Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Showing posts with label Acute Kidney Injury. Show all posts
Showing posts with label Acute Kidney Injury. Show all posts

Thursday, September 22, 2022

Dynamic nomogram for predicting acute kidney injury in patients with acute ischemic stroke: A retrospective study

 And somehow in your two functioning brain cells you think predicting damage rather than preventing such damage was worthwhile research?

Dynamic nomogram for predicting acute kidney injury in patients with acute ischemic stroke: A retrospective study

Ganggui Zhu1, Zaixiang Fu2, Taian Jin2, Xiaohui Xu3, Jie Wei2, Lingxin Cai2 and Wenhua Yu1*
  • 1Department of Neurosurgery, Hangzhou First People's Hospital, School of Medicine, Zhejiang University, Hangzhou, China
  • 2Department of Neurosurgery, The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China
  • 3Department of Neurosurgery, The Fourth Affiliated Hospital, School of Medicine, Zhejiang University, Yiwu, China

Background: This study sought to develop and validate a dynamic nomogram chart to assess the risk of acute kidney injury (AKI) in patients with acute ischemic stroke (AIS).

Methods: These data were drawn from the Medical Information Mart for Intensive Care III (MIMIC-III) database, which collects 47 clinical indicators of patients after admission to the hospital. The primary outcome indicator was the occurrence of AKI within 48 h of intensive care unit (ICU) admission. Independent risk factors for AKI were screened from the training set using univariate and multifactorial logistic regression analyses. Multiple logistic regression models were developed, and nomograms were plotted and validated in an internal validation set. Based on the receiver operating characteristic (ROC) curve, calibration curve, and decision curve analysis (DCA) to estimate the performance of this nomogram.

Results: Nomogram indicators include blood urea nitrogen (BUN), creatinine, red blood cell distribution width (RDW), heart rate (HR), Oxford Acute Severity of Illness Score (OASIS), the history of congestive heart failure (CHF), the use of vancomycin, contrast agent, and mannitol. The predictive model displayed well discrimination with the area under the ROC curve values of 0.8529 and 0.8598 for the training set and the validator, respectively. Calibration curves revealed favorable concordance between the actual and predicted incidence of AKI (p > 0.05). DCA indicates the excellent net clinical benefit of nomogram in predicting AKI.

Conclusion: In summary, we explored the incidence of AKI in patients with AIS during ICU stay and developed a predictive model to help clinical decision-making.

Introduction

Stroke remains the second most common disease threatening humans worldwide (1). Stroke places a tremendous burden on patients, families, and society, especially in developing countries (2). The American Heart Association and the American Stroke Association project that the total medical cost of stroke will reach $1,841 billion from 2012 to 2030 (3). Ischemic stroke, usually caused by a blood clot blocking an artery in the brain, is the leading type of stroke (4). Tissue plasminogen activator (tPA) is the only drug currently approved by the United States Food and Drug Administration (FDA) for the treatment of ischemic strokes. Patients outside of the time window for tPA use may be treated with other therapies, such as thrombectomy, anticoagulants, blood pressure-lowering, and cholesterol-lowering drugs. Nevertheless, the effectiveness of treatment for ischemic stroke is unsatisfactory. Stroke kills ~6 million people each year, accounting for more than 10% of all deaths (5). Therefore, in the management of ischemic stroke, early identification of patients who may have a poor prognosis and timely intervention is important to improve the quality of patient survival later in life.

Acute kidney injury (AKI) is a common condition in critically ill patients and occurs in ~30–50% of intensive care unit (ICU) patients (6). High mortality is one of its characteristics, with ~20–25% of patients dying during hospitalization (7, 8). AKI manifests itself as a dramatic deterioration of renal function and a decrease in urine output, which leads to water and electrolyte disturbances and high circulating blood volume, resulting in a series of negative effects on other organs (9). After the stroke, activation of the sympathetic nervous system, the renin-angiotensin-aldosterone pathway impairs the self-regulatory function of the kidney (10). Moreover, the immune response induced by stroke leads to a massive release of inflammatory factors, resulting in decreased renal function (11). Therefore, early identification, recognition, and intervention can reduce the probability of AKI and slow down its progression (12).

However, there are no validated clinical models to predict the occurrence of AKI in patients with acute ischemic stroke (AIS). Therefore, there is a need to effectively predict the occurrence of AKI or screen for potential risk factors to guide early clinical intervention to improve prognosis. Based on several key variables and parameters, nomograms, especially dynamic nomograms, provide a powerful and easy-to-use method to predict the outcomes of individual events (13–16). The main objective of this study was to identify factors that independently predict the occurrence of AKI in patients with AIS. The patient cohort and factors were selected from the Medical Information Mart for Intensive Care III (MIMIC-III) database, and the nomogram was concurrently developed to predict the incidence of AKI in the AIS population during ICU (17).

More at link.

Tuesday, May 10, 2022

Greater coffee consumption correlates with lower risk for AKI( Acute kidney injury), compared with no coffee

Once again useless information, greater means nothing. But I'm doing as much coffee as I can on a daily basis for dementia, Parkinsons prevention and CVD reduction. But I don't know how much, so to not miss out I do a 12 cup pot of coffee daily.  I bet your stroke hospital incompetently does not have a 24 hour coffee station for patients. 

