Risk group stratification according to KDIGO guideline on CKD may prove useful in predicting graft outcome, but this should be confirmed in larger cohorts.
Botulinum neurotoxins (BoNTs) are responsible for botulism in humans and vertebrates, being one of the six most catastrophic potential bioterrorism agents. This are ~150 kDa proteins, assembled as a ~50 kDa light chain (LC) and a ~100 kDa heavy chain (HC). The LC acts like a zinc metalloproteinase that cleaves three proteins in neurons, members of the SNARE (Soluble N-ethylmaleimide sensitive fusion attachment protein receptors) family: VAMP (vesicle-associated membrane protein) / synaptobrevin, SNAP-25 (synaptosomal-associated protein 25) and syntaxin. After cleavage of any of this proteins, neurotransmission is blocked and flaccid paralysis of the muscle is installed. This extraordinary restricted tropism for the cholinergic presynaptic membrane makes this drug unique regarding its toxicity, pharmacological and therapeutic use. Taking into consideration the potential of this substance, this paper aims to summarize the most relevant data regarding the mechanism of actions and its main clinical applications, in order to improve medical practice. Therefore, we presented the mechanism of action in order to understand its usage in different pathologies, such as dystonias, spasticity, nephrologic and urologic conditions, cosmetic use, depression, gastroenterologic and proctologic diseases, dermatologic conditions, pathologies specific to plastic surgery and also the role of BoNT therapy in pain management. It is well documented in the literature that important discoveries have been made through recent experimental and clinical studies. Even so, there is still much to learn about the therapeutic action of this drug in terms of molecular and pathophysiological mechanisms, in order to benefit of the whole healing potential of this amazing toxin.
The prevalence of mineral bone disorders in chronic kidney disease (MBD-CKD) and the cardiovascular risk are increased in hemodialysis (HD) patients. Hyperphosphatemia is one of the complications often associated with increased cardiovascular risk, and in CKD patients, the reduced renal excretion of phosphate is an important cause of elevated serum of this microelement. Physical activity represents another contributing factor in evaluating the risk of cardiovascular disease. The aim of our study was to determine the influence of physical activity on serum phosphate levels in HD patients. The inclusion criteria of this 3-months study were: age > 18 years old, dialysis vintage > 6-months, diuresis > 500 mL/day, PTH values between 100-500 pg/mL, similar dialysis protocol, phosphate daily intake and MBD-CKD therapy. The following parameters were monitored: dry weight, diuresis, associated comorbidities, hemoglobin, serum calcium, phosphate, sodium, potassium, serum albumin, intact parathormon, bicarbonate. The physical activity was assessed during 4 days (3 week-days and 1 during the week-end) for 3 months, and the patients had to complete a questionnaire, too. 49 patients were included and divided in 5 groups, depending on their physical activity. Analyzing the parameters influence on serum phosphate levels, we observed that physical activity, serum calcium and albumin were the only parameters statistically significant (p = 0.001, p = 0.033, and p = 0.47, respectively). The nutritional recommendations of chronic HD patients should be adapted to their individual level of physical activity, in order to avoid an abnormal increase of serum phosphate level, and to improve to over-all outcome.
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