Consensus recommendations on fasting during Ramadan for patients with kidney disease: review of available evidence and a call for action (RaK Initiative).

Ramadan fasting (RF) involves abstaining from food and drink during daylight hours; it is obligatory for all healthy Muslims from the age of puberty. Although sick individuals are exempt from fasting, many will fast anyway. This article explores the impact of RF on individuals with kidney diseases through a comprehensive review of existing literature and consensus recommendations. This study was conducted by a multidisciplinary panel of experts.The recommendations aim to provide a structured approach to assess and manage fasting during Ramadan for patients with kidney diseases, empowering both healthcare providers and patients to make informed decisions while considering their unique circumstances.

Serum potassium changes during hypothermia and rewarming: a case series and hypothesis on the mechanism.

Introduction: Hypokalemia is known to occur in association with therapeutically induced hypothermia and is usually managed by the administration of potassium (K+). Methods: We reviewed data from 74 patients who underwent a therapeutic hypothermia protocol at our medical institution. Results: In four patients in whom data on serum K+ and temperature were available, a strong positive correlation between serum K+ and body temperature was found. Based on the close positive relationship between serum K+ and total body temperature, we hypothesize that serum K+ decreases during hypothermia owing to decreased activity of temperature-dependent K+ exit channels that under normal conditions are sufficiently active to match cellular K+ intake via sodium/K+/adenosine triphosphatase. Upon rewarming, reactivation of these channels results in a rapid increase in serum K+ as a result of K+ exit down its concentration gradient. Conclusion: Administration of K+ during hypothermia should be done cautiously and avoided during rewarming to avoid potentially life-threatening hyperkalemia. K+ exit via temperature-dependent K+ channels provides a logical explanation for the rebound hyperkalemia. K+ exit channels may play a bigger role than previously appreciated in the regulation of serum K+ during normal and pathophysiological conditions.

Activation of Angiopoietin-Tie2 Signaling Protects the Kidney from Ischemic Injury by Modulation of Endothelial-Specific Pathways.

SIGNIFICANCE STATEMENT: Ischemia-reperfusion AKI (IR-AKI) is common and causes significant morbidity. Effective treatments are lacking. However, preclinical studies suggest that inhibition of angiopoietin-Tie2 vascular signaling promotes injury, whereas activation of Tie2 is protective. We show that kidney ischemia leads to increased levels of the endothelial-specific phosphatase vascular endothelial protein tyrosine phosphatase (VE-PTP; PTPRB), which inactivates Tie2. Activation of Tie2 through VE-PTP deletion, or delivery of a novel angiopoietin mimetic (Hepta-ANG1), abrogated IR-AKI in mice. Single-cell RNAseq analysis showed Tie2 activation promotes increased Entpd1 expression, downregulation of FOXO1 target genes in the kidney vasculature, and emergence of a new subpopulation of glomerular endothelial cells. Our data provide a molecular basis and identify a candidate therapeutic to improve endothelial integrity and kidney function after IR-AKI. BACKGROUND: Ischemia-reperfusion AKI (IR-AKI) is estimated to affect 2%-7% of all hospitalized patients. The significant morbidity and mortality associated with AKI indicates urgent need for effective treatments. Previous studies have shown activation of the vascular angiopoietin-Tie2 tyrosine kinase signaling pathway abrogates ischemia-reperfusion injury (IRI). We extended previous studies to (1) determine the molecular mechanism(s) underlying kidney injury and protection related to decreased or increased activation of Tie2, respectively, and (2) to test the hypothesis that deletion of the Tie2 inhibitory phosphatase vascular endothelial protein tyrosine phosphatase (VE-PTP) or injection of a new angiopoietin mimetic protects the kidney from IRI by common molecular mechanism(s). METHODS: Bilateral IR-AKI was performed in VE-PTP wild-type or knockout mice and in C57BL/6J mice treated with Hepta-ANG1 or vehicle. Histologic, immunostaining, and single-cell RNA sequencing analyses were performed. RESULTS: The phosphatase VE-PTP, which negatively regulates the angiopoietin-Tie2 pathway, was upregulated in kidney endothelial cells after IRI, and genetic deletion of VE-PTP in mice protected the kidney from IR-AKI. Injection of Hepta-ANG1 potently activated Tie2 and protected the mouse kidney from IRI. Single-cell RNAseq analysis of kidneys from Hepta-ANG1-treated and vehicle-treated mice identified endothelial-specific gene signatures and emergence of a new glomerular endothelial subpopulation associated with improved kidney function. Overlap was found between endothelial-specific genes upregulated by Hepta-ANG1 treatment and those downregulated in HUVECs with constitutive FOXO1 activation, including Entpd1 / ENTPD1 that modulates purinergic receptor signaling. CONCLUSIONS: Our data support a key role of the endothelium in the development of IR-AKI, introduce Hepta-ANG1 as a putative new therapeutic biologic, and report a model to explain how IRI reduces Tie2 signaling and how Tie2 activation protects the kidney. PODCAST: This article contains a podcast at https://dts.podtrac.com/redirect.mp3/www.asn-online.org/media/podcast/JASN/2023_05_23_JSN_Ang_EP23_052323.mp3.

Essentials of Vascular Access for Home Hemodialysis.

Hemodialysis (HD) at home has gained increasing popularity in recent years because of regulatory and financial issues. Creation and maintenance of a well-functioning, cannulatable vascular access is essential for performance of home HD (HHD). A vascular access team-based approach to creation, maintenance, and troubleshooting of vascular access can facilitate removing barriers to cannulation at home related to fear of pain and bleeding associated with large bore needles. Frequent cannulation of HD access is associated with more frequent access complications, especially infections. Thus, proper cannulation of arteriovenous access requires careful training of rope ladder and buttonhole techniques to avoid infectious and traumatic complications that can lead to dire consequences. Development of better methods of creating buttonholes and single needles for dialysis can facilitate HHD. A culture of self-cannulation at dialysis centers can also promote HHD.

New Directions in Ensuring Catheter Safety.

Tunneled dialysis catheters remain the most common vascular access used to initiate hemodialysis. Unfortunately, their use is associated with higher morbidity and mortality when compared with arteriovenous fistulae or grafts. Different types of catheters with different designs and material properties function differently. Additional devices and medications can be used to decrease the rates of infection and thrombosis. The current available tunneled dialysis catheters remain far from the desired goal and innovation in the field of dialysis vascular access remains in dire need.

Avoiding problems in tunneled dialysis catheter placement.

Tunneled dialysis catheters (TDCs) remain the predominant vascular access for initiation of hemodialysis (HD) worldwide. TDCs are also utilized in a significant number of prevalent patients for continuation of dialysis and during the periods of complications related to arteriovenous (AV) accesses. TDC placement is a routine procedure, but can be associated with mechanical and infectious complications related to placement. Imaging guidance with ultrasound and fluoroscopy has made the placement of TDC safer and more successful. Adequate operator training, careful technique, utilization of a checklist, and barrier precautions are essential to avoid problems related to TDC placement.