Humans

Importance Accurate assessment of intravascular volume facilitates management decisions about fluid management in patients with volume overload.

Objective To identify the most accurate clinical examination, radiographic, and laboratory findings for assessing volume overload in nonintubated patients.

Data Sources and Study Selection MEDLINE was searched (1946 to January 6, 2026) to identify peer-reviewed English-language studies about the diagnostic accuracy of the clinical examination of spontaneously breathing patients with intravascular volume overload.

Data Extraction and Synthesis Three authors independently extracted data for each finding and calculated sensitivity, specificity, and likelihood ratios (LRs). A 2-level mixed logistic regression model was used to pool estimates.

Results Forty studies, involving 11 490 adult patients, were included, with a prevalence of volume overload of 35% to 69%. Thirty-three of those studies evaluated patients with dyspnea. Prevalence of volume overload was more likely when the physical examination revealed jugular venous distention with the highest point of pulsation more than 3 cm in a vertical line above the sternal angle (LR, 4.1 [95% CI, 2.9-5.6]; specificity, 92%), lower extremity edema (LR, 2.2 [95% CI, 1.5-3.1]; specificity, 80%), or crackles on auscultation (LR, 2.7 [95% CI, 1.7-4.5]; specificity, 81%). Vascular congestion on chest radiography increased the likelihood of intravascular volume overload (LR, 5.9 [95% CI, 2.9-12.0]; specificity, 91%). Point-of-care ultrasonography that identified bilateral pulmonary B-lines suggested volume overload (LR, 4.0 [95% CI, 2.6-6.1]; specificity, 77%), and absence of pulmonary B-lines made volume overload unlikely (LR, 0.09 [95% CI, 0.04-0.23]; sensitivity, 93%). Inferior vena cava collapsibility index of less than 50% increased the likelihood of volume overload (LR, 3.9 [95% CI, 2.5-6.1]; specificity, 79%), and a collapsibility index of at least 50% made it less likely (LR, 0.22 [95% CI, 0.11-0.45]; sensitivity, 82%). Point-of-care ultrasonographic measurement of jugular venous pressure (JVP; >8 cm) also increased the likelihood of volume overload (LR, 2.8 [95% CI, 2.2-3.5]; specificity, 71%), although JVP of 8 cm or less identified patients less likely to have volume overload (LR, 0.26 [95% CI, 0.20-0.33]; sensitivity, 81%). A plasma brain-type natriuretic peptide (BNP) level of 100 ng/mL or higher was the single best test to identify those most likely to have volume overload (LR, 6.9 [95% CI, 2.4-20.4]; specificity, 87%), and a normal value made it less likely (LR, 0.14 [95% CI, 0.08-0.24]; sensitivity, 87%).

Conclusions and Relevance A BNP level of 100 ng/mL or higher and presence of vascular congestion on chest radiography may be the most useful tests to identify patients with volume overload. Absence of pulmonary B-lines using point-of-care ultrasonography or BNP levels of less than 100 ng/mL may be most useful to exclude volume overload.

Aim: The "2026 ACC/AHA/AACVPR/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA Guideline on the Management of Dyslipidemia" retires and replaces the "2018 AHA/ACC/AACVPR/AAPA/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA Guideline on the Management of Blood Cholesterol."

Methods: A comprehensive literature search was conducted from October 2024 to December 2024 to identify clinical studies, systematic reviews and meta-analyses, and other evidence conducted on human participants that were published in English from MEDLINE (through PubMed), EMBASE, the Cochrane Library, Agency for Healthcare Research and Quality, and other selected databases relevant to this guideline.

Structure: The focus of this clinical practice guideline is to address the evaluation, management, and monitoring of individuals with dyslipidemias, including high blood cholesterol, hypertriglyceridemia, and elevated lipoprotein(a).

Keywords: ACC/AHA clinical practice guideline; HDL; LDL; anticholesteremic agents; atherosclerosis; atherosclerotic disease; cardiovascular disease; cardiovascular diseases; cholesterol; drug interactions; dyslipidemia(s); hydroxymethylglutaryl-CoA reductase inhibitors; hypercholesterolemia; hyperlipid(a)emia/s; hyperlipoproteinemia type II; hypertriglyceridemia; hypolipidemic agents; lipids; lipoprotein(a); primary prevention; risk adjustment; risk assessment; risk factors; simvastatin; statin(s); triglycerides.

The risk of recurrent ischemic stroke can be reduced by managing modifiable risk factors and instituting a regimen of mechanism-specific secondary stroke prevention. Strategies for secondary prevention should be instituted as early as possible. Poststroke monitoring of risk metrics, lifestyle behaviors, and medication recommendations is of key importance.

Importance IgA nephropathy (IgAN) is a chronic kidney disease involving deposition of IgA-containing immune complexes in the glomerulus, causing glomerular inflammation and scarring. It is the most common immune-mediated glomerular disease worldwide, and affects an estimated 198 887 to 208 184 persons in the US. Up to 50% of patients with IgAN develop kidney failure within 10 years of diagnosis.

Observations IgAN typically presents with nephritic syndrome and usually occurs in younger adults, with a mean age at diagnosis of 34 to 45 years. Incidence is highest in East Asia. Approximately 60% of cases are detected incidentally with hematuria or proteinuria on urinalysis. Up to 30% of patients present with episodic visible hematuria, often concomitantly with an upper respiratory or gastrointestinal tract infection (synpharyngitic hematuria). Less common presentations include nephrotic syndrome (<5%) and rapidly progressive glomerulonephritis (<5%). When IgAN is suspected (due to hematuria, proteinuria, or reduced kidney function), initial workup should include quantification of proteinuria and assessment for other causes of nephritic syndrome (eg, lupus nephritis). Adults with suspected IgAN and proteinuria greater than or equal to 0.5 g per day should undergo kidney biopsy. The diagnosis of primary IgAN is based on presence of IgA-dominant immune deposits in the glomerular mesangium after excluding other causes of this histologic appearance, ie, IgA vasculitis, IgA-dominant infection-related glomerulonephritis, and secondary IgAN from diseases such as cirrhosis, inflammatory bowel disease, celiac disease, infection (eg, viral hepatitis), and autoimmune diseases (eg, axial spondyloarthritis). Based on the Kidney Disease: Improving Global Outcomes 2025 clinical practice guideline for the management of IgAN, treatment for patients with proteinuria greater than 0.5 g per day includes behavioral modifications (eg, dietary sodium <2 g/d, smoking cessation, weight control, exercise), antihypertensive medications for goal blood pressure less than 120/70 mm Hg, and therapies to reduce the formation of IgA-containing immune complexes (eg, targeted-release budesonide), decrease glomerular injury (eg, systemic glucocorticoids, iptacopan), and manage existing IgAN-induced nephron loss (eg, renin-angiotensin system inhibitor or dual endothelin angiotensin receptor antagonist [eg, sparsentan] alone or in combination with a sodium-glucose cotransporter 2 inhibitor).

Conclusions and Relevance IgAN is the leading cause of immune-mediated glomerular disease worldwide. Patients with suspected IgAN and proteinuria greater than or equal to 0.5 g per day should undergo kidney biopsy to confirm the diagnosis. Treatment of IgAN includes behavioral modifications, blood pressure management, and therapies to decrease formation of IgA-containing immune complexes (eg, targeted-release budesonide), reduce immune complex–mediated glomerular injury (eg, systemic glucocorticoids, iptacopan), and manage IgAN-induced nephron loss (eg, renin-angiotensin system inhibitor, dual endothelin angiotensin receptor antagonist, and sodium-glucose cotransporter 2 inhibitor).