Publications by authors named "Tilman Drueke"
Cardiac arrythmias are common in patients undergoing maintenance hemodialysis. In this issue, Charytan et al. showed that in patients with hyperkalemia (serum potassium concentration 5.
View Article and Find Full Text PDFAssociations of chronic kidney disease (CKD) with metabolic syndrome and cardiovascular disease (CVD) have long been recognized. Until recently, such associations were mainly limited to interrelationships between either heart and kidney, heart and metabolic syndrome, or metabolic syndrome and kidney. It is the merit of the American Heart Association (AHA) to have set up a work group of cardiologists, endocrinologists, and nephrologists for the purpose of combining all 3 disorders in a single entity, as an appreciation of their pathophysiological interrelatedness.
View Article and Find Full Text PDFPurpose Of Review: This review is a critical analysis of treatment results obtained in clinical trials conducted in patients with chronic kidney disease (CKD) and secondary hyperparathyroidism (SHPT), hyperphosphatemia, or both.
Recent Findings: Patients with CKD have a high mortality rate. The disorder of mineral and bone metabolism (CKD-MBD), which is commonly present in these patients, is associated with adverse outcomes, including cardiovascular events and mortality.
Article Synopsis
- The study investigates how chronic kidney disease (CKD) affects sex differences in cardiovascular disease (CVD) risk, specifically distinguishing between atheromatous CVD (ACVD) and nonatheromatous CVD (NACVD).
- Utilizing data from a cohort of nearly 3,000 patients with moderate to severe CKD across France, the results indicate that women have a significantly lower rate of ACVD compared to men, but no significant difference in NACVD rates was found between the sexes.
- The findings highlight that as kidney function declines (measured by eGFR), the sex differences in ACVD risk diminish, whereas NACVD risk remains consistent across both sexes, suggesting gender impacts risk differently based on CVD
Background: The trajectories of haemoglobin in patients with chronic kidney disease (CKD) have been poorly described. In such patients, we aimed to identify typical haemoglobin trajectory profiles and estimate their risks of major adverse cardiovascular events (MACE).
Methods: We used 5-year longitudinal data from the CKD-REIN cohort patients with moderate to severe CKD enrolled from 40 nationally representative nephrology clinics in France.
Article Synopsis
- Vascular calcification in chronic kidney disease (CKD) is an active process influenced by cell death mechanisms.
- Apoptosis of vascular smooth muscle cells leads to the release of bodies that help calcium crystals form and deposit.
- Recent research by Ye et al. reveals that ferroptosis, another type of cell death, also plays a role in vascular calcification in CKD.
The most important contributors to the anemia of patients with chronic kidney disease are insufficient erythropoietin production and erythropoietin hyporesponsiveness, decreased red blood cell half-life, iron deficiency, and inflammation. However, in contrast to the role of kidney failure, that of proteinuria and nephrotic syndrome is less clear. Bissinger et al.
View Article and Find Full Text PDFArticle Synopsis
- Chronic kidney disease (CKD) is linked to increased cardiovascular risk, and kidney transplant recipients (KTRs) have a higher overall mortality rate compared to matched CKD patients (CKDps).
- A study analyzed aortic stiffness in KTRs and CKDps, revealing that KTRs had significantly lower stiffness one year after transplant despite similar conditions at three months post-transplant.
- The findings suggest that KTRs experience reduced aortic stiffness compared to CKDps, indicating distinct mechanisms behind cardiovascular disease development in these two groups.
In chronic kidney disease, parathyroid hormone (PTH), like all proteins, can undergo post-translational modifications, including oxidation. This can lead to structural and functional changes of the hormone. It has been hypothesized that currently used PTH measurement methods do not adequately reflect PTH-related bone and cardiovascular abnormalities in chronic kidney disease owing to the presence of oxidized, biologically inactive PTH in the circulation.
View Article and Find Full Text PDF