Chiefs’ Inquiry Corner – 9/9/2019

September 9, 2019


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Kidney Disease – Improving Global Outcomes (KDIGO) guidelines recommend treating non-diabetic adults with chronic kidney disease (CKD) and urine albumin excretion greater than 300 mg / day or equivalent with an angiotensin-converting enzyme (ACE) inhibitor or angiotensin receptor blocker (ARB). This recommendation is based on a meta-analysis of 11 randomized controlled trials, including 1860 patients, which found that reduction of proteinuria using an ACE inhibitor or ARB was associated with less progression of CKD, independent of blood pressure control. Unfortunately, the combination of an ACE inhibitor and ARB has not been shown to further reduce proteinuria and prevention of CKD progression.

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Functional mitral regurgitation (MR) refers to valvular insufficiency secondary to a dilated left ventricle in the setting of heart failure. Percutaneous valve repair has traditionally been reserved for patients with primary MR. The COAPT trial, however, found that in patients with persistent functional moderate to severe MR despite goal directed medical therapy, percutaneous valve repair decreased hospitalization and mortality. The smaller MITRA-FR trial, however, did not reproduce these findings, and guidelines have not yet updated their recommendations. Importantly, patients with severely reduced EF (<20%) or dilated left ventricle (left internal diastolic diameter >70mm) were excluded from these trials. 

References: 
HIV infection contributes to a chronic inflammatory state, which increases the risk of comorbid conditions such as cardiovascular disease, cancer, and autoimmune disease. However, while successful antiretroviral therapy reduces inflammation in most patients, inflammatory markers remain elevated in some, even with undetectable viral loads. As expected, those with persistently elevated inflammatory markers have a higher burden of comorbid disease. The pathophysiology behind this is unclear and a variety of mechanisms have been proposed, including ongoing low level viral replication, immune dysregulation, or microbial translocation. 

References: Inflammation in HIV

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