Search

Zusammenfassung Hintergrund: Die chronische metabolischen Azidose (cmA) ist eine häufige Komplikation bei chronischer Niereninsuffizienz, deren Behandlung bei niereninsuffizienten Patienten mit Diabetes mellitus die Insulinresistenz verbessern kann. Um die aktuelle Therapiesituation der cmA im diabetologischen Umfeld abzubilden und mehr über die Zusammenarbeit von Diabetologen und Nephrologen zu erfahren, wurden diabetologisch tätige Haus- und Fachärzte zur cmA befragt. Methoden An 5863 Ärzten mit diabetologischer Zusatzqualifikation wurde postalisch ein Fragebogen versandt. Alle 97 erhaltenen Antwortbögen wurden deskriptiv ausgewertet. Ergebnisse Die meisten Teilnehmer sind Internisten mit diabetologischer Zusatzqualifikation (46 %) und behandeln im Median 50 (10; 112) Patienten mit Typ-1-Diabetes bzw. 210 (100; 450) Patienten mit Typ-2-Diabetes pro Quartal. Eine cmA wurde von 12 % der Teilnehmer in den letzten 12 Monaten bei median 4 (2; 6) Patienten mit Typ-1-Diabetes und 10 (3; 30) Patienten mit Typ-2-Diabetes beobachtet. Die cmA wird überwiegend durch Bestimmung des Serum-Bikarbonats (27; 28 %) und des Base Excess (19; 20 %) diagnostiziert. 38 (39 %) der Teilnehmer erhalten regelmäßig von Nephrologen die Empfehlung zur Behandlung der cmA. Sie wird von knapp 1 Drittel als relevant (29 %) und gut umsetzbar (27 %) betrachtet. Zur Behandlung der cmA wird vor allem orales Bikarbonat empfohlen (Bikarbonat: 39 %, Zitrat: 5 %, sonst: keine Angabe). Maßnahmen, die die Mehrheit der Diabetologen in der Verantwortung der Nephrologen sehen, sind ergänzende Diagnostik (87; 90 %) einschließlich Blutgasanalyse (59 %) sowie die Behandlung der cmA (62 %) und renalen Anämie (53 %). 34 % der Diabetologen gaben an, bisher noch keine cmA-Fälle in der Praxis behandelt zu haben. Die meisten Diabetologen überlassen die Behandlung und Überwachung der cmA dem Nephrologen (38 %). Dabei wird die Zusammenarbeit mit den Nephrologen als zufriedenstellend (81 %) bewertet. 38 % der Befragten haben in der täglichen Praxis beobachtet, dass die Einstellung der cmA auch die Insulinresistenz positiv beeinflusst. Eine CME-Fortbildung in der Diabetologie speziell zur cmA würden 76 (78 %) begrüßen. Diskussion Bei der Behandlung der cmA wird die Kooperation zwischen Diabetologen und Nephrologen generell gut bewertet, wobei die Diagnose, Behandlung und Überwachung einer cmA in der Verantwortung des Nephrologen gesehen werden. Da die Behandlung der cmA die Insulinresistenz verringern kann, sollte der Stellenwert der cmA-Therapie im diabetologischen Umfeld nicht unterschätzt werden. Um die cmA-Behandlung bei diabetischer Nephropathie zu optimieren, wären CME-Fortbildungen zur cmA geeignet. Zudem könnten Schulungen im Rahmen einer interdisziplinären Kooperation mit Diätberatern die Umsetzbarkeit diätetischer Interventionen zur Behandlung der cmA verbessern.

Surgical aortic valve replacement (SAVR) in kidney transplant recipients (KTR) is associated with high morbidity and mortality, and an increased risk of postoperative graft failure potentially leading to graft loss. Transcatheter aortic valve implantation (TAVI) emerged as an alternative in high-risk patients. However, data on TAVI in kidney transplant recipients are limited. We performed a retrospective analysis of 40 KTR in which aortic valve replacement was performed at our center between 2005 and 2015. The outcomes and follow-up of TAVI (n=20; 2010-2015) and SAVR (n=20; 2005-2015) were analyzed with respect to patient and graft survival. Baseline characteristics in both groups were comparable. Hospital stay after TAVI was significantly shorter compared to SAVR (19 [11.5-21.75] days vs. 33 [21-62] days, p=0.001). Acute graft failure occurred more frequently after SAVR (45% vs. 89.5%; p=0.006). Thirty-day mortality was 10% in both groups. However, in-hospital mortality reached 25% in the SAVR group (TAVI 10%), indicating a more complicated course after surgery. Moreover, during a median follow-up time of 1928 days in TAVI patients and 2717 days in patients after SAVR, graft loss occurred only in the surgically treated group (n=7). While one-year survival after TAVR was 90% compared to 69% after SAVR, long-term follow-up showed comparable results (at 5 years: TAVI 58% vs. 52% SAVR; log-rank-test: p=0.86). In KTR, TAVI can be performed with good mid- to long-term results. Compared to SAVR, renal outcomes seem to be improved after TAVI, suggesting better graft survival.

