Hearing in renal failure

Abstract

The incidence of sensorineural hearing loss among patients with chronic renal failure (CRF) is considerably higher than in the general population. Bazzi et al. [1] found an incidence of 77% including patients with mild and very mild hearing loss. Ozturan and Lam [2] found a moderate to severe hearing loss in 46% of the tested patients. The general consensus in audiometric findings among patients with CRF claims a high frequency hearing loss [3,4] with a notch at 6 kHz [2]. Presence of hearing loss and estimation of type and degree constitute one of the most common methods used to investigate the effects of renal disease on the auditory system. Degree of hearing loss may give an indication of the extent of damage to auditory function, whereas the type of hearing loss may distinguish between lesions in the outer and middle ear (conductive hearing loss) or the cochlea and the neural pathways (sensorineural hearing loss). In addition to these indicators, the reports to be reviewed in the following sections have also described auditory function in CRF with methods such as otoacoustic emissions (OAEs) (namely transient evoked OAEs, TEOAEs and distorion product OAEs, DPOAEs), and auditory evoked potentials (AEPs). OAEs are low level sounds emitted by the cochlea in the process of receiving the sound vibrations and transforming them to cellular and neural stimulation. Recording of OAEs implies a functioning cochlea and healthy middle ear mechanism. TEOAEs are produced by the action of the hair cells, and they reflect special characteristics of the stimulus. DPOAEs are produced when the ear is stimulated with a combination of pure tones that are close in frequency (the primary tones). DPOAEs reflect non-linear processes of hair cell motion. Both TEOAEs and DPOAEs are generated by the active cochlear mechanisms responsible for enhancing basilar membrane vibration; this is known as the ‘cochlear amplifier’ [5]. AEPs represent neural activity related to auditory stimulation. They show summated neural energy at the various synaptic levels of the auditory pathway; this activity is generated by specific stimuli and extracted from the ongoing EEG activity by specialized technical manipulation. AEPs are recorded from the scalp representing activity in the cochlea and brainstem, thalamus and cortical areas. They are distinguished in early, middle and late evoked potentials, respectively. AEPs recorded from the cochlea include the cochlear microphonic (CM), the summating potential (SP) and the auditory nerve action potential (AP). The CM originates in the outer hair cells and mirrors the incoming signal. The SP also reflects hair cell function. The auditory nerve AP represents the sum of synchronous responses of auditory nerve fibers at the level of the cochlea. The largest component of the AP is the N1, a characteristic wave that constitutes also the first identifiable component of the auditory brainstem response (ABR). The ABR is also an ‘early’ evoked response, as it reflects neural function along the ascending auditory pathway, from the cochlea to the inferior colliculus. The five distinct waves of the normal ABR waveform are mainly generated by successive nuclei in the ascending auditory pathway: waves I and II originate from the distal and proximal portions of the auditory nerve, respectively, wave III originates from the cochlear nucleus, wave IV originates from the superior olivary complex and wave V originates from the lateral lemniscus/inferior colliculus. Each higher level order wave receives contributions from lower levels of the pathway [6]. The AEP reflecting function from auditory cortical areas is the Auditory Late Response (ALR). Major identifiable waves of the ALR are the N1 and P2 waves. ALR measurements reflect higher-level auditory function [7]. In general, latency of AEP waves indicates speed of neural function, whereas amplitude is a variable indicator of response robustness. The cochlea and kidney have similar physiological mechanisms, namely the active transport of fluid Correspondence and offprint requests to: Dr Chryssoula ThodiPetrou Cyprus, Audiology Center, Kallipoleos and 1Damaskinos Str, 1070, P.O. Box 20739, 1663 Nicosia, Cyprus. Email: DrC@cyprusaudiologycenter.com Nephrol Dial Transplant (2006) 21: 3023–3030