Sanai T, Okuda S, Onoyama K, Oochi N, Oh Y, Kobayashi K, Shimamatsu K, Fujimi S, Fujishima M
Second Department of Internal Medicine, Faculty of Medicine, Kyushu University, Fukuoka, Japan.
Nephron. 1990;54(1):53-60. doi: 10.1159/000185810.
Chronic renal failure developed in 5 patients who were taking germanium dioxide (GeO2)-containing compounds. Renal functional deterioration was slow but progressive and dialysis treatment was necessitated temporarily in 2 patients. After the discontinuation of GeO2, the impaired renal function tended to improve but remained abnormal for an observation period of 10-40 months. The lack of proteinuria and hematuria was characterized as the clinical manifestations. Renal biopsy specimens revealed the tubular epithelial cell degeneration containing hematoxylin-positive fine granules on light microscopy, and electron-dense inclusions in the swollen mitochondria on electron microscopy. These findings localized mainly in distal segment of the tubules. In the rats given GeO2 orally for 10 weeks, similar histological lesions were evident, as manifested by marked weight loss, anemia, azotemia, and negative proteinuria. In the rats given carboxyethylgermanium sesquioxide, these changes were not observed and Ge concentration of kidney was significantly lower than in the rats given GeO2. The present study indicates that chronic GeO2 intake causes progressive renal dysfunction characterized by the degeneration of distal tubules.
5名服用含二氧化锗（GeO2）化合物的患者出现了慢性肾衰竭。肾功能恶化缓慢但呈进行性，2名患者需要临时进行透析治疗。停用GeO2后，受损的肾功能有改善趋势，但在10至40个月的观察期内仍未恢复正常。临床表现的特点是无蛋白尿和血尿。肾活检标本在光镜下显示肾小管上皮细胞变性，含有苏木精阳性细颗粒，在电镜下显示肿胀线粒体中有电子致密包涵体。这些发现主要局限于肾小管的远端节段。给大鼠口服GeO2 10周后，出现了类似的组织学病变，表现为体重明显减轻、贫血、氮质血症和阴性蛋白尿。给大鼠服用羧乙基锗倍半氧化物后，未观察到这些变化，且肾脏的Ge浓度明显低于服用GeO2的大鼠。本研究表明，长期摄入GeO2会导致以远端肾小管变性为特征的进行性肾功能障碍。