BACKGROUND Varices of the upper gastrointestinal tract are due to portal hypertension and can result from occlusion of the portal venous system. This report is of a 55-year-old man with recurrent gastrointestinal bleeding due to stricture of the portal vein anastomotic site to inferior vena cava (IVC) 12 years after combined pancreas and kidney transplantation. CASE REPORT A 55-year-old man presented bleeding episodes requiring transfusion of more than 70 units of red blood cells (RBCs), complicated by bacterial and viral infection episodes including cytomegalovirus (CMV) reactivation and hepatitis E and transient impairment of function of the renal allograft. Endoscopy, computed tomography (CT) scan, and angiography revealed jejunal varices due to anastomotic stricture at the portal vein to IVC as the cause of the hemorrhage. Neither conservative therapy nor an anastomosis between the splenic vein of the graft and the internal iliac vein as a bypass could stop the life-threatening bleeding. During the recurrent bleeding, CD4 T lymphocytes were low, indicating immunodeficiency despite paused immunosuppressive therapy. After the hemorrhage resolved and immunosuppression was restarted, CD4 T lymphocyte levels normalized. Finally, to stop the hemorrhage and save the transplanted kidney and the patient's life, graft pancreatectomy was performed. Long-term damage to the renal transplant was not found. CONCLUSIONS This report is of a rare case of portal hypertension as a long-term complication of transplant surgery. Although acute venous thrombosis at the anastomotic site is a recognized postoperative complication of pancreatic transplant surgery, this case highlights the importance of post-transplant follow-up and diagnostic imaging.

Acute kidney injury is associated with mortality in COVID-19 patients. However, host cell changes underlying infection of renal cells with SARS-CoV-2 remain unknown and prevent understanding of the molecular mechanisms that may contribute to renal pathology. Here, we carried out quantitative translatome and whole-cell proteomics analyses of primary renal proximal and distal tubular epithelial cells derived from human donors infected with SARS-CoV-2 or MERS-CoV to disseminate virus and cell type-specific changes over time. Our findings revealed shared pathways modified upon infection with both viruses, as well as SARS-CoV-2-specific host cell modulation driving key changes in innate immune activation and cellular protein quality control. Notably, MERS-CoV infection-induced specific changes in mitochondrial biology that were not observed in response to SARS-CoV-2 infection. Furthermore, we identified extensive modulation in pathways associated with kidney failure that changed in a virus- and cell type-specific manner. In summary, we provide an overview of the effects of SARS-CoV-2 or MERS-CoV infection on primary renal epithelial cells revealing key pathways that may be essential for viral replication.

Mineralocorticoid receptor antagonists have beneficial effects on left ventricular remodeling, cardiac fibrosis, and arrhythmia in heart failure, but efficacy and safety in dialysis patients is less clear. We evaluated the effect of spironolactone on left ventricular mass (LVM), an independent predictor of all-cause and cardiovascular mortality, in hemodialysis patients. In this placebo-controlled, parallel-group trial, 97 hemodialysis patients (23% female; mean age 60.3 years) were randomized to spironolactone 50 mg once daily (n=50) or placebo (n=47). The primary efficacy endpoint was change in LVM index (LVMi) from baseline to 40 weeks as determined by cardiac magnetic resonance imaging. Safety endpoints were development of hyperkalemia and change in residual renal function. There was no significant change in LVMi in participants randomized to spironolactone compared to placebo (-2.86±11.87 vs. 0.41±10.84 g/m2). There was also no difference in the secondary outcomes of mean 24-hour systolic or diastolic ambulatory blood pressure, left ventricular ejection fraction, 6-minute walk test distance, or New York Heart Association functional class. Moderate hyperkalemia (pre-dialysis potassium levels of 6.0-6.5 mmol/L) was more frequent with spironolactone treatment (155 vs. 80 events), but severe hyperkalemia (≥6.5 mmol/L) was not (14 vs. 24 events). Changes in residual urine volume and measured glomerular filtration rate did not differ between groups. There were no deaths in the spironolactone group and 4 deaths in the placebo group. Thus, treatment with 50 mg spironolactone did not change left ventricular mass index, cardiac function, or blood pressure in hemodialysis patients. Spironolactone increased the frequency of moderate hyperkalemia, but did not increase severe hyperkalemia.

