During exertion, your muscles convert the stored creatine molecules into energy, which assists in muscle contraction. However, creatine is mainly stored in its phosphorylated form, known as phosphocreatine or creatine phosphate. Creatine is transported via blood flow to the skeletal muscles where it is stored in free and phosphorylated forms. So, how does your body generate creatinine? It starts with creatine, which is mainly synthesized in the kidneys, pancreas, and liver. It simply stays in the blood until reaching the kidneys, where it’s filtered and eliminated through urination. Creatinine itself doesn’t have a specific physiological function-it’s just a waste product. Creatinine is a natural byproduct of muscle use, caused by the breakdown of a chemical called creatine. What is creatinine?Įveryone has certain serum creatinine levels in their bloodstream. While it might be the last thing you think about while exercising, your blood creatinine levels can be a key indicator of your renal health and kidney function. When your muscles break down during exercise, they slowly build back up, increasing muscle mass, but this process also releases waste products into your blood, primarily creatinine. But there’s a whole lot more going on under the surface. Like most people, you’re acutely aware of how physical activity makes your body feel- the breathing, sweat, and heat. And when you’re done, nothing feels better than a warm shower, a cold glass of water, and a seat on the couch. You’re breathing fast, and your muscles are on fire. You’re 10 minutes into your afternoon jog, powering through your daily exercise routine, or biking around the neighborhood. ![]() What is creatinine? | Good creatinine level | How to prepare for creatinine testing | Abnormal creatinine levels | How to lower creatinine levels | How to increase creatinine levels A.Share on Facebook Facebook Logo Share on Twitter Twitter Logo Share on LinkedIn LinkedIn Logo Copy URL to clipboard Share Icon URL copied to clipboard Matsue, Y., van der Meer, P., Damman, K., Metra, M., O'Connor, C. The PROTECT trial was supported by NovaCardia, a subsidiary of Merck.Ĭleland, Professor John and Damman, Dr Kevin In Cox regression analysis, higher than normal range of BUN/creatinine ratio group was an independent predictor for all-cause death (HR: 1.86, 95% CI 1.29 to 2.66) and death or cardiovascular or renal rehospitalisation (HR: 1.37, 95% CI 1.03 to 1.82), but not for HF rehospitalisation (HR: 1.23, 95% CI 0.81 to 1.86) after adjustment for other prognostic factors including both creatinine and BUN.Ĭonclusions: In patients with AHF, BUN/creatinine higher than age-specific and sex-specific normal range is associated with worse prognosis independently from both creatinine and BUN. Results: In a cohort of patients with AHF, 482 (24.6%) and 28 (1.4%) patients with HF were classified into higher and lower than normal range groups, respectively. Association of abnormal range to prognosis was tested in 2033 patients with AHF for the outcome of all-cause death through 180 days, death or cardiovascular or renal rehospitalisation through 60 days and heart failure (HF) rehospitalisation within 60 days. ![]() Methods: In 4484 subjects from the general population without cardiovascular comorbidities, we calculated age-specific and sex-specific normal values of the BUN/creatinine ratio, deriving a higher and lower than normal range of BUN/creatinine ratio (exceeding the 95% prediction intervals). The aim of this study is to define the normal range of BUN/creatinine ratio and to investigate its clinical significance in patients with AHF. Objective: The blood urea nitrogen-to-creatinine (BUN/creatinine) ratio has been proposed as a useful parameter in acute heart failure (AHF), but data on the normal range and the added value of the ratio compared with its separate components in patients with AHF are lacking.
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