다중혈관 관상동맥 환자에서 y-문합을 이용하여 양쪽 내흉동맥만을 사용한 우회술의 조기 성적

The Modification of Diet in Renal Disease (MDRD) Study equation underestimates glomerular filtration rate (GFR) in patients with mild kidney disease. Levey and associates therefore developed and va...

/pdf/a-new-equation-to-estimate-glomerular-filtration-rate-5fqjpsnzwg.pdf

A New Equation to Estimate Glomerular Filtration Rate

http://www.klinikaikozpont.u-szeged.hu/pedia/images/pdf/CME_TEL/Full-Text/25.pdf

The Hallmarks of Aging

Background End-stage renal disease substantially increases the risks of death, cardiovascular disease, and use of specialized health care, but the effects of less severe kidney dysfunction on these outcomes are less well defined. Methods We estimated the longitudinal glomerular filtration rate (GFR) among 1,120,295 adults within a large, integrated system of health care delivery in whom serum creatinine had been measured between 1996 and 2000 and who had not undergone dialysis or kidney transplantation. We examined the multivariable association between the estimated GFR and the risks of death, cardiovascular events, and hospitalization. Results The median follow-up was 2.84 years, the mean age was 52 years, and 55 percent of the group were women. After adjustment, the risk of death increased as the GFR decreased below 60 ml per minute per 1.73 m2 of body-surface area: the adjusted hazard ratio for death was 1.2 with an estimated GFR of 45 to 59 ml per minute per 1.73 m2 (95 percent confidence interval, 1....

https://www.nejm.org/doi/pdf/10.1056/NEJMoa041031

Chronic kidney disease and the risks of death, cardiovascular events, and hospitalization

XI. STRATEGIES FOR IMPROVING DIABETES CARE D iabetes is a chronic illness that requires continuing medical care and patient self-management education to prevent acute complications and to reduce the risk of long-term complications. Diabetes care is complex and requires that many issues, beyond glycemic control, be addressed. A large body of evidence exists that supports a range of interventions to improve diabetes outcomes. These standards of care are intended to provide clinicians, patients, researchers, payors, and other interested individuals with the components of diabetes care, treatment goals, and tools to evaluate the quality of care. While individual preferences, comorbidities, and other patient factors may require modification of goals, targets that are desirable for most patients with diabetes are provided. These standards are not intended to preclude more extensive evaluation and management of the patient by other specialists as needed. For more detailed information, refer to Bode (Ed.): Medical Management of Type 1 Diabetes (1), Burant (Ed): Medical Management of Type 2 Diabetes (2), and Klingensmith (Ed): Intensive Diabetes Management (3). The recommendations included are diagnostic and therapeutic actions that are known or believed to favorably affect health outcomes of patients with diabetes. A grading system (Table 1), developed by the American Diabetes Association (ADA) and modeled after existing methods, was utilized to clarify and codify the evidence that forms the basis for the recommendations. The level of evidence that supports each recommendation is listed after each recommendation using the letters A, B, C, or E.