Introduction Prognosis of survivors from cardiac arrest is generally poor. Acute kidney injury (AKI) is a common finding in these patients. In general, AKI is well characterized as a marker of adverse outcome. In-hospital cardiac arrest (IHCA) represents a special subset of cardiac arrest scenarios with differential predisposing factors and courses after the event, compared to out-of-hospital resuscitations. Data about AKI in survivors after in-hospital cardiac arrest are scarce. Methods In this study, we retrospectively analyzed patients after IHCA for incidence and risk factors of AKI and its prognostic impact on mortality. For inclusion in the analysis, patients had to survive at least 48 h after IHCA. Results A total of 238 IHCA events with successful resuscitation and survival beyond 48 h after the initial event were recorded. Of those, 89.9% were patients of internal medicine, and 10.1% of patients from surgery, neurology or other departments. In 120/238 patients (50.4%), AKI was diagnosed. In 28 patients (23.3%), transient or permanent renal replacement therapy had to be initiated. Male gender, preexisting chronic kidney disease and a non-shockable first ECG rhythm during resuscitation were significantly associated with a higher incidence of AKI in IHCA-survivors. In-hospital mortality in survivors from IHCA without AKI was 29.7%, and 60.8% in patients after IHCA who developed AKI (p

Background Pneumocystis jirovecii pneumonia (PcP) remains a life-threatening opportunistic infection after solid organ transplantation, even in the era of Pneumocystis prophylaxis. The association between risk of developing PcP and low CD4+ T cell counts has been well established. However, it is unknown whether lymphopenia in the context of post-renal transplant PcP increases the risk of mortality. Methods We carried out a retrospective analysis of a cohort of kidney transplant patients with PcP (n = 49) to determine the risk factors for mortality associated with PcP. We correlated clinical and demographic data with the outcome of the disease. For CD4+ T cell counts, we used the Wilcoxon rank sum test for in-hospital mortality and a Cox proportional-hazards regression model for 60-day mortality. Results In univariate analyses, high CRP, high neutrophils, CD4+ T cell lymphopenia, mechanical ventilation, and high acute kidney injury network stage were associated with in-hospital mortality following presentation with PcP. In a receiver-operator characteristic (ROC) analysis, an optimum cutoff of ≤200 CD4+ T cells/µL predicted in-hospital mortality, CD4+ T cell lymphopenia remained a risk factor in a Cox regression model. Conclusions Low CD4+ T cell count in kidney transplant recipients is a biomarker for disease severity and a risk factor for in-hospital mortality following presentation with PcP.

