Evaluation of s100β, NSE and GFAP Levels in Renal Transplantation

Encephalopathy, thiamine deficiency, uremia, hypertension, electrolyte imbalance after dialysis are clinical pictures with high incidences in case of renal failure. There are multifactor reasons in its pathophysiology such as hormonal imbalance, oxidative stress, accumulation of metabolites in time, disorders in excitatory and inhibitory transmitters and intermediary metabolisms.

Neurological disorders that affect renal transplant patients during the waiting list period do not only significantly affect preoperative morbidity and even mortality, but also show important predictive factors for neurological symptoms after the transplantation. A rigorous neurological assessment before transplantation is important for identifying the severity and distribution of the neurological disorder as well as defining the abnormalities that are responding to the current treatments and foreseeing potential postoperative prognosis. Specific indexes preferred for neurological assessment before the transplant may vary depending on the clinic; however, correct and differential diagnosis of various symptoms may be difficult despite the use of various diagnostic tools such as biochemical, neurophysiologic, neuropsychological and neuroimaging tools.

S100β is a 10.4 kDa protein. S100β is synthesized in the brain through endfeet processes of astrocytes and it belongs to the superfamily of low molecular weight EF-hand type acidic calcium-binding proteins. This protein is metabolized in the kidneys first and foremost and then discharged through urine. It has been shown that S100β does not differ depending on ethnic groups and genders and is not affected by circadian rhythm. Even though S100β may be found in other tissues, it may be used as an early marker for brain damage since it is found in higher concentration in the brain.

Astrocytes are the key agents for homeostasis regulation in the central nervous system (CNS) and they secrete S100β after brain damage. Certain studies show that increased levels of S100β may be used as an early marker of intracerebral changes in the brains of patients with acute or chronic liver failure and hepatic encephalopathy (HE) before the development of cerebral edema.

Moreover, some studies suggest that increased levels of S100β in serum concentrations may predict HE. However, there are few pieces of evidence that prove the correlation between S100β levels and HE's presence.

NSE (neuron-specific enolase) is a CNS protein found in neurons and neuroendocrine tissues. NSE functions in the glycolytic path of neurons as an intracytoplasmic enzyme and its serum levels increase in case of neuron damage. S100β is a marker of astroglial dysfunction while NSE is a marker of neuronal dysfunction.

And Glial fibrillary acidic protein (GFAP) is reported to be more specific to brain tissue compared to S100β. There are studies showing that prognosis is worse when both GFAP and S100β levels are seen to increase in the assessment of neurological damage, especially in cases of head traumas, thus supporting the use of both proteins for higher prognostic accuracy. GFAP is also a biomarker used for neurodegenerative diseases and ischemic cases other than cases of trauma.

The aim of the present study is to analyze neurological damage in renal transplant patients through S100β, NSE and GFAP serum concentrations and assess their impacts on the prognosis.