BackgroundThe definition of glomerular hyperfiltration has not been agreed upon and the pathophysiological mechanisms have not been well explored. Low serum creatinine concentrations may be associated with increased risk of coronary heart disease (CHD) or cardiopulmonary events the impact of which needs further study.MethodsConsecutive applicants to a cardiovascular hospital free of moderate/severe chronic kidney disease (age 55.6 ± 8.2 years) were grouped into those without (“healthy”, n = 469) and with CHD (320 stable and acute coronary syndrome cases) at baseline and into sex-specific quartiles of CKD-EPI equation-estimated glomerular filtration rate (eGFR). New or recurrent cardiovascular (myocardial infarction, stroke, heart failure [HF]) events, obstructive pulmonary disease (COPD) and death were determined during 3-years’ follow-up.ResultsAmong 25 deaths and 75 cardiopulmonary events, HF was the leading nonfatal event. Age, serum uric acid and left ventricular ejection fraction proved the best independent inverse covariates of eGFR in the “healthy” sample. The highest eGFR quartile (“hyperfiltrators”), exhibiting significantly lower serum LDL-cholesterol levels, significantly predicted the combined outcome (at a RR of 6) in “healthy” subjects, after adjustment for sex, age, body mass index, smoking status and presence of hypertension. This finding was paralleled by the highest eGFR quartile calculated also by the MDRD equation, replicating this also in the CHD group.ConclusionRenal “hyperfiltrators” represent individuals with autoimmune activation (involving serum creatinine, partly escaping assay), are misclassified into optimal renal function and actually are at significantly higher risk of death, HF or cardiopulmonary events. Low serum creatinine levels may represent a clue to the existence of autoimmune activation.
Gender differences exist in cardiovascular or metabolic disease risk, beyond the protective effect of estrogens, mostly burdening the postmenopausal female. We aimed to review herein sex differences in pro-inflammatory states, the independence of inflammation from insulin resistance, differences in high-density lipoprotein dysfunction, in gene-environment interactions, and in the influence of current and former smoking on cardiometabolic risk. Sex differences in absorption of long-chain fatty acids are highlighted. Differences exist in the first manifestation of cardiovascular disease, men being more likely to develop coronary heart disease as a first event, compared to women who have cerebrovascular disease or heart failure as a first event. Autoimmune activation resulting from pro-inflammatory states, a fundamental mechanism for numerous chronic diseases in people prone to metabolic syndrome, is much more common in women, and these constitute major determinants. Therapeutic approaches to aspects related to sex difference are briefly reviewed.
The generally high age-adjusted overall mortality in Turkey displays significant differences across geographic regions. Age-adjusted CHD incidence is not regressing sufficiently, and is especially high among men of the Mediterranean and women of the Southeast regions.
Two highly prevalent diseases, Type-2 diabetes mellitus and coronary heart disease (CHD), share risk factors. Excess levels of LDL-cholesterol have been overemphasized to uniformly encompass the development of CHD, and the origin of insulin resistance underlying Type-2 diabetes has not been fully elucidated. Autoimmune response has been recognized to be responsible only of a small minority of diabetes. The increasing trend in the worldwide prevalence of diabetes and the risk factors for both diseases are reviewed, the independent mediation for CHD of (central) adiposity in both diseases and the 'hypertriglyceridemic waist' phenotype are outlined. Evidence is described that serum lipoprotein (Lp)(a) concentrations, not only in excess, but also in apparently 'reduced' levels, as a result of autoimmune response, underlie both disorders and are closely related to insulin resistance.
Overall and coronary mortality in Turkish adults continue to be high, while an elicited annual increase of 5% in the age-controlled prevalence of diabetes is virtually alarming and requires new public health policies.
Inverse association of HbA(1c) with adverse outcomes in men and nondiabetic people indicates the involvement of HbA(1c) levels in autoimmune activation. The weaker inverse association with prevalent diabetes and in women is consistent with the operation of more pronounced confounding autoimmune processes.
To what extent is the metabolic syndrome (MetS) determined beyond its recognized components? In 1702, middle-aged men and women without MetS at baseline, MetS development was identified in 546 participants at a mean of 10.1-year follow-up. Participants subsequently developing MetS had, beyond higher values of MetS traits, significantly higher total and low-density lipoprotein cholesterol, apolipoprotein B, C-reactive protein (CRP), γ-glutamyl transferase (GGT), and lower high-density lipoprotein cholesterol. Females were significantly more frequent never smokers and males had lower values of total testosterone. In logistic regression analyses, adjusted for sex, age, and smoking status, MetS was predicted disparately in the sexes, whereas males exhibited, beyond abdominal obesity, CRP, GGT, and sex hormone-binding globulin (SHBG) as independent predictors, abdominal obesity was not an independent predictor in females in whom other than age, CRP conferred MetS risk, whereas SHBG was and current smoking tended to be protective. A surrogate of hepatic steatosis proved a major mediator of abdominal obesity in determining incident MetS (relative risk, 5.6 [95% confidence interval, 3.4-9.3]) in each sex. We confirm that GGT and SHBG are novel independent MetS determinants. Hepatic steatosis is the major predictor of MetS mediating adiposity in each sex. Abdominal obesity is not an independent determinant in Turkish women in whom autoimmune activation seems to prevail before MetS development.
Primary Hyperparathyroidism (PHP) in pregnancy constitutes a serious danger to mother and fetus. The diagnosis of PHP in pregnancy presents a challenge, and PHP commonly goes unidentified and untreated in pregnancy. We present four case reports about patients having PHP, which is very rare condition in pregnancy and their treatment modalities. Three patients, not to be controlled biochemically, denied the parathyroidectomy operation although they are informed about the details of their disease. They are followed up with medical therapy. The first one had no maternal or fetal complications, the second one acquired nephrolithiasis crisis in the last trimester and the third one gave birth to a premature baby who succumbed to tetany. The fourth patient who underwent parathyroidectomy operation in the second trimester had no maternal or fetal complications. PHP in pregnancy is a preventable cause of fetal and maternal mortality and morbidity. Thus, suspecting from PHP during the pregnancy and early diagnosis is critically important in terms of maternal and fetal wellness.
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