Chronic metabolic acidosis (CMA) is a common complication of chronic kidney disease (CKD). Its treatment in patients with diabetes mellitus and CKD could also improve insulin resistance. We investigated the current therapeutic approaches in diabetes mellitus (DM) with CKD in a survey among diabetologic specialists and general practitioners with additional qualification in diabetology about their approach to CMA and cooperation with nephrologists.5863 practitioners were invited to complete a 27 item survey. 97 completed surveys were analysed descriptively.Most participants were internists with additional qualification in diabetology (46 %). They cared for median 50 (10; 112) patients with DM type I and 210 (100; 450) patients with diabetes m, type II per quarter. CMA was observed by 12 % of practitioners during the last 12 months in median 4 (2; 6) patients with DM type I and 10 (3; 30) with type II. CMA was mainly diagnosed via serum bicarbonate (28 %) or base excess (20 %). 39 % received a recommendation from the nephrologic colleagues about treatment of CMA. About one third of diabetologists rated this recommendation as highly relevant (29 %) and feasible (27 %). For treatment of CMA, oral bicarbonate is preferred (39 %). Most participants preferred their nephrological colleagues doing specialist diagnostics (90 %) including blood gas analysis, as well as taking care of the treatment of CMA (62 %) and anemia (53 %). 34 % had not treated CMA in their practice so far. The cooperation between the participants and nephrologists was evaluated good (81 %). Most participants (78 %) would appreciate further education with a focus on CMA.Cooperation between diabetologists and nephrologists works well. Nephrologists are mainly responsible for diagnosis and treatment of CMA. However, because CMA may worsen insulin resistance, its relevance for DM treatment appears to be underestimated. Further education may be required in this field.Die chronische metabolischen Azidose (cmA) ist eine häufige Komplikation bei chronischer Niereninsuffizienz, deren Behandlung bei niereninsuffizienten Patienten mit Diabetes mellitus die Insulinresistenz verbessern kann. Um die aktuelle Therapiesituation der cmA im diabetologischen Umfeld abzubilden und mehr über die Zusammenarbeit von Diabetologen und Nephrologen zu erfahren, wurden diabetologisch tätige Haus- und Fachärzte zur cmA befragt.An 5863 Ärzten mit diabetologischer Zusatzqualifikation wurde postalisch ein Fragebogen versandt. Alle 97 erhaltenen Antwortbögen wurden deskriptiv ausgewertet.Die meisten Teilnehmer sind Internisten mit diabetologischer Zusatzqualifikation (46 %) und behandeln im Median 50 (10; 112) Patienten mit Typ-1-Diabetes bzw. 210 (100; 450) Patienten mit Typ-2-Diabetes pro Quartal. Eine cmA wurde von 12 % der Teilnehmer in den letzten 12 Monaten bei median 4 (2; 6) Patienten mit Typ-1-Diabetes und 10 (3; 30) Patienten mit Typ-2-Diabetes beobachtet. Die cmA wird überwiegend durch Bestimmung des Serum-Bikarbonats (27; 28 %) und des Base Excess (19; 20 %) diagnostiziert. 38 (39 %) der Teilnehmer erhalten regelmäßig von Nephrologen die Empfehlung zur Behandlung der cmA. Sie wird von knapp 1 Drittel als relevant (29 %) und gut umsetzbar (27 %) betrachtet. Zur Behandlung der cmA wird vor allem orales Bikarbonat empfohlen (Bikarbonat: 39 %, Zitrat: 5 %, sonst: keine Angabe). Maßnahmen, die die Mehrheit der Diabetologen in der Verantwortung der Nephrologen sehen, sind ergänzende Diagnostik (87; 90 %) einschließlich Blutgasanalyse (59 %) sowie die Behandlung der cmA (62 %) und renalen Anämie (53 %). 34 % der Diabetologen gaben an, bisher noch keine cmA-Fälle in der Praxis behandelt zu haben. Die meisten Diabetologen überlassen die Behandlung und Überwachung der cmA dem Nephrologen (38 %). Dabei wird die Zusammenarbeit mit den Nephrologen als zufriedenstellend (81 %) bewertet. 38 % der Befragten haben in der täglichen Praxis beobachtet, dass die Einstellung der cmA auch die Insulinresistenz positiv beeinflusst. Eine CME-Fortbildung in der Diabetologie speziell zur cmA würden 76 (78 %) begrüßen.Bei der Behandlung der cmA wird die Kooperation zwischen Diabetologen und Nephrologen generell gut bewertet, wobei die Diagnose, Behandlung und Überwachung einer cmA in der Verantwortung des Nephrologen gesehen werden. Da die Behandlung der cmA die Insulinresistenz verringern kann, sollte der Stellenwert der cmA-Therapie im diabetologischen Umfeld nicht unterschätzt werden. Um die cmA-Behandlung bei diabetischer Nephropathie zu optimieren, wären CME-Fortbildungen zur cmA geeignet. Zudem könnten Schulungen im Rahmen einer interdisziplinären Kooperation mit Diätberatern die Umsetzbarkeit diätetischer Interventionen zur Behandlung der cmA verbessern.

Zusammenfassung Hintergrund Die chronische metabolische Azidose ist eine häufige Begleiterkrankung niereninsuffizienter Patienten, auch unter Hämodialysetherapie. Aktuelle Ergebnisse der DOPPS-Studie zeigen, dass hohe Bicarbonatkonzentrationen während der Dialyse mit einer erhöhten Mortalität der Patienten assoziiert sind. Vor diesem Hintergrund wurde die aktuelle Situation in deutschen Dialysezentren evaluiert: Inwiefern kommen Leitlinienempfehlungen in der täglichen Routine an und gilt dies auch für neue Studiendaten? Methoden Es wurde eine Umfrage unter 2096 deutschen Nephrologen durchgeführt, um mehr über das aktuelle Vorgehen bei der Therapie chronischer metabolischer Azidose zu erfahren. Es wurden 280 auswertbare Antworten erhalten und deskriptiv ausgewertet. Ergebnisse Eine Blutgasanalyse wurde von 75 (27 %) der befragten Nephrologen wöchentlich durchgeführt, von 56 (20 %) monatlich, von 54 (19 %) alle drei Monate, von 14 (5 %) seltener oder nicht routinemäßig (8 [3 %]). Für den Zeitpunkt der Blutgasanalyse wurde in den meisten Fällen „vor der Dialyse“ angegeben (232; 83 %). 57 (20 %) der Befragten gaben an, darüber hinaus routinemäßig eine Blutgasanalyse auch am Ende der Dialysesitzung durchzuführen, 9 (3 %) auch während der Dialysesitzung, 55 (20 %) zusätzlich „bei Bedarf“. Orales Bicarbonat wird von 155 (66 %) der befragten Nephrologen bei Dialysebeginn abgesetzt. 62 von diesen (22 %) verwenden grundsätzlich kein orales Bicarbonat, 123 (44 %) setzen es zunächst ab und verordnen nur bei Bedarf neu. 94 (34 %) der Befragten behalten eine Behandlung mit oralem Bicarbonat bei und passen bei Bedarf die Dosierung an. Diskussion Es besteht vereinzelt Bedarf an Implementierung neuester Studienevidenz und Leitlinien zur Diagnostik und Therapie chronischer metabolischer Azidose: Etwa ein Viertel der befragten Nephrologen führt eine Blutgasanalyse nur alle 3 Monate oder seltener durch, obwohl die KDIGO-Leitlinien eine monatliche Blutgasanalyse empfehlen. Auch erfolgt eine Überprüfung des Bicarbonatstatus nach der Dialyse nur selten. Sollten hierbei vermehrt alkalotische Episoden festgestellt werden, ist statt der Zufuhr von Bicarbonat über die Dialyse eine regelmäßige Therapie mit oralem, magensaftresistentem Bicarbonat eine gute Alternative.

