CLINICAL AND NEUROLOGICAL MANIFESTATIONS OF PATHOLOGY OF THE NERVOUS SYSTEM IN CHRONIC KIDNEY DISEASE IN CHILDREN

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Abstract

The purpose of the study: to analyze the main clinical and neurological manifestations of pathology of the nervous system in chronic kidney disease (CKD) in children.


Materials and methods: 30 conditionally healthy and 120 children aged 7-15 years with different forms of CKD were examined. The stages of CKD were determined in accordance with the K/DOQI classification approved by the Congress of Pediatric Nephrologists of Russia. Patients by stages of CKD were divided into 4 groups: 1st – CKD C1 (12); 2nd – CKD C2 (50); 3rd - CKD C3a (34); 4th – CKD C3b and the presence of signs of PE (24). The neurological status was assessed jointly with neurologists. 3 main syndromes were analyzed: astheno-vegetative; encephalopathic and intellectual-mnestic. The digital material was processed by the method of variation statistics.


Results: Asthenovegetative syndrome in patients with CKD was more often detected in children with C3b stage of CKD and to a greater extent in the presence of PE, manifested mainly by headaches and emotional lability of a transient nature. Along with this, clinical manifestations of encephalopathic syndrome were noted: anisoreflexia, paresis of the VII – XII pair of PMN, coordination disorders and horizontal nystagmus. The frequency of detection of anisoreflexia and horizontal nystagmus depended on the degree of damage to the nitrogen-releasing function of the kidneys and sharply increased in the group of children with PE. Children with C1 and C2 stages of CKD had cognitive impairments, manifested by emotional and behavioral disorders, decreased memory and attention due to the emotional state of the child. In the group of children with stages 3a and 3b of CKD, especially with the presence of PE, low productivity of attention and its stability are clearly interrelated with disorders in the emotional sphere and disorders of various types of memory.


Conclusion: The results obtained dictate the need to monitor the manifestations of hepatic encephalopathy and the appropriate correction of neuroprotection.

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