:
Bronchial asthma is one of the most common and severe diseases among children. The
phenomenon of creatinuria (CU) in patients with bronchial asthma (BA) has been acknowledged for
a relatively long time.
Aims:
The Aim of the research is to study the level of creatinuria, creatinemia, creatine kinase
activity, and the concentration of calcium in biological medium (blood, saliva, urine) in children
suffering from an intermittent and persistent form of asthma during the period of exacerbation.
Material and methods::
The research consists of 102 children with asthma who were treated in
inpatient department in Simferopol Clinic. The intermittent course of asthma was recorded in 49
children and a persistent course of asthma was recorded in 53 children. The subject of study was
blood serum and daily urine of observed patients. The level of calcium in the biological medium was
studied using the "Filisit" test kit (Dnipro) and the activity of the creatine kinase by test set "Lahma".
The levels of creatine and creatinine were determined using a colorimetric method based on a color
reaction with picric acid.
Results and conclusion: :
The analysis testifies that creatinuria in children with persistent BA is
caused by the disorder of the phosphorylation process rather than the disorder of creatinin
rephosphorylation synthesis, that is testified by the normal creatinine level. In children with
persistent BA, there is а decrease of creatinine concentration in the blood serum and urine during the
exacerbation period and early post exacerbation period. The low activity of creatinine kinase at the
background of creatinine elimination is typical for the children in the phase of exacerbation of
persistent form of BA, though its level remains to be sufficient for the synthesis of the necessary
amount of creatinine phosphate.
Conclusion:
The processes of creatinuria and calciuria in children suffering from a persistent form of
BA are interdependent, that is testified by the data of correlative analysis. In connection with this, it
is possible to consider the change of calcium homeostasis in the pathogenesis of the disease as one of
the causes of distributing the creatinine metabolism on the cellular level.
Separate nuclear genes encode sarcomere-specific and ubiquitous human mitochondrial creatine kinase isoenzymes.
