Herpes zoster ophthalmicus.

Neurology

This article is part of a review series on water and electrolyte disorders, based on the annual "Electrolyte Winter Seminar" for early-career nephrologists in Japan. The seminar features interactive case-based discussions, some of which are included as self-assessment questions. The fifth installment addresses the management of hyperkalemia. Hyperkalemia frequently occurs in patients with chronic kidney disease (CKD) and can become life-threatening when severe, necessitating prompt treatment regardless of its underlying cause. Renin-angiotensin system inhibitors (RASi) are a recognized risk factor for hyperkalemia in CKD; however, discontinuing RASi in response to elevated potassium levels may adversely affect patient outcomes. Although there are no formal criteria distinguishing acute from chronic hyperkalemia, symptoms presentation and potassium levels offer a practical guide for clinical management. This review covers standard treatment strategies for severe (symptomatic or acute) hyperkalemia in emergency and inpatient settings and discusses how to manage mild-to-moderate (asymptomatic or chronic) cases in CKD patients while continuing RASi therapy.

Management of hyperkalemia: strategic clinical actions in real-world practice.

Clinical and Experimental Nephrology

The "2025 AHA/ACC/AANP/AAPA/ABC/ACCP/ACPM/AGS/AMA/ASPC/NMA/PCNA/SGIM Guideline for the Prevention, Detection, Evaluation, and Management of High Blood Pressure in Adults" retires and replaces the "2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA Guideline for the Prevention, Detection, Evaluation, and Management of High Blood Pressure in Adults."

A comprehensive literature search was conducted from December 2023 to June 2024 to identify clinical studies, reviews, and other evidence performed on human subjects that were published since February 2015 in English from MEDLINE (through PubMed), EMBASE, the Cochrane Library, the Agency for Healthcare Research and Quality, and other selected databases relevant to this guideline.

The focus of this clinical practice guideline is to create a living, working document updating current knowledge in the field of high blood pressure aimed at all practicing primary care and specialty clinicians who manage patients with hypertension.

2025 AHA/ACC/AANP/AAPA/ABC/ACCP/ACPM/AGS/AMA/ASPC/NMA/PCNA/SGIM Guideline for the Prevention, Detection, Evaluation and Management of High Blood Pressure in Adults: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines.

Circulation

Cardiogenic shock (CS) is a state of critical end-organ hypoperfusion caused by primary cardiac failure, in which the heart cannot generate sufficient output despite adequate preload and is associated with very high mortality rates. The emergence of precision medicine may enable tailored interventions based on individual patient profiles, including genetic, biomarker, imaging, and clinical data. Advanced hemodynamic monitoring, mechanical circulatory support devices with smaller profiles and higher flow, and targeted pharmacologic therapies have expanded the therapeutic possibilities in CS. However, integrating these novel approaches into clinical practice requires careful alignment with evidence-based medicine. Balancing innovation with robust clinical evidence is crucial. Many technologies enter the clinical sphere before comprehensive trials confirm their benefit, creating potential risks in vulnerable CS patients. Precision medicine must therefore be grounded on rigorous data from randomized-controlled trials, registries, and meta-analyses to ensure safety and efficacy. Collaborative efforts, including large-scale data sharing and international research networks, are essential to bridge the gap between innovation and evidence. The goal is to move beyond a one-size-fits-all model toward a more nuanced, patient-centered approach while maintaining scientific rigor.

Cardiogenic shock: diagnosis, phenotyping and management.

