1. Young, sub-totally nephrectomized rats were used to study the altered mineral metabolism of renal failure and its effects on bone growth and mineral maturation.
2. Rats killed at 4 weeks after sub-total nephrectomy demonstrated less bone growth than the age-matched control animals. These differences diminished in successive 4 week periods and were not significant at 12 weeks after operation.
3. The major differences in bone mineral composition between the uraemic rats and the control rats were: (i) lower CO23;− concentrations, and (ii) higher PO34;− and HPO24;− concentrations.
4. These differences are consistent with the view that bone mineral matures by the conversion of an acidic calcium phosphate precursor into a carbonate-containing apatite, an essential feature of this conversion being the replacement of PO34;− or HPO24;− by CO23;−. By this definition, uraemic rats at 4 weeks after operation contained more immature bone mineral than the control rats. These differences corresponded to the changes in bone weight, and were similarly unaffected at 12 weeks after operation.
5. The effects observed were transient and were reversed as renal function recovered. If renal failure is sustained, however, as in patients with end-stage renal disease, the maturation defect could become a feature of renal bone disease. Specific aetiological factors are discussed, but not identified.