Biological Trace Element Research

, Volume 29, Issue 3, pp 267–280

Nephrotoxicity and neurotoxicity in humans from organogermanium compounds and germanium dioxide

  • Alexander G. Schauss

DOI: 10.1007/BF03032683

Cite this article as:
Schauss, A.G. Biol Trace Elem Res (1991) 29: 267. doi:10.1007/BF03032683


There is no known biological requirement for germanium (Ge), germanates, or any organogermanium compound. Ge deficiency has not been demonstrated in any animal. The estimated average dietary intake of Ge in humans is 1.5 mg/d. Ge is widely distributed in edible foods, all of which, with few exceptions, contain less than 5 ppm Ge, since higher levels are toxic to most plants. Ingestion of Ge compounds has been shown to produce toxic effects in experimental animals.

In recent years inorganic germanium salts and novel organogermanium compounds, such as carboxyethyl germanium sesquioxide (Ge-132) and lactate-citrate-germanate (Ge lactate citrate) have been sold as “nutritional supplements” in some countries for their purported immunomodulatory effects or as health-producing elixirs, resulting sulting in intakes of Ge significantly exceeding the estimated average dietary intake. Since 1982, there have been 18 reported cases of acute renal dysfunction or failure, including two deaths, linked to oral intake of Ge elixirs containing germanium dioxide (GeO2) or Ge-132. In these cases, biopsies show vacuolar degeneration in renal tubular epithelial cells, without proteinuria or hematuria, in the absence of glomerular changes. Serum creatinine levels have been well above 400 μmol/L in such patients. In 17 of 18 cases, accumulated elemental Ge intakes reportedly ranged between 16 to 328 g over a 4–36 mo period, or between 100 to 2000 times the average estimated dietary intake for human. In surviving patients, renal function improved after discontinuation of Ge supplementation. However, in no case was recovery complete.

One organogermanium compound, an azaspiran organogermanium compound, 2-aza-8-germanspiro[4,5] decane-2-propamine-8,8-diethyl-N,N-dimethyl dichloride (spirogermanium), has been found to cause both neurotoxicity and pulmonary toxicity in phase I and II studies examining its chemotherapeutic potential as an antitumor drug in the treatment of various malignancies. In cancer patients given the drug spirogermanium, 40% experienced marked, yet transient neurotoxicity. Two patients suffered from pulmonary toxicity. Results of phases I and II human cancer trials for spirogermanium have not been favorable, with the exception of moderate benefits for three types of malignancies.

It is recommended that patients exposed to long-term (>3 mo) Ge supplementation at levels well above the estimated daily intake be medically supervised and monitored for potential renal-, pulmonaryor neurotoxicity. Further study regarding the mechanism of Geinduced nephrotoxicity in human is warranted.

Index Entries

Germaniumgermanium toxicity—humansgermanium dioxideorganogermanium compoundscarboxyethyl germanium sesquioxide (Germanium-132 or Ge-132)spirogermaniumgermanium lactate citrategermanatesacute renal failure resulting from germanium toxicitygermanium-induced nephrotoxicitygermanium neurotoxicity

Copyright information

© The Humana Press, Inc 1991

Authors and Affiliations

  • Alexander G. Schauss
    • 1
  1. 1.Life Sciences DivisionAmerican Institute for Biosocial Research, Inc.Tacoma