Intensive Care Medicine

Nephrolithiasis is the most common health condition affecting the kidney and urinary tract and constitutes a major global health-care problem. The prevalence of nephrolithiasis has increased substantially over the past five decades, irrespective of age, sex or ethnicity. Kidney stones cause substantial morbidity, reduced quality of life and enormous health-care expenditure, largely due to their frequent recurrence. Furthermore, nephrolithiasis is now recognized as a systemic condition associated with increased risks of chronic kidney disease, cardiovascular disease, metabolic syndrome and low bone mass. Nephrolithiasis exhibits marked pathophysiological heterogeneity. Dietary and environmental exposures interact with genetic predisposition to shape individual disease risk. Calcium oxalate stones are most prevalent, commonly driven by hypercalciuria, hyperoxaluria, hypocitraturia and low urine volume, whereas the formation of uric acid and calcium phosphate stones is commonly linked to urinary pH. A comprehensive clinical evaluation can uncover underlying metabolic abnormalities, distinguish idiopathic, secondary and Mendelian forms of nephrolithiasis, identify systemic disease associations and guide therapy. Recurrence prevention requires individualized strategies that combine dietary and pharmacological interventions. For established stones, surgical management is effective, with ureteroscopy and percutaneous nephrolithotomy achieving high stone-free rates. Despite its considerable clinical and societal burden, nephrolithiasis remains under-recognized, underserved and under-researched. Greater awareness and investments in research, innovation and education are urgently needed.

Kidney stone disease: risk factors, pathophysiology and management.

Nature Reviews. Nephrology

The pressure-flow relationship is fundamental to circulatory hemodynamics of any organ. In the kidney, renal perfusion pressure (RPP), defined as the gradient between mean arterial pressure and renal venous pressure or mean systemic filling pressure, serves as the principal driving pressure for renal blood flow (RBF). This concept recognizes that both arterial hypotension and venous congestion can reduce the pressure gradient for renal perfusion, potentially contributing to renal dysfunction or acute kidney injury (AKI). In health, whenever RPP fluctuates, the kidney autoregulates intrarenal vascular resistance to maintain stable RBF and glomerular filtration rate over a range of RPP. However, in critical illness, autoregulatory capacity may be impaired, and the degree of impairment can vary not only between patients but also within the same patient depending on the disease context or stage of illness. Therefore, during critical illness, inadequate RPP tends to overwhelm renal autoregulation capacity earlier than anticipated, leading to tissue hypoperfusion and increased risk of AKI. Relying on standard blood pressure targets to optimize RPP may not account for such inter- or intra-individual variations in autoregulation. Experimental models have shown that AKI can develop without overt macrocirculatory changes, implicating microcirculatory dysfunction as an important contributor too. Dynamic, multi-modal assessment of renal perfusion may offer a more precise approach to renal protection. Additionally, the focus of research has shifted towards providing new insights into individualized perfusion targets and refining RPP-guided strategies to prevent AKI among high-risk patients in ICU. The objective of this review is to describe the role of RPP, implications of dysregulated renal perfusion, approaches to monitoring renal perfusion, and potential therapies targeting RPP on the horizon for critically ill patients.

Renal perfusion pressure: role and implications in critical illness.

Annals of Intensive Care

Heart failure (HF) is a clinical condition characterized by the heart's inability to pump blood effectively enough to meet the body's metabolic demands; typically this happens because of impaired ventricular filling or ejection. HF affects millions of people in the United States, with increasing prevalence, hospitalizations, and deaths. Classification of HF by left ventricular ejection fraction divides it into HF with preserved ejection fraction (HFpEF), mildly reduced ejection fraction, and reduced ejection fraction (HFrEF). Early diagnosis and appropriate staging, using tools such as natriuretic peptides and echocardiography, are essential for identifying HF and implementing effective treatment. In patients with HFrEF, guideline-directed medical therapy, comprising renin-angiotensin system inhibitors, beta blockers, mineralocorticoid receptor antagonists, and sodium-glucose cotransporter-2 inhibitors, has demonstrated reductions in morbidity, mortality, and hospitalizations. Management of comorbidities such as the use of glucagon-like peptide-1 receptor agonists for obesity in patients with HFpEF has improved outcomes. Advanced therapies, cardiac rehabilitation, and supportive interventions, including vaccinations and mental health screening, contribute to improved patient quality of life. Focusing on pharmacologic and nonpharmacologic strategies is essential to reduce HF progression, minimize hospitalizations, and improve overall survival.

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