Uric Acid and Hypertension: Cause or Effect?

Uric acid was first associated with primary hypertension in 1874, yet its role in this condition remains unclear. Historically, uric acid was thought to be a secondary response to hypertension or its associated conditions. However, more recent experimental and clinical studies suggest that uric acid could have a contributory role in the pathogenesis of elevated blood pressure. More studies are needed to help dissect the potential mechanisms by which uric acid could initiate this response. It remains possible that uric acid is a marker for xanthine oxidase–associated oxidants and that the latter could be driving the hypertensive response. However, the weight of the evidence suggests that uric acid is a true modifying and possibly causal factor for human primary hypertension. Hence, early management of hyperuricemia might delay the development of essential hypertension.     

Inflammatory Bowel Disease: One or Two Diseases?

This chapter addresses the longstanding question of whether inflammatory bowel disease (IBD) is really one or two diseases. The straightforward answer is that ulcerative colitis (UC) and Crohn’s disease (CD) embody separate diseases more than a single syndrome. In reality, however, the question is more complex. This chapter makes the case that there are actually many more than just two diseases under the rubric of IBD.     

Atrial Fibrillation and Heart Failure: Cause or Effect?

Atrial fibrillation (AF) and heart failure (HF) are two epidemics of the century that have a close and complex relationship. The mechanisms underlying this association remain an area of ongoing intense research. In this review, we will describe the relationship between these two public health concerns, the mechanisms that fuel the development and perpetuation of both, and the evolving concepts that may revolutionize our approach to this dual epidemic.     

Hypertension in CKD Pregnancy: a Question of Cause and Effect (Cause or Effect? This Is the Question)

Chronic kidney disease (CKD) is increasingly encountered in pregnancy, and hypertension is frequently concomitant. In pregnancy, the prevalence of CKD is estimated to be about 3 %, while the prevalence of chronic hypertension is about 5–8 %. The prevalence of hypertension and CKD in pregnancy is unknown. Both are independently related to adverse pregnancy outcomes, and the clinical picture merges with pregnancy-induced hypertension and preeclampsia. Precise risk quantification is not available, but risks linked to CKD stage, hypertension, and proteinuria are probably multiplicative, each at least doubling the rates of preterm and early preterm delivery, small for gestational age babies, and related outcomes. Differential diagnosis (based upon utero-placental flows, fetal growth, and supported by serum biomarkers) is important for clinical management. In the absence of guidelines for hypertension in CKD pregnancies, the ideal blood pressure goal has not been established; we support a tailored approach, depending on compliance, baseline control, and CKD stages, with strict blood pressure monitoring. The choice of antihypertensive drugs and the use of diuretics and of erythropoiesis-stimulating agents (ESAs) are still open questions which only future studies may clarify.     

Is Vimentin the Cause or Effect of Obstructive Sleep Apnea Development?

Lung - In obstructive sleep apnea (OSA), hypoxia secondary to apnea and hypopnea and the resulting systemic inflammatory response are the main causes of comorbidities. The aim of this study was to...     

Painful and Painless Diabetic Neuropathy: One Disease or Two?

Painful diabetic polyneuropathy (PDPN) is generally considered a variant of diabetic polyneuropathy (DPN) but the identification of distinctive aspects that characterize painful compared with painless DPN has however been addressed in many studies, mainly with the purpose of better understanding the mechanisms of neuropathic pain in the scenario of peripheral nerve damage of DPN, of determining risk markers for pain development, and also of recognizing who might respond to treatments. This review is aimed at examining available literature dealing with the issue of similarities and differences between painful and painless DPN in an attempt to respond to the question of whether painful and painless DPN are the same disease or not and to address the conundrum of why some people develop the insensate variety of DPN whilst others experience distressing pain. Thus, from the perspective of comparing painful with painless forms of DPN, this review considers the clinical correlates of PDPN, its distinctive framework of symptoms, signs, and nerve functional and structural abnormalities, the question of large and small fiber involvement, the peripheral pain mechanisms, the central processing of pain and some new insights into the pathogenesis of pain in peripheral polyneuropathies and PDPN.     

Inflammation and C-Reactive Protein in Atrial Fibrillation: Cause or Effect?

Atrial fibrillation is associated with substantial morbidity and mortality rates. The incompletely understood pathogenesis of this cardiac dysrhythmia makes it difficult to improve approaches to primary and secondary prevention. Evidence has accumulated in regard to a relationship between inflammation and atrial fibrillation. Investigators have correlated the dysrhythmia with myocarditis, pericardiotomy, and C-reactive protein levels, suggesting that inflammation causes atrial fibrillation or participates in its onset and continuation. Conversely, other investigators suggest that atrial fibrillation induces an inflammatory response. In this review, we summarize and critically discuss the nature and clinical role of inflammation and C-reactive protein in atrial fibrillation.