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Funding Acknowledgements Type of funding sources: None. Introduction In general, most people spend their day in a non-fasting state. Hence, it is suggested that the changes in atherosclerosis happen mainly under the influence of non-fasting lipids. Up to date, the studies in the postprandial state were primarily performed on healthy subjects. Aim This exploratory, cross-sectional study investigates the change in lipid profile, in biomarkers of inflammation, as well as markers of platelet activation in patients with different cardiovascular risk profiles in the postprandial state. Methods The studied population consists of 66 patients with different cardiovascular risk: patients with a history of chronic coronary syndrome (CCS) and diabetes mellitus type 2 (DM2) (n=20), CCS without DM2 (n=25), and a healthy control group (n=21). Lipid variables and markers of platelet function were assessed during the fasting state (baseline) and three and five hours after a standardized fat meal using a standardized oral fat tolerance test (OFTT), a milkshake with 90g of fat. Platelet activity was measured with the Multiplate Assay using adenosine diphosphate (ADP), arachidonic acid (ASPI) and thrombin-receptor activating peptide (TRAP) as stimulants. Results Patients with CCS and DM2 were significantly older and had the highest BMI. All patients with CCS were on acetylsalicylic acid, and 95% of CCS patients were on high-dose statins. HDL-c decreased significantly during the OFTT, with a peak after five hours (3.46±0.4 mg/dL, p Conclusion This study showed that a standardized fatty meal changes HDL-c and TG concentrations and leads to an increased postprandial inflammation response irrespective of the cardiovascular risk and to increased platelet activity in healthy subjects, while there was no increase in platelet activity in higher-risk CCS patients.

Introduction Measuring lipid panel in the fasting state can be inconvenient for patients and may aggravate their compliance. Moreover, people spend most of the day in the nonfasting state. Hence, it suggests that the changes in the process of atherosclerosis happen mainly under the influence of nonfasting lipids. Up to date, the studies in the postprandial state were primarily performed in healthy subjects. Aim This exploratory study investigates the change in lipid profile and platelet activity in patients with different cardiovascular risk profiles in the postprandial state. Methods The studied population consists of 66 patients with different cardiovascular risks: patients with coronary artery disease (CAD) and diabetes mellitus type 2 (DM2) (n=20), CAD without DM2 (n=25), and a healthy control group (n=21). Lipid variables and markers of platelet function were assessed during the fasting state and 3 and 5 hours after a standardized fat meal using a standardized oral fat tolerance test (OFTT), a milkshake with 90g of fat. The platelet activity was measured with a Multiplate test using ADP, ASPI and TRAP reagents. Results Patients with CAD and DM2 were significantly older and had the highest BMI. All patients with CAD were on acetylsalicylic acid, and 95% of CAD patients were on high-dose statins. Total cholesterol, LDL-c, Apolipoprotein A1, and Apolipoprotein B did not change during the OFTT, irrespective of the group. However, HDL-c decreased statistically significantly three and five hours after the fat loading with a peak after five hours (3.46±0.4 mg/dL, p Conclusion This study showed that fatty meal causes worsening of lipid profile and leads to increased platelet activity in subjects irrespective of cardiovascular risk profile. Funding Acknowledgement Type of funding sources: None.

After taking a patient's history and physical examination, lung ultrasound can immediately reveal numerous causes and complications in patients suffering from respiratory tract infection and/or dyspnea. It can thus facilitate decisions on further diagnostic and first therapeutic procedures, even in patients with a SARS-CoV‑2 infection who present to the emergency room. This review article highlights the typical findings of lung ultrasound in patients with COVID-19 and discusses its value compared to other imaging methods.

Hermansky-Pudlak Syndrome (HPS) is a rare disease caused by mutations in the genes coding for various HPS proteins. HPS proteins are part of multi-subunit complexes involved in the biogenesis of organelles from the lysosomal-endosomal-system. In humans, this syndrome is characterized by the presence of albinism, platelet dysfunction and pulmonary fibrosis. The renal component to the disease remains unstudied and untreated in patients with HPS. Here we demonstrate that in humans, HPS proteins have a high renal expression with active transcription of HPS1, 3, 4 and 5 in human podocyte cell culture, suggesting that impaired function of HPS proteins could directly impact renal function. Therefore, we developed a zebrafish model to study the renal involvement of HPS proteins in proteinuric kidney disease. Remarkably, knockdown of HPS genes in zebrafish causes glomerular injury with edema, proteinuria and structural changes of the glomerular filtration barrier. Moreover, reduced expression of HPS proteins in zebrafish recapitulates other important disease hallmarks, like hypopigmentation and accumulation of intracellular debris characteristic of lysosomal disorders. In conclusion, we present a valid zebrafish model that highlights the previously underestimated relevance of renal disease in HPS. This draws attention to the therapeutic options available to manage this component of the syndrome.

