Shigematsu T, Caverzasio J, Bonjour JP Department of Medicine, University Hospital of Geneva, Switzerland.
Kidney Int 1993 Jul;44(1):173-181

The influence of PTH in the progression of renal failure induced by a high protein diet was investigated in either sham operated (SHAM) or parathyroidectomized (PTX) and subtotally nephrectomized (NX) rats. NX-SHAM rats were pair-fed either a high (HPr, 40% casein) or a normal (NPr, 20% casein) protein diet and NX-PTX rats a HPr diet. The results indicate that PTX markedly improved the survival rate and prevented the deterioration of renal function induced by the HPr diet. The number of rats alive after 33 weeks was 0 of 11, 6 of 10, and 9 of 10 in NX-SHAM-HPr, NX-PTX-HPr and NX-SHAM-NPr, respectively. The increases in plasma urea and creatinine were consistently delayed or prevented in NX-PTX as compared to NX-SHAM rats fed the HPr diet. The increment in the mass and calcium content of the kidney remnant induced by HPr was prevented by parathyroidectomy. In addition, PTX completely prevented the rise in the circulating level of cholesterol observed in response to HPr. Normalization of plasma calcium in NX-PTX rats with 1,25-dihydroxyvitamin D3 restored the increment in the renal mass and calcium content and reduced the protective effect of PTX on the progression of renal failure induced by high protein diet. In conclusion, in the subtotal nephrectomized rat model of chronic renal failure, the progression of kidney damage induced by a high protein diet can be prevented by removal of the parathyroid glands. This observation suggests that PTH could be implicated in the mechanism whereby a high protein regimen accelerates the course of chronic renal failure.