[What To Do In Case Of Hematuria? - Step By Step]. / Was tun bei Hämaturie? ­ Schritt für Schritt.

Hematuria is a common clinical finding and has a wide spectrum of possible causes. Erythrocytes can originate from any part of the genitourinary tract. An urine dipstick test is the first step in diagnostic approach. Medical history may help to narrow down the range of causes: arterial hypertension or a family history of renal disease may indicate a renal disease. Risk factors for an urinary tract malignoma point to an urological origin. If the microscopy shows more than 5 % acanthocytes in the urine sediment, a glomerular cause can be assumed. Normal erythrocytes suggest a non-glomerular cause. A nephrologist should be consulted if urine sediment microscopy and other clinical features (e. g. clinically relevant proteinuria, elevated serum creatinine) indicate a renal disease. In this case, a renal biopsy should be considered to confirm the diagnosis of glomerulopathy and to develop a treatment plan. If an urological pathology is suspected, sonography should be complemented by a multi-phasic computed tomography. Based on the imaging results, a retrograde ureteroscopy should be considered. Repeated urinalysis on an annual basis for two consecutive years is recommended, if no diagnosis can be established.

Systemic reaction to and interference with urine protein measurements after intravenous fluorescein injection.

BACKGROUND: Fluorescein angiography is an important and frequently used diagnostic tool in ophthalmological practice. In this case report we describe a patient who experienced an anaphylactic reaction after the injection of fluorescein. Furthermore, we report an interference with laboratory testing by fluorescein in this patient and summarize the literature on this topic. CASE PRESENTATION: An 86-year old Caucasian woman undergoing fluorescein angiography due to suspected peripapillary neovascularizations collapsed after the injection of fluorescein. The patient developed an anaphylactic reaction. With fluid resuscitation and oxygen therapy, the patient regained consciousness after a few minutes. The patient was admitted to the geriatric ward for observation, and routine blood and urine tests were performed. Urine protein concentration appeared to be falsely increased as a consequence of disturbance of the laboratory analysis by the presence of fluorescein. CONCLUSIONS: Serious complications can occur with fluorescein angiography, such as an anaphylactic reaction. In the case of anaphylaxis appropriate supportive measures including the use of oxygen and epinephrine (e.g. EpiPen), should be available to prevent morbidity and mortality from this test. Furthermore, these potential complications should be taken into consideration when choosing the healthcare setting for fluorescein angiography, such as the immediate availability of an acute medical team. Several studies have demonstrated the interference of laboratory analyses by fluorescein. The majority of these studies were published 10 to 30 years ago. By presenting this case, the authors hope to bring renewed attention to this phenomenon among clinicians, as falsely increased or decreased laboratory values can result in unnecessary diagnostics and/or therapy.

Metabolic preference of nitrate over oxygen as an electron acceptor in foraminifera from the Peruvian oxygen minimum zone.

Benthic foraminifera populate a diverse range of marine habitats. Their ability to use alternative electron acceptors-nitrate (NO3-) or oxygen (O2)-makes them important mediators of benthic nitrogen cycling. Nevertheless, the metabolic scaling of the two alternative respiration pathways and the environmental determinants of foraminiferal denitrification rates are yet unknown. We measured denitrification and O2 respiration rates for 10 benthic foraminifer species sampled in the Peruvian oxygen minimum zone (OMZ). Denitrification and O2 respiration rates significantly scale sublinearly with the cell volume. The scaling is lower for O2 respiration than for denitrification, indicating that NO3- metabolism during denitrification is more efficient than O2 metabolism during aerobic respiration in foraminifera from the Peruvian OMZ. The negative correlation of the O2 respiration rate with the surface/volume ratio is steeper than for the denitrification rate. This is likely explained by the presence of an intracellular NO3- storage in denitrifying foraminifera. Furthermore, we observe an increasing mean cell volume of the Peruvian foraminifera, under higher NO3- availability. This suggests that the cell size of denitrifying foraminifera is not limited by O2 but rather by NO3- availability. Based on our findings, we develop a mathematical formulation of foraminiferal cell volume as a predictor of respiration and denitrification rates, which can further constrain foraminiferal biogeochemical cycling in biogeochemical models. Our findings show that NO3- is the preferred electron acceptor in foraminifera from the OMZ, where the foraminiferal contribution to denitrification is governed by the ratio between NO3- and O2.

Regulation of podocyte survival and endoplasmic reticulum stress by fatty acids.

