Apolipoprotein A-IV Concentrations and Clinical Outcomes In A Large CKD Cohort
ApoA-IV appears to be an independent risk marker for reduced all-cause mortality, cardiovascular events and heart failure in a large cohort of patients with CKD.
KEY FINDINGS: The data support a link between elevated apoA-IV concentrations and reduced inflammation in moderate CKD. ApoA-IV appears to be an independent risk marker for reduced all-cause mortality, cardiovascular events and heart failure in a large cohort of patients with CKD.
BACKGROUND: Chronic kidney disease (CKD) represents a chronic proinflammatory state and is associated with very high cardiovascular risk. Apolipoprotein A-IV (apoA-IV) has antiatherogenic, antioxidative, anti-inflammatory and antithrombotic properties and levels increase significantly during the course of CKD. Study aimed to investigate the association between apoA-IV and all-cause mortality and cardiovascular outcomes in the German Chronic Kidney Disease study.
DETAILS: This was a prospective cohort study including 5141 Caucasian patients with available apoA-IV measurements and CKD. The majority of the patients had an estimated glomerular filtration rate (eGFR) of 30-60 ml/min/1.73m2 or an eGFR >60 ml/min/1.73m2 in the presence of overt proteinuria. Median follow-up was 6.5 years. The association of apoA-IV with comorbidities at baseline and endpoints during follow-up was modelled adjusting for major confounders. Mean apoA-IV concentrations of the entire cohort were 28.9 ± 9.8 mg/dl. Patients in the highest apoA-IV quartile had the lowest high-sensitivity C-reactive protein values despite the highest prevalence of diabetes, albuminuria and the lowest eGFR. Each 10 mg/dl higher apoA-IV translated into lower odds of prevalent cardiovascular disease (1289 cases, odds ratio = 0.80, 95% confidence interval [CI] 0.72-0.86, p = 0.0000003). During follow-up, each 10 mg/dl higher apoA-IV was significantly associated with a lower risk for all-cause mortality (600 cases, hazard ratio [HR] = 0.81, 95% CI 0.73-0.89, p = 0.00004), incident major adverse cardiovascular events (506 cases, HR = 0.88, 95% CI 0.79-0.99, p = 0.03) and death or hospitalizations due to heart failure (346 cases, HR = 0.84, 95% CI 0.73-0.96, p = 0.01).
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Copyright © John Wiley & Sons, Inc. All rights reserved
Source: Schwaiger, J. P., Kollerits, B., Steinbrenner, I., et al. (2022). Apolipoprotein A-IV Concentrations And Clinical Outcomes In A Large Chronic Kidney Disease Cohort: Results from the GCKD Study. Journal of Internal Medicine. 2022; 291(5): 622-636. Published: May, 2022. DOI: 10.1111/joim.13437.
Hypopigmentation Following Picosecond Laser Treatment for Melasma
While hypopigmentation is rare with PSL treatment, it can occur even with conservative low-fluence settings and adequate intervals between sessions. One possible mechanism is thermal beam- stacking, where slow hand movement during treatment may lead to repeated pulses on the same area. This can result in localised thermal accumulation, potentially causing subcellular disruption of melanosomes without overt melanocyte loss.
Summary
A Case Series
[Posted 13/Jan/2026]
AUDIENCE: General Surgery, Dermmatology, Internal Medicine
KEY FINDINGS: While hypopigmentation is rare with PSL treatment, it can occur even with conservative low-fluence settings and adequate intervals between sessions. One possible mechanism is thermal beam- stacking, where slow hand movement during treatment may lead to repeated pulses on the same area. This can result in localised thermal accumulation, potentially causing subcellular disruption of melanosomes without overt melanocyte loss. These findings suggest the need for clinician vigilance in monitoring for hypopigmentation, as re-pigmentation may not be achievable. Larger, controlled studies are needed to clarify risk factors and guide safer practice.
BACKGROUND: Picosecond lasers (PSL) are increasingly used for treating melasma, with fewer adverse effects reported compared to Q-switched lasers (QSL). However, the incidence of hypopigmentation following PSL treatment remains unexplored in detail. This case series aims to explore outcomes of hypopigmentation following PSL therapy in patients with melasma, and explore potential contributing factors.
