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• W1977462463 abstract "Dear Sir,Depression is the most common psychiatric finding in chronic renal failure (CRF) [1]. Studies demonstrating the relation between parathyroid hormone (PTH) which is a uremic toxin, and depression are scarce and contradictory [1, 2, 3]. In this study, we aimed at examining the relationship of depression and secondary hyperparathyroidism (SHPT) in patients with CRF.The mean age of the study group was 49.1 ± 1.1 years, and the age range was 18–72 years. There was a total of 31 patients, 18 males and 13 females. The diagnosis included: 12 chronic glomerulonephritis (38.7%), 6 diabetic nephropathy (16.4%), 5 amyloidosis (16.4%), 5 pyelonephritis (16.4%), and 3 CRF secondary to vesicoureteral reflux (9.7%). None of the patients had dialysis. The duration of the illness was 24.3 ± 5.3 months.The patients were administered the Hamilton Depression Scale and the Mini Mental State Examination (MMSE), and a complete neuropsychiatric examination was performed. On the same day a blood sample was drawn from each patient to measure BUN, creatinine and electrolytes, intact PTH, urinary electrolytes and the glomerular filtration rate (GFR). X-rays and computerized brain tomography were performed on subjects with depression, and those with organic lesions were excluded from the study.In all patients, while the MMSE was normal there was depression in 15 patients (48.4%). The duration of illness was 13.5 ± 1.1 months in patients with depression and 18.6 ± 2 months in those without depression; the difference was statistically non-significant (p > 0.05). The serum PTH levels of the patients with depression were significantly higher than in the non-depression group (p < 0.001). On the other hand there was no correlation between depression and BUN, creatinine, serum electrolytes, sex, GFR, and duration of illness (p > 0.05; table 1).In the literature, hyperparathyroidism has been considered the psycho-organic origin of mental disorders with PTH having a direct and reversible neurotoxic effect. But controversy regarding this concept remains [1, 2, 3, 4, 5]. Only a few studies show the correlation between psychopathologic symptoms and pathologically high levels of PTH in CRF. It has also been reported that cerebral functions showed improvement after parathyroidectomy [5], that electroencephalographic changes are related to PTH [4] and that development of uremic encephalopathy results from cerebral Ca overload [6]. Other studies did not verify these findings [7]. In SHPT, changes in the metabolism of some neurotransmitters have been reported [7]. In our study the serum Ca and P levels of all the patients with depression were normal, and brain scans revealed no cerebral calcification.The mechanism of depression in CRF has not been clarified as yet. The depression found in our patients cannot be explained by reactive depression due to chronic illness. The serum PTH levels of the patients with depression were found to be quite high, which may be due to some unknown mechanism causing metabolic changes that result in depression.As a result of our findings, it has been concluded that high levels of PTH can play an important role in the pathogenesis of depression in CRF. We propose keeping SHPT under control rather than giving non-specific antidepressants in the treatment of this type of depression. Further controlled studies are indicated, to elucidate the physiopathology of depression seen in CRF." @default.
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• W1977462463 date "1998-01-01" @default.
• W1977462463 modified "2023-10-18" @default.
• W1977462463 title "Depression and Secondary Hyperparathyroidism in Chronic Renal Failure" @default.
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• W1977462463 doi "https://doi.org/10.1159/000045115" @default.
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