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Asymptomatic hyperuricemia is frequently observed in patients with kidney disease. Although a substantial number of epidemiologic studies have suggested that an elevated uric acid level plays a causative role in the development and progression of kidney disease, whether hyperuricemia is simply a result of decreased renal excretion of uric acid or is a contributor to kidney disease remains a matter of debate. Over the last two decades, multiple experimental studies have expanded the knowledge of the biological effects of uric acid beyond its role in gout. In particular, uric acid induces immune system activation and alters the characteristics of resident kidney cells, such as tubular cells, endothelial cells, and vascular smooth muscle cells, toward a proinflammatory and profibrotic state. These findings have led to an increased awareness of uric acid as a potential and modifiable risk factor in kidney disease. Here, we discuss the effects of uric acid on the immune system and subsequently review the effects of uric acid on the kidneys mainly in the context of inflammation.Recently, research has redirected its interests in uric acid (UA) from gout, an inflammatory disease in joints, to groups of closely interrelated pathologies associated with cardiovascular and kidney dysfunction. Many epidemiological, clinical, and experimental studies have shown that UA may play a role in the pathophysiology of the cardiorenal syndrome continuum; however, it is still unclear if it is a risk factor or a causal role. Hyperuricemia has been well studied in the past two decades, revealing mechanistic insights into UA homeostasis. Likewise, some epidemiological and experimental evidence suggest that hypouricemia can lead to cardiorenal pathologies. The goal of this mini-review is to highlight why studying both hyperuricemia and hypouricemia is warranted as well as to summarize the relevance of UA to kidney function.Changes in mitochondrial function are central to many forms of kidney disease including acute injury, diabetic nephropathy, hypertension and chronic kidney diseases. As such, there is an increasing need for reliable and fast methods for assessing mitochondrial respiratory function in renal cells. Despite being indispensable for many mechanistic studies, cultured cells or isolated mitochondria, however, often do not recapitulate in vivo or close-to-in vivo situations. Cultured and/or immortalized cells often change their bioenergetic profile and phenotype compared to in vivo or ex vivo situations, and isolated mitochondria are simply removed from their cellular milieu. This is especially important for extremely complex organs such as the kidney. Here we report the development and validation of a new approach for rapid assessment of mitochondrial oxygen consumption on freshly isolated glomeruli or proximal tubular (PT) fragments using the Agilent SeaHorse XFe24 and XF96 Extracellular Flux Analyzers. We validated the technique in several healthy and diseased rodent models - the C57BL/6J mouse, the diabetic db/db mouse and their matching db/+ control and the Dahl salt sensitive rat. We compared the data to respiration from isolated mitochondria. The method can be adapted and used for rapid assessment of mitochondrial oxygen consumption from any rodent model of the investigator's choice. The isolation methods presented here ensure viable and functional PT fragments and glomeruli, with preserved cellular environment for studying mitochondrial function within the context of their surroundings and interactions.MALDI-TOF MS provides fast, easy to perform and cost-effective diagnosis in clinical microbiology laboratories, however in some cases results of MALDI-TOF MS should be confirmed with additional tests. This confirmation is especially important for causes of life-threatening infections like Neisseria meningitidis. In our laboratory, three isolates were identified as N. meningitidis by Bruker MALDI Biotyper (BD, USA) between April 2018 and March 2019 from clinical specimens of blood, sputum, and urine. 16S rRNA sequencing was performed for further investigation. Two of the isolates were identified as Neisseria subflava and only one was confirmed as N. meningitidis by sequencing. These results show that MALDI-TOF MS is not always reliable in the diagnosis of N. meningitidis and clinical microbiologists should confirm these results with additional tests. Also, clinical correlations should be determined. Accurate identification of this microorganism is very important because of the necessity of prophylactic antimicrobial usage and biosafety precautions. Enlarged databases of Neisseria species are needed to overcome this problem.This study aimed to evaluate the routine identification tools available in Lebanon for differentiation of Escherichia coli and Shigella spp. The identification of 43 isolates defined as Shigella spp. [https://www.selleckchem.com/products/spop-i-6lc.html SPOP-i-6lc inhibitor] by Api 20E was accessed using MALDI-TOF, serological testing, duplex PCR targeting ipaH (present in Shigella spp. and enteroinvasive E. coli "EIEC") and lacY (found in E. coli including EIEC but not Shigella spp.) as well as gyrB gene sequencing. Antibiotic susceptibility was investigated as well as Shiga-toxin production. All isolates were identified as E. coli by MALDI-TOF while the PCR showed a disparate group of 26 EIEC, 11 Shigella spp., 5 E. coli and 1 inactive E. coli. However, the sequencing of gyrB gene, which was recently described as a suitable marker for distinguishing E. coli and Shigella spp., identified all isolates as E. coli. Antibiotic resistance was noticeable against ß-lactams, rifampicin, trimethoprim-sulfamethoxazole, gentamicin, and ciprofloxacin. The most common variants of beta-lactamase genes were blaTEM-1, blaCTX-M-15, and blaCTX-M-3. A great discordance between the used methods in identification was revealed herein. An accurate identification technique able to distinguish E. coli from Shigella spp. in routine laboratories is a pressing need in order to select the appropriate treatment and assess the epidemiology of these bacteria.Streptococcus suis is an emerging zoonotic human pathogen, which is a causative agent of invasive infections in people who are in close contact with infected pigs or contaminated pork products. It is associated with severe systemic infections, most commonly meningitis and sepsis, which may lead to high rates of morbidity and mortality. Serotype 2 is the most prevalent type in S. suis infections in humans. We have reported a case of a very rapidly proceeding fatal human S. suis infection in a splenectomized, but otherwise immunocompetent patient in Hungary. We would like to highlight the attention for this pathogen for the risk group patients, not only pig breeders, veterinarians, abattoir workers, meat processing and transport workers, butchers and cooks, that those persons who are immunocompromised including those with spleen removed, persons with diabetes mellitus, cancer and alcoholism, are also at greater risk of infection.