Summary Kidney injury significantly increases overall mortality. Neutrophilic granulocytes (neutrophils) are the most abundant human blood leukocytes. They are characterized by a high turnover rate, chiefly controlled by granulocyte colony stimulating factor (G‐CSF). The role of kidney injury and uremia in regulation of granulopoiesis has not been reported. Kidney transplantation, which inherently causes ischemia–reperfusion injury of the graft, elevated human neutrophil expression of the surface glycoprotein CD177. CD177 is among the most G‐CSF‐responsive neutrophil genes and reversibly increased on neutrophils of healthy donors who received recombinant G‐CSF. In kidney graft recipients, a transient rise in neutrophil CD177 correlated with renal tubular epithelial G‐CSF expression. In contrast, CD177 was unaltered in patients with chronic renal impairment and independent of renal replacement therapy. Under controlled conditions of experimental ischemia–reperfusion and unilateral ureteral obstruction injuries in mice, renal G‐CSF mRNA and protein expression significantly increased and systemic neutrophilia developed. Human renal tubular epithelial cell G‐CSF expression was promoted by hypoxia and proinflammatory cytokine interleukin 17A in vitro. Clinically, recipients of ABO blood group‐incompatible kidney grafts developed a larger rise in neutrophil CD177. Their grafts are characterized by complement C4d deposition on the renal endothelium, even in the absence of rejection. Indeed, complement activation, but not hypoxia, induced primary human endothelial cell G‐CSF expression. Our data demonstrate that kidney injury induces renal G‐CSF expression and modulates granulopoiesis. They delineate differential G‐CSF regulation in renal epithelium and endothelium. Altered granulopoiesis may contribute to the systemic impact of kidney injury., Our prospective study in kidney graft recipients shows that human neutrophil CD177, a major G‐CSF target gene, significantly and reversibly increases after transplantation. Two mouse models demonstrate enhanced renal G‐CSF expression and granulopoiesis after acute kidney injury under controlled conditions in vivo. Experiments in primary human cells revealed differential regulation of G‐CSF in human renal tubular epithelium and vascular endothelium by hypoxia, IL‐17A and complement activation as possible underlying mechanisms.

Background Peritoneal dialysis (PD)-associated peritonitis remains by far the most important complication requiring patients to transfer to hemodialysis and has a major impact on patient morbidity and mortality. Current International Society for Peritoneal Dialysis (ISPD) guidelines on peritonitis recommend analysis of peritonitis episodes only in trained patients. In a large tertiary care center, we analyzed peritonitis episodes accounting for different groups of untrained patients and compared these with episodes in the trained patient population. Methods We analyzed data collected prospectively over a 15-year time span regarding differences between peritonitis episodes in trained patients and episodes in untrained patients post-catheter insertion but prior to training completion as well as on in-center intermittent PD with respect to incidence rates, pathogenic organisms, outcome, and peritonitis predictors. Results In 275 patients, a total of 160 peritonitis episodes in trained patients were counted. A total of 27 additional episodes in untrained patients were recorded. When accounting for these episodes, the peritonitis incidence significantly increased and the percentage of peritonitis-free patients decreased. Peritonitis episodes in untrained patients were most often culture-negative and the pathogen spectrum differed significantly compared with episodes counted as per ISPD recommendations, while outcome of peritonitis episodes did not differ. Predictors of peritonitis after multivariate logistic regression analysis included glomerulonephritis as primary kidney disease, being on home PD rather than being on in-center intermittent PD, and higher dialysis vintage. Conclusions Depending on local practice patterns, we argue that centers should additionally monitor peritonitis episodes in untrained patients because computation of statistics as per ISPD recommendations could underestimate peritonitis incidence and may depict a distorted pathogen spectrum.