Standards of Medical Care in Diabetes

Normal circadian rhythm of blood pressure (BP) shows a diurnal variation with the highest BP levels reached during the morning and then declining to a trough value around midnight. In the early morning, an abrupt and steep acceleration of BP occurs on arising from sleep. There is an increased risk of stroke, myocardial infarction, and sudden death in the first few hours after waking, but the reasons for this remain speculative. Although it has been postulated that the morning BP surge is directly related to the risk for cardiovascular (CV) events, it is unclear whether this increased risk is related to the morning BP itself, or to an extreme nocturnal decline (ie, exaggerated “dipping”) defined as more than a 20% difference between daytime and nighttime BP readings. A study by Kario and colleagues of silent cerebral infarcts and stroke assessed by brain magnetic resonance imaging in elderly hypertensive patients calculated the mean systolic BP (SBP) during the 2 hours after awakening minus the SBP during the lowest hour of sleep BP. After an average of 41 months, 44 stroke events occurred, with the highest likelihood in the 53 patients (top decile) whose morning SBP surge was greater than 55 mm Hg. This group had a higher baseline prevalence of multiple infarcts and a higher stroke incidence during the follow-up period than the group with less BP increase on arising. The relationship of morning BP surge to stroke events in the highest decile was independent of 24-hour BP, nocturnal dipping, and baseline prevalence of silent brain infarction. The study has limitations in that it was performed in an older Japanese population known to have a higher risk of stroke and may not be readily applicable to populations in the United States or Europe. A recent retrospective study from Brazil of 632 hypertensive adults confirmed these findings using a cutoff of 41 mm Hg for the morning surge in SBP. On the other hand, an Italian investigation of the association between morning surge in SBP and risk for stroke in 1191 elderly treated hypertensive patients divided according to tertiles of morning surge in SBP and dipping status showed no significant association with ischemic stroke during 9 years of follow-up. However, the stroke risk was different when nondippers and dippers were analyzed separately. They observed that the stroke risk was not associated with morning surge in nondippers, but, in dippers, stroke risk was significantly higher in the third tertile (>23 mm Hg) of morning surge in SBP. Stroke risk was similarly high in dippers with SBP morning surge greater than 23 mm Hg and in nondippers, arguing that higher morning surge values predicted stroke risk in dippers but not in nondippers because nondippers are at risk for stroke with or without a threshold value for morning surge. Finally, in another study from Italy, 2051 patients were followed up for 16 years logging the occurrence of CV events and all-cause deaths with the addition of echocardiography to assess for left ventricular hypertrophy 10 years after the baseline visit. In this population with a wide age spectrum (25–74 years), morning BP surge was not found to be an independent predictor of cardiovascular death, all-cause death, or the development of high cardiovascular risk (as documented by new-onset left ventricular hypertrophy). Our take on this is threefold. First, losing circadian variation in BP is not a good thing. Second, extreme dipping or an exaggerated morning surge in SBP may be two sides of the same coin. Lastly, when morning surge does exist it could represent a plausible intervention target for clinical trials, which are sorely needed to guide us in what to do. It may also be useful to tell patients with an early morning SBP surge to avoid intense physical exercise in the early morning. But what is the level of morning surge that is significant? We’re going to sleep on that one, for now.

https://www.onlinelibrary.wiley.com/doi/pdf/10.1111/jch.12438

Is it morning blood pressure surge or extreme nocturnal dipping that accounts for the increased stroke risk in the morning waking hours

Hypertension is a common disorder with well-recognized consequences on the heart, brain, and kidney as target organs. Guidelines espouse a treatment goal of blood pressure reduction to <140 mm Hg for the systolic pressure and <90 mm Hg for the diastolic pressure in most hypertensive patients. In this review, the basis for these recommendations, the practical achievement of these goals in various practice settings, and the risk versus the benefit of achieving such goals in most hypertensive patients are examined.

Can we justify goal blood pressure of <140/90 mm Hg in most hypertensives?

In the 1950s, electrocortin, as aldosterone was then known,1 was a relatively novel hormone, the importance of which in human pathophysiology was established by reports of cases of aldosterone excess by Conn in 1955.2 Despite more than 50 yr of study, the breadth of many actions of aldosterone continues to unfold in basic, translational, and clinical milieus.

From a basic aspect, aldosterone has typical genomic effects. After receptor binding, aldosterone exposure initiates transcriptional processes, which increase protein synthesis in pathways that enhance sodium retrieval from tubular lumens, salivary and sweat glands, and colon. Nongenomic aspects have been reported in which aldosterone infusion reduces the caliber of isolated afferent and efferent arterioles3 through the activation of systems that inhibit endothelial nitric oxide action.4

From a translational aspect, the synthetic pathways detailing aldosterone production offer the opportunity for studying genes such as CYP11B2 , which regulates production of 11β-hydroxylase, a key enzyme in corticosteroid production.5 Population studies of polymorphisms in the CYP11B2 gene suggest that compensation for reduced activity of CYP11B2 , through modest increases in the release of ACTH, results in upregulation of other …

/pdf/aldosterone-blockade-in-diabetic-nephropathy-relative-risks-4n66gj4ptp.pdf

Aldosterone Blockade in Diabetic Nephropathy: Relative Risks and Potential Promise

https://www.ackdjournal.org/article/S1548-5595(14)00121-9/pdf

Blood Pressure Targets in CKD

In this issue, Jafar and colleagues address three questions about the management of patients with nondiabetic kidney disease and hypertension: Does the amount of urinary protein affect outcomes? Ar...

Raymond R. Townsend

Papers

Is it morning blood pressure surge or extreme nocturnal dipping that accounts for the increased stroke risk in the morning waking hours

Can we justify goal blood pressure of <140/90 mm Hg in most hypertensives?

Aldosterone Blockade in Diabetic Nephropathy: Relative Risks and Potential Promise

Blood Pressure Targets in CKD

Guiding lights for antihypertensive treatment in patients with nondiabetic chronic renal disease: proteinuria and blood pressure levels?