[Contrast medium-induced acute kidney injury-Consensus paper of the working group "Heart and Kidney" of the German Cardiac Society and the German Society of Nephrology]. / Kontrastmittelinduzierte akute Nierenschädigung ­ Konsensuspapier der Arbeitsgemeinschaft "Herz ­ Niere" der Deutschen Gesellschaft für Kardiologie ­ Herz- und Kreislaufforschung e. V. und der Deutschen Gesellschaft für Nephrologie e. V.

This consensus paper summarizes the expert consensus and recommendations of the working group "Heart and Kidney" of the German Cardiac Society (DGK) and the German Society of Nephrology (DGfN) on contrast medium-induced acute kidney injury. Potentially nephrotoxic contrast agents containing iodine are frequently used in interventional medicine and for computer tomography diagnostics. Acute kidney injury occurs in approximately 8-17% of patients exposed to contrast media. The risk factors and underlying pathophysiology are discussed and recommendations for the prophylaxis and treatment of contrast medium-induced acute nephropathy are presented.

[Baroreceptor activation therapy for therapy-resistant hypertension: indications and patient selection : Recommendations of the BAT consensus group 2017]. / Barorezeptorakivierungstherapie bei therapierefraktärer Hypertonie: Indikation und Patientenselektion : Empfehlungen der BAT-Konsensusgruppe 2017.

Baroreceptor activation therapy (BAT) has been available for several years for treatment of therapy-refractory hypertension (trHTN). This procedure is currently being carried out in a limited number of centers in Germany, also with the aim of offering a high level of expertise through sufficient experience; however, a growing number of patients who are treated with BAT experience problems that treating physicians are confronted with in routine medical practice. In order to address these problems, a consensus conference was held with experts in the field of trHTN in November 2016, which summarizes the current evidence and experience as well as the problem areas in handling BAT patients.

[Anticoagulation in patients with chronic kidney disease : Recommendations from the working group "Heart-Kidney" of the German Cardiac Society and the German Society of Nephrology]. / Antikoagulation bei Patienten mit chronischer Niereninsuffizienz : Empfehlungen der Arbeitsgemeinschaft "Herz ­ Niere" der Deutschen Gesellschaft für Kardiologie ­ Herz- und Kreislaufforschung und der Deutschen Gesellschaft für Nephrologie.

Indications for anticoagulation are thromboembolic events, prosthetic heart valves, and atrial fibrillation with a corresponding risk score. Clinical trials have excluded patients with advanced chronic kidney disease and these data cannot be always generalized to patients with chronic kidney disease. Non-vitamin K antagonist oral anticoagulants (NOACs) are mostly not recommended or are contraindicated in advanced stages of chronic kidney disease. Observational studies have shown that dialysis patients with atrial fibrillation do not profit from coumarin anticoagulants; prospective studies are lacking.

[Dialysis and ultrafiltration therapy in patients with cardio-renal syndrome: recommendations of the working group "heart-kidney" of the German Cardiac Society and the German Society of Nephrology]. / Dialyse- und Ultrafiltrationsverfahren bei kardio-renalem Syndrom. Empfehlung der Arbeitsgemeinschaft "Herz--Niere" der Deutschen Gesellschaft für Kardiologie--Herz- und Kreislaufforschung e.V. und der Deutschen Gesellschaft für Nephrologie e.V.

Renal failure is common in patients with severe heart failure. This complex pathophysiological interaction has been classified as cardio-renal syndrome. In these patients hydropic decompensation is the main cause of hospitalization. In patients with refractory heart failure, characterized by diuretic resistance and congestion due to volume overload, ultrafiltration has to be considered. In acute decompensated heart failure with worsening of renal function, extracorporeal ultrafiltration is the preferred treatment modality. On the other hand, patients suffering from chronic decompensated heart failure, particularly patients with ascites, will profit from the treatment specific advantages of peritoneal ultrafiltration. Prerequisite for an optimized care of patients with cardio-renal syndrome is the close collaboration among intensive care doctors, cardiologists and nephrologists.

[Is there a correlation between C-reactive protein and calcification inhibitors with cardiovascular parameters and risk factors in hemodialysis patients?]. / Korrelieren C-reaktives Protein und Verkalkungsinhibitoren bei Hämodialyse-Patienten mit kardiovaskulären Parametern und Risikofaktoren?

BACKGROUND AND OBJECTIVE: Patients on hemodialysis exhibit a drastically increased cardiovascular mortality. Inflammation, hyperphosphatemia and lack of calcification inhibitors are uremia-associated risk factors for vascular calcification. Functional and morphological vascular parameters are used to assess cardiovascular risk. The aim of our study was to analyse the relation between pulse wave velocity (PWV) and intima-media-thickness (IMT) with calcification inhibitors. METHODS: A cohort of 97 hemodialysis patients was consecutively selected and investigated (age 56 +/- 9 years). Carotid-femoral PWV, carotid IMT, left ventricular ejection fraction and septum thickness were determined. These parameters were correlated with serum levels of CRP and calcification inhibitors (fetuin-A and osteoprotegerin [OPG]). RESULTS: Both PWV and IMT showed a positive correlation with age and systolic blood pressure and a negative correlation with Kt/V (dialysis efficiency). Additionally, fetuin-A was negatively associated with CRP and positively with cholesterol and triglycerides. Serum levels of the calcification inhibitors fetuin-A and OPG were not correlated to PWV or IMT. CONCLUSION: The lack of correlation of calcification inhibitors with PWV and IMT means that functional and morphological measurements of vascular properties can not necessarily be replaced by analysing "biomarkers".

Eurotransplant Senior Program 'old for old': results from 10 patients.

