Hearing loss is a common finding in patients with end-stage renal failure. Uremic toxins, ototoxins, and axonal uremic neuropathy appear to be likely pathogenic factors. We analyzed whether an improvement in hearing capacity can be achieved with an improvement of anemia by erythropoietin (EPO) administration. Fifty patients on long-term hemodialysis in a single center were examined audiologically by otoscopy, tympanometry, pure tone audiometry, and the short increment sensitivity index. Twenty-five patients were treated with EPO in a dose of 120 U/kg per week over a period of 5 to 8 months, and the remaining 25 patients were not treated with EPO (controls). Both groups were reexamined audiologically after the study period, and the results were compared. In the group treated with EPO, the hemoglobin level increased from 7 +/- 0.9 to 11 +/- 0.8 g/dL, as against the control group, whose hemoglobin increased from 7.1 +/- 0.9 to 8 +/- g/dL. The audiologic tests were repeated at the end of the study period, and a significant improvement of hearing was found in the patients treated with EPO as compared with the control group (p < .001). Our study suggests that improvement of anemia in patients on long-term hemodialysis by administration of EPO is associated with an improvement in hearing capacity in a significant number of patients. Thus, anemia seems to be an important factor responsible for hearing disorders in patients with end-stage renal failure. Studies with larger numbers of patients are required to confirm this observation.

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Background: Urinary albumin excretion has been purported to be strongly linked to cardiovascular events in hypertensive patients. The prevalence of microalbuminuria in patients with essential hypertension and its relationship with target organ damage was evaluated with the present study, as the correlation of microalbuminuria and target organ damage except cardiovascular events has not been deliberated upon much in the past. Objectives: To evaluate the relationship between microalbuminuria and reduced creatinine clearance with subclinical target organ damage in asymptomatic nondiabetic hypertensive patients. Methodology: 120 hypertensive cases were studied from January 2019 to December 2020 in Dr VRK Womens Medical College, Hyderabad. Cases were evaluated for microalbuminuria, creatinine clearance, left ventricular hypertrophy and hypertensive retinopathy. Creatinine clearance was estimated by the Cockcroft-Gault formula. Left ventricular hypertrophy was determined by ECG and echocardiography. Retinal vascular changes were evaluated by direct ophthalmoscopy. Microalbuminuria was detected in 24 hours urine sample by immunoturbidimetric, assay. Results: There was significant association between microalbuminuria (30%) and reduced creatinine clearance (38%) with target organ damage i.e. left ventricular hypertrophy [p < 0.002 & p 0.002 respectively] and hypertensive retinopathy [p 0.005 & p 0.03 respectively]. Patients with urine microalbumin had 30 times risk [95% CI: 3.6-253, p 0.001] and those with reduced creatinine clearance had 5.9 times the risk [95% CI: 1.7-19.4, p 0.0035] of developing target organ damage. But when present together the risk increased to 39.4 times [95% CI: 2.2-703, p 0.0124]. Conclusion:Results show that a reduction in creatinine clearance and/or presence of microalbuminuria is a marker of subclinical organ damage in patients with primary hypertension. Microalbuminuria showed better association with target organ damage than reduced creatinine clearance.