Damage to kidney cells can occur due to a variety of ischemic and toxic insults and leads to inflammation and cell death, which can result in acute kidney injury (AKI) [...]

Gliflozins are inhibitors of the renal proximal tubular sodium-glucose co-transporter-2 (SGLT-2), that inhibit reabsorption of urinary glucose and they are able to reduce hyperglycemia in patients with type 2 diabetes. A renoprotective function of gliflozins has been proven in diabetic nephropathy, but harmful side effects on the kidney have also been described. In the current project, primary highly purified human renal proximal tubular epithelial cells (PTCs) have been shown to express functional SGLT-2, and were used as an in vitro model to study possible cellular damage induced by two therapeutically used gliflozins: empagliflozin and dapagliflozin. Cell viability, proliferation, and cytotoxicity assays revealed that neither empagliflozin nor dapagliflozin induce effects in PTCs cultured in a hyperglycemic environment, or in co-medication with ramipril or hydro-chloro-thiazide. Oxidative stress was significantly lowered by dapagliflozin but not by empagliflozin. No effect of either inhibitor could be detected on mRNA and protein expression of the pro-inflammatory cytokine interleukin-6 and the renal injury markers KIM-1 and NGAL. In conclusion, empa- and dapagliflozin in therapeutic concentrations were shown to induce no direct cell injury in cultured primary renal PTCs in hyperglycemic conditions.

Pneumocystis jirovecii pneumonia (PcP) remains a life-threatening opportunistic infection after solid organ transplantation, even in the era of Pneumocystis prophylaxis. The association between risk of developing PcP and low CD4We carried out a retrospective analysis of a cohort of kidney transplant patients with PcP (n = 49) to determine the risk factors for mortality associated with PcP. We correlated clinical and demographic data with the outcome of the disease. For CD4In univariate analyses, high CRP, high neutrophils, CD4Low CD4

Profound left ventricular (LV) hypertrophy with diastolic dysfunction and heart failure is the cardinal manifestation of heart remodelling in chronic kidney disease (CKD). Previous studies related increased T1 mapping values in CKD with diffuse fibrosis. Native T1 is a non-specific readout that may also relate to increased intramyocardial fluid. We examined concomitant T1 and T2 mapping signatures and undertook comparisons with other hypertrophic conditions.In this prospective multicentre study, consecutive CKD patients (n = 154) undergoing routine clinical cardiac magnetic resonance (CMR) imaging were compared with patients with hypertensive (HTN, n = 163) and hypertrophic cardiomyopathy (HCM, n = 158), and normotensive controls (n = 133).Native T1 was significantly higher in all patient groups, whereas native T2 in CKD only (p 0.001 vs. all groups). Native T1 and T2 were interrelated in patient groups and the strength of association was condition-specific (CKD r = 0.558, HTN r = 0.324, both p 0.001; HCM r = 0.157, p = 0.05). Native T1 and T2 were similarly correlated in all CKD stages (S3 r = 0.501, S4 0.586, S5 r = 0.424, p 0.001 for all). Native T1 was the strongest myocardial discriminator between patients and controls (area under the curve, AUC HCM: 0.97; CKD: 0.97, HTN 0.98), native T2 between CKD vs HCM (AUC 0.90) and native T1 and T2 between CKD vs HTN (AUC: 0.83 and 0.80 respectively), p 0.001 for all.Our findings reveal different CMR signatures of common hypertrophic cardiac phenotypes. Native T1 was raised in all conditions, indicating the presence of pathologic hypertrophic remodelling. Markedly raised native T2 was CKD-specific, suggesting a prominent role of intramyocardial fluid.

