Increased Risk of Getting Sudden Sensorineural Hearing Loss in Patients with
Chronic Kidney Disease: A Population-Based Cohort Study
Key Discussion
The current study indicated that patients with CKD had a higher risk of developing SSHL.
For patients with CKD between 50 to 64 years of age, the risk of developing SSHL increased
remarkably. Comorbidity with diabetes significantly aggravates the risk of developing SSHL.
This observation may prompt early detection and timely treatment for high-risk patients. Further
investigations with large numbers of study subjects are helpful to identify any hearing
preservation effect among treatment methods for CKD.
The present patients with newly diagnosed CKD were found to have substantially higher
incidence of SSHL than their non-CKD counterparts (Figure 1). The present study is the first
report of the relationship between SSHL and CKD in English literatures. Although hearing
impairment among patients with chronic renal failure has been a common finding in studies
investigating the effects of renal failure on auditory function;16, 19 only a few cases report
proposed coincidence of SSHL in patients with chronic renal failure. For example, Lasisi et al.
reported two cases with chronic kidney disease sustained SSHL after 5 and 7 sessions of
hemodialysis.6 With a large sample size, the present study indicated the elevated risk of getting
SSHL in patients who sustained chronic kidney disease. Meanwhile, both animal studies and
human temporal bone studies have consistently reported a supporting evidence for the
correlations between CKD and risk of developing SSHL.14, 20-26
Evidence from induced renal insufficiency in animal studies has constantly reported the
correlation between CRF and sensorineural hearing impairment.20-23 A general consensus of
animal models was that cochlea is the site of auditory lesion in induced CRF.20 For example,
Ohashi et al. found that with greater renal damage, the amplitudes of the cochlear potentials N1
and CM were smaller and latency of N1 was prolonged, but the AP was within normal range.21
Ikeda et al. measured the cochlear potentials of guinea pigs with induced renal failure at 1, 2 and
3 months post-operatively.22 They found small changes in the compound AP and CM, which
were exacerbated with time. They proposed that CRF affects the cochlear hair cells. Shvili et al.
measured ABRs of cats with induced renal failure after 3 months. They found prolongation of
wave I, with normal I–V interpeak latency.23 Those suggested a site of damage either at the
cochlea or along the proximal part of the acoustic nerve.
Evidence from human temporal bone studies has also continuously approved the
occurrence of cochlear damage in patients with CRF.14, 24, 25 For example, in a temporal bone
study of patients with renal failure, Charachon et al. reported a case with bilateral deafness
associated with demyelinization of the preganglionic cochlear fibers, and a cell loss of about 25%
in the spiral ganglion.26 The high incidence of hearing loss in this group was attributed to the
premature aging caused by renal failure. Rizvi and Holmes reported a patient with progressive
hearing loss parallel to progression of CRF, peritoneal dialysis and hemodialysis.14 They found
anatomic changes in the labyrinth (collapse of the endolymphatic system, edema and atrophy),
which they attributed to osmotic disequilibrium caused by haemodialysis. As previous notion,
Uremic neuropathy of renal failure may also contribute to auditory dysfunction.27, 28
For patients with CKD who experienced SSHL, 50% of them contracted SSHL after the
forth follow-up year. The age subgroup of 50-64 years of age and that of ≥65 years of age were
the majority (71.4%). The annual incidence of SSHL after patients who sustained chronic kidney
disease is still unknown in the English literature. Nevertheless, several studies have investigated
the correlations between hearing impairment and disease duration of chronic renal failure. Rizvi
and Holmes (1980) reported a patient with progressive hearing impairment parallel to progression
of CRF, peritoneal dialysis and hemodialysis.14 Zeigelboim et al. (2001) measured thresholds
between 9 and 18 kHz in 37 patients with CRF undergoing conservative treatment and a control
group with normal hearing function.33 A more severe high frequency hearing impairment in the
group with chronic renal failure was noted. Hearing impairment among patients with CRF
seemed to deteriorate further a year after the first evaluation. However, Henrich et al. (1977)
found that 75% of the patients with chronic renal failure showed no deterioration of hearing
during the 4-year time of follow-up.34 In contrast to the debate regarding the correlation between
sensorineural hearing impairment and disease duration of chronic renal insufficiency, our study
indicated that the risk of getting SSHL increased by years after patients sustained chronic kidney
disease.
The association between diabetes and sensorineural hearing impairment has been
consistently reported. We have reported that the incidence of SSHL increased significantly higher
in the patients with diabetes compared with subjects without diabetes. Microangiopathy was one
of the proposed mechanisms for diabetic patients developing sensorineural hearing impairment.
Meanwhile, several literatures have reported the association between microangiopathy and
SSHL.35-38 Aimoni et al. (2010) described that the risk of getting SSHL tended to increase as the
number of cardiovascular risk factors increased.39 Mosnier et al. (2011) reported that the
personal/familial history of cardiovascular events was more prevalent in patients with SSHL
compared with subjects without.40 Further more, Lin et al. (2008) found that the risk of stroke in
patients with SSHL increased to a HR of 1.64 (p < 0.001), compared with patients without SSHL.
In accord with above literature, we observed a synergic effect between CKD and diabetes
mellitus comorbidities regarding the occurrence of SSHL.41 A novel finding was that incidence of
SSHL increased to an adjusted HR of 1.31 for CKD with diabetes compared with CKD patients
without diabetes comorbid (95% CI=1.003-1.711). This may infer that both CKD and SSHL
shared similar pathological risk of microangiopathy as diabetes.
The knowledge regarding the elevated risk of getting SSHL for patients with CKD would
prompt the early detection and treatment of the SSHL. Shaheen et al. (1997) found that
improvement of anemia in patients on long-term hemodialysis by administration of
erythropoietin is associated with an improvement in hearing capacity.40 They proposed anemia as
an important factor responsible for hearing disorders in patients with end-stage renal failure.
Accordingly, further observation and study are needed to make claim on the treatment methods
for hearing preservation in patients with chronic renal disease. Furthermore, it is noteworthy that
the growth of risk of getting stroke to a HR of 2.75 (p < 0.001) had been found in diabetic
patients with SSHL, compared with non-diabetic patients.41 Meanwhile, relevant reports have
noted that the risk of getting stroke increased in patients with renal failure. In retrospective study
of 3711 hypertensive patients in China, Zheng et al. (2012) reported that the risk of ischemic
stroke in patients with decreased glomerular filtration rate (60 ml/min versus 90 ml/min per 1.73
m) increased to a HR of 3.79 (95% CI 1.33-10.81).43 Kudo et al. (2012) examined 525 incident
stroke patients in Japan. They found that the prevalence of ischemic stroke was significantly
higher in patients with kidney damage (75.9%) than in those without (58.9%).44 Consequently, it
would never be overemphasized to address the prevention of stroke after SSHL in patients with
comorbidities of CKD and diabetes.