DETAILS: A retrospective chart review identified four patients with hypopigmentation following PSL treatment for melasma, including one referral from another clinic. Across the cohort, 796 patients underwent 3096 sessions between 2021 and 2025. Treatments used 755 and/or 1064-nm wavelengths at low fluences, with intervals of 4–12 weeks. Three in-clinic patients (0.38%, 95% CI 0.13%–1.10%) and one referral developed hypopigmentation. Changes occurred across both wavelengths and beam profiles. Histology demonstrated preserved melanocyte density with reduced melanin pigment and melanosome content. None of the cases showed meaningful re-pigmentation at 6-month follow-up. No cases of post-inflammatory hyperpigmentation (PIH) were observed.
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Cardiac Allograft Vasculopathy Inhibition With Alirocumab
Proprotein convertase subtilisin/kexin 9 inhibition with alirocumab in addition to statin therapy early after HT safely lowers low-density lipoprotein cholesterol but did not reduce coronary artery plaque progression after 1 year compared with rosuvastatin alone in patients with a low baseline low-density lipoprotein cholesterol.
KEY FINDINGS: Proprotein convertase subtilisin/kexin 9 inhibition with alirocumab in addition to statin therapy early after HT safely lowers low-density lipoprotein cholesterol but did not reduce coronary artery plaque progression after 1 year compared with rosuvastatin alone in patients with a low baseline low-density lipoprotein cholesterol.
BACKGROUND: Cardiac allograft vasculopathy is an important cause of mortality after heart transplantation (HT). Dyslipidemia is a major contributor to the development of cardiac allograft vasculopathy. The safety and effectiveness of proprotein convertase subtilisin/kexin 9 inhibition to lower cholesterol and to prevent cardiac allograft vasculopathy early after HT are not well established.
DETAILS: In this investigator-initiated, prospective, multicenter, double-blind randomized trial, participants were randomized early after HT to receive either alirocumab or placebo in addition to rosuvastatin. Before randomization and at 1 year, all participants underwent invasive coronary assessment, including angiography, fractional flow reserve, coronary flow reserve, the index of microcirculatory resistance, and intravascular ultrasound with near-infrared spectroscopy. Lipid values were assessed at baseline and at prespecified intervals. The primary end point was the change in coronary artery plaque volume from baseline to 1 year after HT based on serial intravascular ultrasound. A total of 114 HT recipients were included (57 assigned to alirocumab and 57 assigned to placebo). Baseline characteristics were well matched between the 2 groups. The low-density lipoprotein cholesterol levels decreased significantly from baseline to 1 year in the alirocumab arm (72.7±31.7 to 31.5±20.7 mg/dL; P0.001) and did not change with placebo (69.0±22.4 to 69.2±28.1 mg/dL; P=0.92). Plaque volume increased numerically in both groups from baseline to 12 months (alirocumab, 176.3±95.2 to 184.5±105.4 mm³; P=0.23; placebo 173.7±96.7 to 183.1±109.8 mm3; P=0.15). The change in plaque volume (mean difference in differences) did not differ between groups (1.01 [0.89-1.14]; P=0.86). Fractional flow reserve, coronary flow reserve, and the index of microcirculatory resistance did not change significantly with the addition of alirocumab. There were no significant adverse events related to alirocumab.
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Re-envisioning the Lifespan Approach to Cardiovascular Disease Prevention and Treatment in Women
The anticipated life course of women supports a broadening focus on CVD toward that of lifelong care and emphasize key transitional stages for women - early risk factor onset, pregnancy, menopausal transition, and so on. This review is a call to action to re-envision a health system approach for lifespan prevention, detection, and treatment pathways to reduce CVD risk in women.
KEY FINDINGS:
- Mortality: CVD deaths in women exceed combined deaths from breast and lung diseases.
- Gap in Care: Insufficient sex-specific evidence continues to hinder lifesaving care.
- Call to Action: Transition from episodic care to a lifelong cardiovascular health system for women.
BACKGROUND: Despite the common misconception that respiratory or oncological diseases pose the greatest threat to women, Cardiovascular Disease (CVD) accounts for more female deaths than breast cancer, lung cancer, and chronic lung disease combined, with a comparable mortality to that of men. Historically, both the public and the medical community have underestimated CVD risks in women, leading to diagnostic delays and a scarcity of sex-specific evidence to guide clinical interventions. While advances have been made in the diagnosis, treatment and outcomes of CVD in women, there often remains insufficient evidence to guide effective, lifesaving care of women.