The second most common infection after kidney transplantation is pneumonia, which has a high complication rate, sometimes even resulting in death. The aim of this study was to identify risk factors associated with mortality in nonopportunistic pneumonia.We retrospectively studied all kidney transplant recipients with nonopportunistic pneumonia treated at the University Hospital Frankfurt, Germany, between 2004 and 2017. Patient baseline characteristics, laboratory values, and microbiologic tests were analyzed. We focused specifically on acute and chronic graft failure and the immunosuppressive regimen and included a follow-up period of 7.8 years.One hundred seventy-seven patients (12%) collectively had 270 episodes of pneumonia. Although immunosuppressive therapy was reduced in 42% of patients during infection, there was no increase in graft rejection during hospital stay and follow-up. Significant risk factors for mortality were C-reactive protein10 mg/dL and serum albumin 3 g/dL on admittance, congestive heart failure, autosomal dominant polycystic kidney disease as the underlying renal disease, nosocomial pneumonia, septic shock, intensive care unit admittance, mechanical ventilation, and renal replacement therapy.Using these factors, patients at risk for death can be identified and the outcome of those might be improved by close monitoring and modified therapies.

Introduction Kidney transplant recipients (KTR) represent a high-risk population for cardiovascular disease. Coronary artery disease (CAD) is the most common cause of morbidity and mortality in this population. In KTR, coronary angiography and intervention (CI) can be associated with the risk of acute kidney injury (AKI). Aim Data about the incidence and impact of AKI after CI in this population are rare. The aim of the present study is to describe the incidence and risk factors of AKI, periprocedural bleeding and the prognostic impact on 1-year mortality in KTR undergoing CI. Material and methods This retrospective single-center study includes all KTR undergoing CI at University Hospital Frankfurt between 2005 and 2015. Results A total of 135 CIs in KTR were analyzed. AKI occurred in 31 of 135 CIs (23%, AKI group). Patients of the AKI group were older; other baseline characteristics did not show significant differences. The amount of contrast dye used was higher in the AKI group (p = NS). Periprocedural bleeding defined by BARC criteria occurred more often in the AKI group (23% vs. 5%, p < 0.01) and persisted as a risk factor of AKI in multivariate analysis (odds ratio = 6.43, 95% CI: 1.78-23.20, p = 0.01). In-hospital mortality was 3% in the AKI group; no patient of the non-AKI group died during hospitalization (p = 0.2). One-year-survival was significantly higher in the non-AKI group (94% vs. 81%, p = 0.02). Conclusions AKI is an important prognostic determinant in KTR undergoing coronary angiography and percutaneous coronary intervention (PCI). Periprocedural bleeding events were associated with AKI. Well-known risk factors for AKI such as contrast agent and diabetes were of minor impact.

The kidneys play a vital role in the basic physiological functions of the body. Kidney dysfunction impairs these physiological functions and can lead to a wide range of diseases. Damage to the kidney cells can be caused by a variety of ischemic, toxic or immunological complaints that lead to inflammation and cell death, which can lead to organ damage and, ultimately, complete failure. Although the mechanisms underlying acute kidney injury (AKI) and chronic kidney disease (CKD) are quite distinct, clinical evidence suggests that the two conditions are inextricably interconnected [1]. AKI and CKD, regardless of the underlying cause, have inflammation and activation of the immune system as the common underlying mechanisms. Inflammation, a process aimed, in principle, at detecting and fighting harmful pathogens, is, therefore, a major pathogenic mechanism for both AKI and CKD [1]. While the kidney has the remarkable ability to regenerate after an acute injury and can recover completely, depending on the type of kidney lesion, the options for clinical interventions are currently limited to fluid management and extracorporeal kidney support. However, persistent chronic inflammation can trigger renal fibrosis and chronic kidney disease. The investigation of the molecular mechanisms involved in each individual injury is currently insufficiently understood.

In selected cases, cuffed tunneled catheters via the iliac vein are implanted as a last resort access for hemodialysis. To monitor the correct position, sonography of the inferior vena cava (IVC) is sufficient in most cases. Position control using an X-ray of the abdomen is not routinely recommended when femoral catheters are implanted. In this report, we describe the case of a 59-year-old patient on chronic hemodialysis due to granulomatosis with polyangiitis and complex shunt history with multiple shunt occlusions and revisions. The implantation of an iliac-cuffed tunneled catheter led to complications because the catheter was malpositioned into the left ascending lumbar vein (ALV). It is important to be aware of potential incorrect positioning of dialysis catheters into the ALV. Due to the anatomical relation to the IVC, this happens more frequently on the left side than on the right side. In case of doubt, the correct placement of large-bore catheters via iliac access route should be verified by means of appropriate imaging before hemodialysis is performed.