But I want to know how many cups of coffee to prevent Parkinsons and dementia! Regular or decaf?  What size cup? WHOM WILL BE DOING THAT RESEARCH?

 

Regular consumption of two to three cups of coffee per day could lower CVD risk

How coffee protects against Parkinson’s Aug. 2014  

Coffee May Lower Your Risk of Dementia Feb. 2013

And this: Coffee's Phenylindanes Fight Alzheimer's Plaque December 2018

 

The latest here:

Greater coffee consumption correlates with lower risk for AKI(Acute kidney injury), compared with no coffee

Compared with individuals who never drink coffee, those who consume a large amount of coffee are at a lower risk for incident AKI, according to data published in Kidney International Reports.

“Habitual coffee consumption is associated with the prevention of chronic and degenerative diseases including type 2 diabetes, cardiovascular disease and liver disease,” Kalie L. Tommerdahl, MD, of the department of pediatrics at the Children’s Hospital Colorado and University of Colorado Anschutz Medical Campus in Colorado, and colleagues wrote. “We aimed to assess associations between coffee consumption and incident AKI in a large, diverse population of middle-aged adults and hypothesized that habitual coffee consumption would be associated with a lower risk of incident AKI due to the cardiorenal protective properties of both coffee and caffeine.”

Coffee_Adobe
Source: Adobe Stock

In the Atherosclerosis Risk in Communities (ARIC) study, researchers evaluated 14,207 adults between the ages of 45 and 64 years in the United States. Researchers recruited all participants between 1987 and 1989.

Participants attended seven follow-up visits. At the first visit, researchers asked participants to complete a semiquantitative food frequency questionnaire involving 66 questions to measure coffee consumption.

During the following year, participants reported average coffee consumption of an 8-ounce cup of coffee with the following choices: most never; one to two cups per month; one cup per week; two to four cups per week; five to six cups per week; one cup per day; two to three cups per day; four to six cups per day; and more than six cups per day.

Researchers used the ICD code to define AKI as a hospitalization during the follow-up period.

Researchers identified 1,694 cases of incident AKI during a median of 24 follow-up years among the cohort. Analyses revealed greater coffee consumption correlated with lower risk for AKI vs. no consumption. When accounting for demographic characteristics, socioeconomic status, lifestyle factors and other dietary factors, there was a 15% lower risk of AKI for participants who consumed coffee compared to those who never did.

“Our data support chronic coffee consumption as an opportunity for cardiorenal protection through diet, particularly for the prevention of AKI hospitalizations or procedures,” Tommerdahl and colleagues wrote. “Larger studies evaluating the effects of coffee consumption on kidney perfusion and oxygenation in individuals with impaired kidney function at high risk for AKI, as well as the effects of coffee on anti-inflammatory and antioxidant outcomes, are necessary to fully explain its potential cardiorenal protective effects.”

 

 

 

Tuesday, March 31, 2020

An Association Between Hyperchloremia and Acute Kidney Injury in Patients With Acute Ischemic Stroke

Is your doctor testing for this? Does your hospital have a protocol for this? I had to read up on this to find out what it was.

Hyperchloremia is an electrolyte disturbance in which there is an elevated level of the chloride ions in the blood. The normal serum range for chloride is 96 to 106 mEq/L, therefore chloride levels at or above 110 mEq/L usually indicate kidney dysfunction as it is a regulator of chloride concentration. 

An Association Between Hyperchloremia and Acute Kidney Injury in Patients With Acute Ischemic Stroke

First Published March 25, 2020 Research Article










While an association between hyperchloremia and worse outcomes, such as acute kidney injury and increased mortality, has been demonstrated in hemorrhagic stroke, it is unclear whether the same relationship exists after acute ischemic stroke. This study aims to determine the relationship between moderate hyperchloremia (serum chloride ≥115 mmol/L) and acute kidney injury in patients with ischemic stroke.

This is a multicenter, retrospective, propensity-matched cohort study of adults admitted for acute ischemic stroke. The primary objective was to determine the relationship between moderate hyperchloremia and acute kidney injury, as defined by the Acute Kidney Injury Network criteria. Secondary objectives included mortality and hospital length of stay.

A total of 407 patients were included in the unmatched cohort (332 nonhyperchloremia and 75 hyperchloremia) and 114 patients (57 in each group) were matched based upon propensity scores. In the matched cohort, hyperchloremia was associated with an increased risk of acute kidney injury (relative risk 1.91 [95% confidence interval 1.01-3.59]) and a longer hospital length of stay (16 vs 12 days; P = .03). Mortality was higher in the hyperchloremia group (19.3% vs 10.5%, P = .19), but this did not reach statistical significance.

In this study, hyperchloremia after ischemic stroke was associated with increased rates of acute kidney injury and longer hospital length of stay. Further research is needed to determine which interventions may increase chloride levels in patients with acute ischemic stroke and the association between hyperchloremia and clinical outcomes.