DETAILS: This review of sex-specific and traditional CVD risk and risk-enhancing factors in women identifies areas of knowledge gaps to consider for investigation. A focus on the coronary vasculature reveals physiological differences of clinical relevance which can be interrogated. Inspection of and addressing disadvantage and gender bias in both the medical and lay communities should continue to be addressed. As CVD results from traditional risk factors and emerging risk-enhancing factors, a focus on the detection of preclinical cardiovascular disease may be of particular importance for women. Unique risk markers originate early in pre-menopausal women, as this is considered a healthy period of life. Awareness and implementation of the existing knowledge of sex-specific risk factors and sex-specific thresholds to educate women and physicians are needed. The anticipated life course of women supports a broadening focus on CVD toward that of lifelong care and emphasize key transitional stages for women-early risk factor onset, pregnancy, menopausal transition, and so on. This review is a call to action to re-envision a health system approach for lifespan prevention, detection, and treatment pathways to reduce CVD risk in women.
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Kidney Juxtaglomerular Cells' Renin Shutdown Mechanism in Blood Pressure Regulation
Juxtaglomerular cells monitor calcium levels to toggle renin release. Studying live tissue outperforms isolated cell models for understanding renin regulation. Targeting renin suppression could yield novel hypertension therapies and reduce related complications.
KEY FINDINGS: The findings demonstrate that juxtaglomerular cells shut down renin production through calcium-mediated mechanisms observed directly in kidney tissue. This approach highlights the brakes on hormone systems, differing from traditional focus on activation pathways.
BACKGROUND: Juxtaglomerular cells in the kidney serve as key sensors for blood pressure homeostasis. These cells release renin, a hormone that elevates blood pressure when levels drop too low. They rely on intracellular calcium as an on-off switch to control renin production, preventing hypotension.
DETAILS: Juxtaglomerular cells function as the body's primary baroreceptors, constantly assessing systemic blood pressure through mechanosensory mechanisms in the afferent arterioles. When pressure falls, these cells detect reduced stretch and rising intracellular calcium, triggering renin release to activate the renin-angiotensin-aldosterone system (RAAS). This study shifts focus to the inhibitory phase: how elevated calcium levels or other signals in intact kidney tissue suppress renin synthesis, acting as a regulatory "brake" to prevent overactivation. Traditional research emphasized renin induction using isolated cell cultures, which overlooked tissue-specific interactions like interstitial signaling and vascular coupling. By contrast, this work analyzed living kidney slices, revealing precise calcium-dependent shutdown pathways that halt transcription and secretion in real-time. This tissue-level insight explains why excessive renin persists in hypertension, potentially due to faulty off-switches, and opens avenues for therapies targeting suppression rather than blockade alone—such as modulating calcium channels or downstream inhibitors.
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Medical Policy Brief: Shift in Universal Hepatitis B Vaccine Recommendation
The ACIP voted 8-3 to end the universal HepB birth dose recommendation. Vaccination at birth is recommended only for infants of mothers who are positive for HepB or have unknown status. Mothers who test negative are advised to consult their healthcare provider to decide the timing of their child's vaccination. A change in the recommendation, if approved by the CDC Director, could affect state policies and private insurance coverage of the vaccine.
KEY FINDINGS:
- Vote Margin: The ACIP voted 8-3 to end the universal HepB birth dose recommendation.
- New Guidance: Vaccination at birth is recommended only for infants of mothers who are positive for HepB or have unknown status.
- Negative Mothers: Mothers who test negative are advised to consult their healthcare provider to decide the timing of their child's vaccination.
- Policy Impact: A change in the recommendation, if approved by the CDC Director, could affect state policies and private insurance coverage of the vaccine.
BACKGROUND: The Hepatitis B (HepB) vaccine has historically been universally recommended for all infants at birth by the Centers for Disease Control and Prevention's Advisory Committee on Immunization Practices (ACIP). This policy ensures protection against perinatal transmission and helps reduce the overall disease burden.
DETAILS: The CDC's Advisory Committee on Immunization Practices (ACIP) recently held a vote to reconsider the universal recommendation for the HepB vaccine at birth. The panel voted by a margin of 8-3 to cease the blanket recommendation that all infants receive the vaccine at birth. The new guidance maintains the recommendation only for infants whose mothers test positive for the infection or have unknown status. Mothers who test negative for Hepatitis B would be advised to "talk with their healthcare provider and decide themselves when to vaccinate their child." The discussion involved controversy, including a newly appointed ACIP member without medical training who reportedly argued against the universal birth dose, claiming vaccines had "never tested (the vaccines) appropriately." Dr. Cody Meissner, the sole continuing ACIP member, criticized the proposed change, stating "no rational science [had] been presented" to justify it. The ACIP voted in favor of changing the recommendations. These recommendations must now go to the CDC director for approval. While states ultimately set their own immunization policies, they generally rely on CDC guidelines. A change in ACIP recommendations can also influence insurance coverage, as most private insurers are required to cover recommended vaccines.
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