy qualitatively determines cellular viability by removing protein aggregates and damaged cytoplasmic constituents, and contributes significantly to the degree of myocardial ischemia-reperfusion (I/R) injury. This tightly orchestrated catabolic cellular 'housekeeping' process provides cells with a new source of energy to adapt to stressful conditions. This process was first described as a pro-survival mechanism, but increasing evidence suggests that it can also lead to the demise of the cell. Autophagy has been implicated in the pathogenesis of multiple cardiac conditions including myocardial I/R injury. However, a debate persists as to whether autophagy acts as a protective mechanism or contributes to the injurious effects of I/R injury in the heart. This controversy may stem from several factors including the variability in the experimental models and species, and the methodology used to assess autophagy. This review provides updated knowledge on the modulation and role of autophagy in isolated cardiac cells subjected to I/R, and the growing interest towards manipulating autophagy to increase the survival of cardiac myocytes under conditions of stress-most notably being I/R injury. Perturbation of this evolutionarily conserved intracellular cleansing autophagy mechanism, by targeted modulation through, among others, mammalian target of rapamycin (mTOR) inhibitors, adenosine monophosphate-activated protein kinase (AMPK) modulators, calcium lowering agents, resveratrol, longevinex, sirtuin activators, the proapoptotic gene Bnip3, IP3 and lysosome inhibitors, may confer resistance to heart cells against I/R induced cell death. Thus, therapeutic manipulation of autophagy in the challenged myocardium may benefit post-infarction cardiac healing and remodeling.