This pre-specified analysis of DAPA-CKD assessed the impact of sodium-glucose cotransporter 2 inhibition on abrupt declines in kidney function in high-risk patients based on having chronic kidney disease (CKD) and substantial albuminuria. DAPA-CKD was a randomized, double-blind, placebo-controlled trial that had a median follow-up of 2.4 years. Adults with CKD (urinary albumin-to-creatinine ratio 200-5000 mg/g and estimated glomerular filtration rate 25-75 mL/min/1.73m2) were randomized to dapagliflozin 10 mg/day matched to placebo (2152 individuals each). An abrupt decline in kidney function was defined as a pre-specified endpoint of doubling of serum creatinine between two subsequent study visits. We also assessed a post-hoc analysis of investigator-reported acute kidney injury-related serious adverse events. Doubling of serum creatinine between two subsequent visits (median time-interval 100 days) occurred in 63 (2.9%) and 91 (4.2%) participants in the dapagliflozin and placebo groups, respectively (hazard ratio 0.68 [95% confidence interval 0.49, 0.94]). Accounting for the competing risk of mortality did not alter our findings. There was no heterogeneity in the effect of dapagliflozin on abrupt declines in kidney function based on baseline subgroups. Acute kidney injury-related serious adverse events were not significantly different and occurred in 52 (2.5%) and 69 (3.2%) participants in the dapagliflozin and placebo groups, respectively (0.77 [0.54, 1.10]). Thus, in patients with CKD and substantial albuminuria, dapagliflozin reduced the risk of abrupt declines in kidney function. HJLH and DC are co-primary authors. The DAPA-CKD Trial Committees and Investigators are listed in the Appendix.

Home blood pressure monitoring in combination with cointerventions can contribute to a better blood pressure control. More complex telemonitoring projects have shown promising initial results in studies in primary care and also in certain patient groups (e.g. pregnant women). The integration into the clinical routine is of crucial importance because "stand-alone" solutions have yet to show convincing effects on blood pressure. The new German Digital Care Act (Digitale-Versorgung-Gesetz, DVG) provides a framework to introduce, validate and prescribe digital applications in routine care financed by the Statutory Health Insurance, when positive effects on care have been confirmed and they are listed in the register of the digital healthcare applications (Verzeichnis der digitalen Gesundheitsanwendungen, DiGA).Heimblutdruckmonitoring in Kombination mit einer Kointervention kann zu einer besseren Blutdruckkontrolle beitragen. Komplexere Telemonitoring-Projekte haben in Studien in der Primärversorgung, aber auch bei bestimmten Patientengruppen (z. B. Schwangere), erste vielversprechende Ergebnisse gezeigt. Entscheidend ist die Integration in die klinische Versorgung, denn „Stand-alone“-Lösungen haben bisher noch keinen überzeugenden Effekt auf den Blutdruck erzielen können. Das Digitale-Versorgung-Gesetz (DVG) ermöglicht die Verordnung von digitalen Anwendungen zulasten der GKV, wenn positive Versorgungseffekte nachgewiesen wurden und eine Listung im Verzeichnis der digitalen Gesundheitsanwendungen (DiGA) erfolgt ist.

Mithilfe des bettseitig, unmittelbar nach Anamnese und klinischer Untersuchung anwendbaren Lungenultraschalls können bei Patienten mit klinischen Zeichen eines Atemwegsinfekts und/oder respiratorischer Insuffizienz zahlreiche Ursachen und Komplikationen auf Anhieb erkannt werden. Damit ermöglicht der Lungenultraschall frühzeitig Entscheidungen über weitere diagnostische und erste therapeutische Maßnahmen auch bei Patienten, die sich mit V. a. SARS-CoV-2-Infektion in der zentralen Notaufnahme vorstellen. In diesem Übersichtsartikel werden die typischen lungensonographischen Befunde bei Patienten mit COVID-19 aufgezeigt und der Stellenwert der Sonographie verglichen mit anderen bildgebenden Verfahren bei dieser neuartigen Erkrankung diskutiert. Video online Die Online-Version dieses Beitrags (10.1007/s10049-020-00767-8) enthält drei ergänzende Videos. Beitrag und Zusatzmaterial stehen Ihnen auf www.springermedizin.de zur Verfügung. Bitte geben Sie dort den Beitragstitel in die Suche ein, das Zusatzmaterial finden Sie beim Beitrag unter „Ergänzende Inhalte“.