More frequently there is the need for renal transplantation of older patients. Against the background of an increasing number of old donors and recipients, Eurotransplant Leiden started the Eurotransplant Senior Program (ESP) 'old for old' in 1999. The ESP works with donors and recipients both over 65 yr. The kidneys are transplanted with short cold ischaemia time regardless of the human leukocyte antigen (HLA) compatibility. Compatibility of blood groups, negative crossmatch and less than 5% cytotoxic antibodies are required. First experiences from 10 patients at Heinrich Heine University hospital are reported here. The course of 10 transplanted patients is described from January 1999 until November 1999 (28.4+/-15.8 wk). Age of donor and recipient, cause of dialysis and concomitant diseases from recipients, function of the transplanted kidney and complications are analysed. Immunosuppression consisted initially of cyclosporin A, mycophenolic acid and steroids. The results of these 10 patients were compared to 14 patients who were transplanted according to the ordinary Eurotransplant criteria (Eurotransplant Kidney Allocation System) in the same period of time. Kidneys from six donors (70.5+/-3.3 yr) were transplanted to 10 different recipients (66.9+/-2.2 yr). The control group consisted of 14 patients (47.6+/-14.4 yr) who received kidneys from 14 donors (48.3+/-10.1 yr). One double kidney transplantation was performed in the senior group, i.e. two kidneys from a marginal donor were transplanted to one recipient ('two in one'). In the ESP group, cold ischaemia time was reduced by 5 h and mean of HLA mismatches was more than doubled. Mean length of hospitalisation of ESP and control groups was 47.2+/-28.2 and 34.2+/-11.6 d, respectively. Intraoperatively, no complications were seen, post-operative care was performed on a normal ward. ESP patients suffered more often from delayed graft function, which led to further need for haemodialysis for 11.2 d. Finally, 9 of 10 patients acquired a satisfactory renal graft function. A total of 13 biopsies were performed in eight cases. Altogether seven acute rejections in 6 patients were found (four interstitial, one vascular, one interstitial+vascular, one clinical). The 9 patients with sufficient renal graft function were discharged with a mean serum creatinine level of 2.3+/-0.5 mg/dL (control: 1.9+/-0.8 mg/dL). Comparing these 10 recipients to a control group consisting of 14 patients, the results are comparable and encouraging. In conclusion, the short-term results of the ESP are promising. Nevertheless, the post-operative care requires more attention due to several complications. Though the HLA compatibility was not considered, all rejections were coped with effectively. Quality of life was improved.

Hypoxia-induced inhibition of adenosine kinase potentiates cardiac adenosine release.

To elucidate the physiological role of the AMP-adenosine metabolic cycle and to investigate the relation between AMP and adenosine formation, the O2 supply of isolated guinea pig hearts was varied (95% to 10% O2). The net adenosine formation rate (AMP-->adenosine) and coronary venous effluent adenosine release rate were measured; free cytosolic AMP was determined by 31P-nuclear magnetic resonance. Switching from 95% to 40% O2 increased free AMP and adenosine formation 4-fold, whereas free cytosolic adenosine and venous adenosine release rose 15- to 20-fold. In the AMP range from 200 to 3000 nmol/L, there was a linear correlation between free AMP and adenosine formation (R2 = .71); however, adenosine release increased several-fold more than formation. At 95% O2, only 6% of the adenosine formed was released; however, this fraction increased to 22% at 40% O2, demonstrating reduced adenosine salvage. Selective blockade of adenosine deaminase and adenosine kinase indicated that flux through adenosine kinase decreased from 85% to 35% of adenosine formation in hypoxia. Mathematical model analysis indicated that this apparent decrease in enzyme activity was not due to saturation but to the inhibition of adenosine kinase activity to 6% of the basal levels. The data show (1) that adenosine formation is proportional to the AMP substrate concentration and (2) that hypoxia decreases adenosine kinase activity, thereby shunting myocardial adenosine from the salvage pathway to venous release. In conclusion, because of the normal high turnover of the AMP-adenosine metabolic cycle, hypoxia-induced inhibition of adenosine kinase causes the amplification of small changes in free AMP into a major rise in adenosine. This mechanism plays an important role in the high sensitivity of the cardiac adenosine system to impaired oxygenation.

Dissociation between adenosine release, MVO2, and energy status in working guinea pig hearts.

Rapid adaptation of ATP formation and coronary flow is required when cardiac work is altered. Cardiac energy status was proposed to control both oxygen consumption (MVO2) and release of vasoactive adenosine (AR). To investigate the hypothesis of a linear relation between free AMP and AR, we employed 31P nuclear magnetic resonance (NMR) in a newly elaborated guinea pig heart performing pressure-volume work. Under basal conditions, MVO2 was 7.8 +/- 1.0 mumol.min-1.g-1, free AMP 297 +/- 189 nM and AR 226 +/- 179 pmol.min-1.g-1 (n = 29). Decreasing arterial PO2 by 50% reduced MVO2 and increased free AMP by 29%; however, AR rose threefold (n = 5). Doubling oxygen content of the perfusion medium (fluorocarbon emulsion) did not alter MVO2, free AMP, or AR (n = 6). When afterload was doubled, MVO2 increased (+45%) and AR decreased (-60%) despite no change in ADP or AMP (n = 6). Dobutamine increased MVO2 (+50%) and AMP (-98%); however, AR rose more than five times (n = 8). Switching substrates from glucose + pyruvate to glucose diminished MVO2 and increased ADP twofold and AMP fourfold, whereas AR remained constant (n = 6). Our findings demonstrate that cardiac energy status is also not the prime regulator of oxidative phosphorylation in the isolated heart. Changes in the oxygen supply-to-demand ratio induced a rise in AR that exceeded by far the increase in free AMP. Thus, additional factors, possibly inhibition of adenosine kinase, influence the release of vasoactive adenosine.