Apoptosis of podocytes is considered critical in the pathogenesis of diabetic nephropathy (DN). Free fatty acids (FFAs) are critically involved in the pathogenesis of diabetes mellitus type 2, in particular the regulation of pancreatic ß cell survival. The objectives of this study were to elucidate the role of palmitic acid, palmitoleic, and oleic acid in the regulation of podocyte cell death and endoplasmic reticulum (ER) stress. We show that palmitic acid increases podocyte cell death, both apoptosis and necrosis of podocytes, in a dose and time-dependent fashion. Palmitic acid induces podocyte ER stress, leading to an unfolded protein response as reflected by the induction of the ER chaperone immunoglobulin heavy chain binding protein (BiP) and proapoptotic C/EBP homologous protein (CHOP) transcription factor. Of note, the monounsaturated palmitoleic and oleic acid can attenuate the palmitic acid-induced upregulation of CHOP, thereby preventing cell death. Similarly, gene silencing of CHOP protects against palmitic acid-induced podocyte apoptosis. Our results offer a rationale for interventional studies aimed at testing whether dietary shifting of the FFA balance toward unsaturated FFAs can delay the progression of DN.

The relationship of cigarette smoking to postoperative complications from dental extractions among female inmates.

OBJECTIVES: The purpose of this study is to assess the contribution of smoking to postoperative complications, including alveolar osteitis (dry socket), after dental extractions. In addition, it attempts to determine the effect of the ban imposed on tobacco use in the prison on postoperative complications. STUDY DESIGN: All inmates having dental extractions at the Federal Correctional Institution in Danbury, CT, during the period January 2004 to April 2005, were included in this study (N = 219; mean age = 37.7 years). Data on postextraction complications were analyzed for association with smoking by using the chi-square test. Significance was set at P < .05. RESULTS: The incidences of overall complications and alveolar osteitis were 19.6% and 5.0%, respectively. It was found that (1) there was a significant difference in overall complications between smokers and nonsmokers (P = .02), (2) there was a significant difference in the incidence of alveolar osteitis between mandibular third molar and other extractions, regardless of smoking status (P = .02), (3) surgical trauma contributed significantly to both an increase in total complications (P = .05) and alveolar osteitis (P = .01), and (4) smoking appeared to be a contributing factor to increased complications among multiple extractions (P = .03). CONCLUSION: In this study, smoking, mandibular third molars, and surgical trauma were significantly associated with the increased incidence of overall complications including alveolar osteitis.

Glomerular podocytes contain neuron-like functional synaptic vesicles.

Although patients with chronic renal failure are increasing worldwide, many aspects of kidney biology remain to be elucidated. Recent research has uncovered several molecular properties of the glomerular filtration barrier, in which podocytes, highly differentiated, ramified cells that enwrap the glomerular basement membrane, have been reported to be mainly responsible for filter's selectivity. We previously described that podocytes express Rab3A, a GTPase restricted to cell types that are capable of highly regulated exocytosis, such as neuronal cells. Here, we first demonstrate by a proteomic study that Rab3A in podocytes coimmmunoprecipitates with molecules once thought to be synapse specific. We then show that podocytes possess structures resembling synaptic vesicles, which contain glutamate, coexpress Rab3A and synaptotagmin 1, and undergo spontaneous and stimulated exocytosis and recycling, with glutamate release. Finally, from the results of a cDNA microarray study, we describe the presence of a series of neuron- and synapse-specific molecules in normal human glomeruli and confirm the glomerular protein expression of both metabotropic and ionotropic glutamate receptors. These data point toward a synaptic-like mechanism of communication among glomerular cells, which perfectly fits with the molecular composition of the glomerular filter and puts in perspective several previous observations, proposing a different working hypothesis for understanding glomerular signaling dynamics.

Functional consequences of integrin-linked kinase activation in podocyte damage.

BACKGROUND: The delicate foot process architecture of glomerular podocytes critically depends on integrin mediated cell-glomerular basement membrane (GBM) interaction. Integrin signaling via the integrin-linked kinase (ILK) is activated in podocyte damage and associated with considerable podocyte phenotype alterations. ILK has been shown to regulate cell fate via nuclear interaction of beta-catenin with lymphoid enhancer factor (LEF-1) transcription factors. The aim of this study was to elucidate the molecular mechanisms of ILK dependant phenotype regulation in podocytes. METHODS: ILK function was evaluated in conditionally immortalized murine glomerular epithelial cells using overexpression of ILK and a small molecule ILK inhibitor in puromycin/adriamycin-induced podocyte damage in vitro and in vivo. RESULTS: Kinase active, but not mutant ILK induced translocation of beta-catenin to the cell nucleus, de novo expression of LEF-1, and nuclear colocalization of beta-catenin and LEF-1. The role of ILK signaling in podocyte damage was evaluated using puromycin, an agent known to cause selective proteinuria and to increase ILK activity. The small molecular ILK inhibitor MC-5 blocked puromycin-induced nuclear translocation of beta-catenin, podocyte detachment, cell proliferation, and repression of the slit membrane molecules P-cadherin and CD2ap. In vivo activation of the beta-catenin pathway could be shown by nuclear colocalization of beta-catenin with WT-1 in adriamycin nephropathy. CONCLUSION: ILK regulates podocyte cell matrix interaction, proliferation, and slit membrane gene expression in podocyte damage. As this pathway is amendable to pharmacologic intervention, further detailed studies of in vivo ILK function in glomerular disease appear justified.