Diabetes & Metabolism - In Press.Proof corrected by the author Available online since lundi 20 juin 2016

Living kidney donation is considered a safe procedure with excellent outcomes. The great demand for organs has changed the suitability criteria for donation and older or hypertensive donors are increasingly accepted.We reviewed the charts of 200 adults who donated a kidney at the University Hospital Hannover. Data regarding diastolic, systolic, mean blood pressure, renal function, and proteinuria at baseline and post-donation follow-up visits were recorded. A Mann-Whitney U test was performed to compare the post-nephrectomy development of blood pressure, estimated glomerular filtration rate (eGFR), and proteinuria between men and women, hypertensives and normotensives, and older (≥65 years) and younger (65 years) donors. Multivariable time-dependent Cox regression models were used to evaluate eGFR decline post-donation, after adjustment for covariates.The majority of donors were female (64.5%), and 29.0% had pre-existing hypertension. The mean age at donation was 49 years, and 9.5% were older than 65 years. During a median follow-up of 3 years, no significant differences in proteinuria and change in renal function were observed between both sexes or hypertensive and normotensive donors. In contrast, older donors exhibited a faster decline in renal function. Mean eGFR (chronic kidney disease epidemiology collaboration equation) pre-donation was 99.6 ± 21.9 mL/min in younger donors and 77.6 ± 17.7 mL/min in older donors (P .001). The respective mean values at the last follow-up visit were 81.3 ± 24.0 and 46.8 ± 17.9 mL/min (P .001). After adjustment for sex and preexisting hypertension, compared to younger donors, older donors had a 2.39 hazard ratio for eGFR decline.Older adults display a faster decline in renal function after donation and thus should be carefully evaluated for suitability before donation.

Primary aldosteronism (PA) is a frequent cause of resistant hypertension. The clinical presentation is heterogeneous, but a suppressed or low normal renin (especially with ACE inhibitors or sartans) should raise suspicion for primary aldosteronism, even when aldosterone levels are in the normal range. Diagnosis of unilateral hormone production from an adrenal adenoma (Conn syndrome), which is curable by surgery, requires adrenal vein sampling, which should be performed in experienced centers.

Kidney involvement is a common complication in patients with plasma cell diseases.This article outlines the spectrum of renal involvement in plasma cell dyscrasia and describes diagnostic and therapeutic measures to guide clinical management.Evaluation and discussion of the current literature as well as existing guidelines and recommendations of professional societies.The clinical manifestations of renal involvement in plasma cell disorders are heterogeneous and range from acute cast nephropathy in multiple myeloma to rare forms of glomerulonephritis. The term monoclonal gammopathy of renal significance (MGRS) was introduced to describe kidney involvement caused by monoclonal gammopathy but without evidence for underlying malignancy. Light chain cast nephropathy is the most common renal manifestation in multiple myeloma, whereas monoclonal immunoglobulin deposition disease (MIDD) and renal light chain (AL) amyloidosis can be found in multiple myeloma and MGRS. Decisive is the extended hematological diagnostics in order to exclude the presence of a hematological neoplasm. The treatment of renal involvement in monoclonal gammopathies involves the reduction of the plasma cell clone with cytoreductive treatment. The reduction of the monoclonal protein in serum is prognostically relevant for the renal response to treatment. In the case of histological evidence of a light chain cast nephropathy, high cut-off dialysis is recommended to reduce the free light chains in serum.The spectrum of renal manifestations in plasma cell dyscrasia has been expanded, particularly since the introduction of the term MGRS. Diagnostic and therapeutic management remain an interdisciplinary challenge.