Bei lebensbedrohlichen Viruserkrankungen ist die Hohe der Viruslast mit der Mortalitat assoziiert. Ein neuer und innovativer therapeutischer Ansatz ist die die Reduktion der Viruslast durch eine extrakorporale Elimination ohne gleichzeitig das Immunsystem durch Entfernung von spezifischen Antikorpern zu schwachen. Dabei wird ein modifizierter Plasmafilter verwendet, der mit einem Lektin – gewonnen aus dem Schneeglockchen- beschichtet ist.

Background Lupus nephritis (LN) is the most common organ manifestation in systemic lupus erythematosus (SLE) and associated with a poor prognosis. Still, a noninvasive but reliable method to diagnose LN has not been established. Thus, we evaluated whether blood sphingolipids could serve as valid biomarkers for renal injury. Methods In this cross-sectional study, 82 participants were divided into three groups: 36 healthy controls and 17 SLE patients without renal injury (both: estimated glomerular filtration rate (eGFR) ≥ 80 ml/min/1.73 m2 and albumin/creatinine ≤ 30 mg/g) and 29 LN patients. LN patients were identified by renal biopsies and impaired renal function (eGFR 30 mg/g). Venous blood was collected from all participants and sphingolipid levels in plasma and serum were measured by LC-MS/MS. Results Most interesting, concentrations of some specific ceramides, C16ceramide (Cer), C18Cer, C20Cer and C24:1Cer, were elevated in both, plasma and serum samples of patients suffering from biopsy-proven LN and impaired renal function, compared to healthy controls as well as SLE patients without renal injury. C24:1dhCer levels were elevated in plasma and serum samples from LN patients compared to SLE patients. Sphingosine levels were higher in plasma and serum of LN patients compared to healthy controls, but not compared to SLE patients. Sphinganine concentrations were significantly elevated in serum samples from LN patients compared to healthy controls and SLE. S1P and SA1P levels were higher in plasma samples of SLE and LN patients compared to healthy controls. Subsequent ROC analyses of plasma and serum data of the most altered ceramide species (C16Cer, C18Cer, C20Cer, C24:1Cer) between LN patients and SLE patients display a high diagnostic differentiation with significant AUCs especially for C24:1Cer serum levels. Further, C24:1Cer serum levels were not affected by glucocorticoid treatment and did not correlate with other renal markers, such as serum creatinine, eGFR and albumin/creatinine ratio. Conclusion Our data reveal that chain-length specific ceramides in blood, most likely C24:1Cer levels in serum, could act as potent biomarkers for renal impairment in patients suffering from SLE.

Stem cell-based therapies require cells with a maximum regenerative capacity in order to support regeneration after tissue injury and organ failure. Optimization of this regenerative potential of mesenchymal stromal/stem cells (MSC) or their conditioned medium by in vitro preconditioning regimens are considered to be a promising strategy to improve the release of regenerative factors. In the present study, MSC were isolated from inguinal adipose tissue (mASC) from C57BL/6 mice, cultured, and characterized. Then, mASC were either preconditioned by incubation in a hypoxic environment (0.5% O2), or in normoxia in the presence of murine epidermal growth factor (EGF) or tumor necrosis factor &alpha, (TNF&alpha, ) for 48 h. Protein expression was measured by a commercially available array. Selected factors were verified by PCR analysis. The expression of 83 out of 308 proteins (26.9%) assayed was found to be increased after preconditioning with TNF&alpha, whereas the expression of 61 (19.8%) and 70 (22.7%) proteins was increased after incubation with EGF or in hypoxia, respectively. Furthermore, we showed the proliferation-promoting effects of the preconditioned culture supernatants on injured epithelial cells in vitro. Our findings indicate that each preconditioning regimen tested induced an individual expression profile with a wide variety of factors, including several growth factors and cytokines, and therefore may enhance the regenerative potential of mASC for cell-based therapies.

Background/Aims: Middle East respiratory syndrome coronavirus (MERS-CoV) and Marburg virus (MARV) are among the World Health Organization’s top 8 emerging pathogens. Both zoonoses share nonspecific early symptoms, a high lethality rate, and a reduced number of specific treatment options. Therefore, we evaluated extracorporeal virus and glycoprotein (GP) elimination by lectin affinity plasmapheresis (LAP). Methods: For both MERS-CoV (pseudovirus) as well as MARV (GPs), 4 LAP devices (Mini Hemopurifiers, Aethlon Medical, San Diego, CA, USA) and 4 negative controls were tested. Samples were collected every 30 min and analyzed for reduction in virus infectivity by a flow cytometry-based infectivity assay (MERS-CoV) and in soluble GP content (MARV) by an immunoassay. Results: The experiments show a time-dependent clearance of MERS-CoV of up to 80% within 3 h (pseudovirus). Up to 70% of MARV-soluble GPs were eliminated at the same time. Substantial saturation of the binding resins was detected within the first treatment hour. Conclusion: MERS-CoV (pseudovirus) and MARV soluble GPs are eliminated by LAP in vitro. Considering the high lethality and missing established treatment options, LAP should be evaluated in vivo. Especially early initiation, continuous therapy, and timed cartridge exchanges could be of importance.