To evaluate the effects of ZIKV infection on non-human primates (NHPs), as well as to investigate whether these NHPs develop sufficient viremia to infect the major urban vector mosquito, Aedes aegypti, four cynomolgus macaques (Macaca fascicularis) were subcutaneously infected with 5.0 log10 focus-forming units (FFU) of DNA clone-derived ZIKV strain FSS13025 (Asian lineage, Cambodia, 2010). Following infection, the animals were sampled (blood, urine, tears, and saliva), underwent daily health monitoring, and were exposed to Ae. aegypti at specified time points. All four animals developed viremia, which peaked 3&ndash, 4 days post-infection at a maximum value of 6.9 log10 genome copies/mL. No virus was detected in urine, tears, or saliva. Infection by ZIKV caused minimal overt disease: serum biochemistry and CBC values largely fell within the normal ranges, and cytokine elevations were minimal. Strikingly, the minimally colonized population of Ae. aegypti exposed to viremic animals demonstrated a maximum infection rate of 26% during peak viremia, with two of the four macaques failing to infect a single mosquito at any time point. These data indicate that cynomolgus macaques may be an effective model for ZIKV infection of humans and highlights the relative refractoriness of Ae. aegypti for ZIKV infection at the levels of viremia observed.

Cytomegalovirus (CMV) infection is a frequent complication of early posttransplantation. This study examines its impact on chronic allograft changes, long-term graft loss, and patient survival. We studied 594 patients who had protocol biopsies at 6 wk, and 3 and 6 mo posttransplantation. Chronic allograft changes were evaluated according to the updated Banff classification [interstitial fibrosis/tubular atrophy (IF/TA), vascular and glomerular lesions]. Follow-up data were available for up to 10 yr. CMV infection was diagnosed in 153 of 594 patients (26%) in the first year after transplantation, mostly within the first 3 mo. Graft survival was reduced in patients with CMV ( P = 0.03) as well as the combined allograft/patient survival ( P = 0.008). Prevalence of IF/TA at 6 wk after transplantation was already threefold higher in patients who experienced CMV infection later on compared with patients without CMV ( P = 0.005). In multivariate analyses, CMV viremia or disease was not a significant factor for graft loss or death. In conclusion, patients with CMV infection posttransplantation show more chronic allograft changes early on, even before CMV infection, and development of IF/TA is not more prevalent in patients with CMV. Our data do not support a significant role of CMV in patient and graft outcomes.

The atypical hemolytic uremic syndrome (aHUS), one of the three major forms of thrombotic microangiopathy, is characterized by genetic alterations in the area of the complement cascade, which can be detected in 40%-60% of all patients with aHUS. Mutations in over 10 different genes have now been identified. The most frequent and clinically relevant of these are mutations that result in a decreased or absent function of factor H, the formation of hybrid genes, or the formation of autoantibodies against factor H. Although genetics are not required for the diagnosis of aHUS, it is of great importance for the decision on how long to treat with the C5 inhibitor eculizumab. Also, knowledge of genetic alterations is absolutely essential if a living related donor is considered, in order to protect the living donor and recipient from developing aHUS.

The IgA nephropathy is the most frequent form of glomerulonephritis worldwide. In approximately 30% of patients a reduction in the glomerular filtration rate of approximately 50% is observed within 10 years. Patients with IgA nephropathy form IgG autoantibodies against galactose-deficient IgA1 antibodies. This results in deposition of these antibodies in the mesangium and activation of complement with mesangial hypercellularity, endocapillary hypercellularity, segmental glomerulosclerosis and atrophying interstitial fibrosis. The basic treatment for patients with IgA nephropathy consists of removing risk factors, in particular hypertension, with blockade of the renin-angiotensin-aldosterone system. Immunosuppressives were also investigated in various studies but a clear advantage was not observed.

In Germany herbal medicines are traditionally frequently used. They represent an important therapeutic option, especially in self-medication.Current systematic review articles and meta-analyses were evaluated and summarized with respect to the evidence of phytotherapeutic drugs for selected psychiatric indications.Apart from the use of St. John's wort for depression, no other herb has so far shown convincing evidence.Due to the promising effects and the low side effect potential within the existing studies, further randomized controlled trials (e. g. for Passiflora incarnata, Rhodiola rosea and Lavendula officinalis) are definitely indicated.

Proteinuria can be induced by impairment of any component of the glomerular filtration barrier (GFB). To determine the role of circulating permeability factors on glomerular damage, we developed a parabiosis-based zebrafish model to generate a common circulation between zebrafish larvae. A morpholino-mediated knockdown of a podocyte specific gene (nephronectin) was induced in one zebrafish larva which was then fused to an un-manipulated fish. Notably, proteinuria and glomerular damage were present in the manipulated fish and in the parabiotically-fused partner. Thus, circulating permeability factors may be induced by proteinuria even when an induced podocyte gene dysregulation is the initiating cause.