The development of new strategies to preserve renal function after acute kidney injury (AKI) is necessary due to limited clinical intervention options. The organ-protective effects of mesenchymal stromal/stem cells (MSCs) and their conditioned medium (CM) have been investigated demonstrating that both separately promoted tubular recovery and ameliorated the outcome of AKI. Nevertheless, strategies to optimise the regenerative potential of both are highly needed. Here we investigated the effects of CM from adipose-derived MSCs (ASCs) preincubated in a hypoxic environment (Hyp). Protective factors were investigated by PCR analysis and a protein array in vitro. The expression of 64 of the 308 proteins assayed was found to be more than two-fold increased after Hyp. CM of Hyp-pretreated ASCs (pCM) was used to enhance regeneration in a mouse model of cisplatin-induced AKI (cisAKI). Renal function was assessed by measurements of markers for AKI and serum cytokine levels. The pCM significantly ameliorated serum creatinine and neutrophil gelatinase-associated lipocalin values, and also the levels of inflammatory cytokines IL-1β and IL-6 in the serum of mice with AKI. Our work clearly showed that a Hyp preconditioning significantly increases the release of protective factors in ASCs and enhances the therapeutic effects of CM in cisAKI in mice.

Purpose: Acute kidney injury (AKI) is a severe complication in medical and surgical intensive care units accounting for a high morbidity and mortality. Incidence, risk factors, and prognostic impact of this deleterious condition are well established in this setting. Data concerning the neurocritically ill patients is scarce. Therefore, aim of this study was to determine the incidence of AKI and elucidate risk factors in this special population. Methods: Patients admitted to a specialized neurocritical care unit between 2005 and 2011 with a length of stay above 48 hours were analyzed retrospectively for incidence, cause, and outcome of AKI (AKI Network-stage ≥2). Results: The study population comprised 681 neurocritically ill patients from a mixed neurosurgical and neurological intensive care unit. The prevalence of chronic kidney disease (CKD) was 8.4% (57/681). Overall incidence of AKI was 11.6% with 36 (45.6%) patients developing dialysis-requiring AKI. Sepsis was the main cause of AKI in nearly 50% of patients. Acute kidney injury and renal replacement therapy are independent predictors of worse outcome (hazard ratio [HR]: 3.704; 95% confidence interval [CI]: 1.867-7.350; P < .001; and HR: 2.848; CI: 1.301-6.325; P = .009). Chronic kidney disease was the strongest independent risk factor (odds ratio: 12.473; CI: 5.944-26.172; P < .001), whereas surgical intervention or contrast agents were not associated with AKI. Conclusions: Acute kidney injury in neurocritical care has a high incidence and is a crucial risk factor for mortality independently of the underlying neurocritical condition. Sepsis is the main cause of AKI in this setting. Therefore, careful prevention of infectious complications and considering CKD in treatment decisions may lower the incidence of AKI and hereby improve outcome in neurocritical care.

Paricalcitol is approved for prevention and therapy of secondary hyperparathyroidism (sHPT) in patients with chronic kidney disease (CKD), with only short-term data in clinical routine settings. A 12-month observational study was conducted in Germany and Austria (90 centers, 761 patients) from 2008 to 2013. Laboratory values, demographical, and clinical data were documented in 629 dialysis patients and 119 predialysis patients. In predialysis patients, median intact parathormone (iPTH) was 180.0 pg/mL (n = 105) at the start of the study, 115.7 pg/mL (n = 105) at last documentation, and 151.8 pg/mL (n = 50) at month 12, with 32.4% of the last documented iPTH values in the KDOQI (Kidney Disease Outcomes Quality Initiative) target range. In dialysis patients, median iPTH was 425.5 pg/mL (n = 569) at study start, 262.3 pg/mL (n = 569) at last documentation, and 266.1 pg/mL (n = 318) at month 12, with 36.5% of dialysis patients in the KDOQI target range. Intravenous paricalcitol showed more homogenous iPTH control than oral treatment. Combined analysis of all dialysis patients indicated comparable and stable mean serum calcium and phosphate levels throughout the study. Clinical symptoms, such as itching, bone pain, and fatigue, were improved compared with study entry. The spectrum and frequency of adverse events mirrored the known pattern for patients on dialysis. Paricalcitol is efficacious and has a consistent safety profile in sHPT over 12 months.