Hyperphosphatemia: a factor that provokes severe experimental acute renal failure
Zager, R.A.
Journal of Laboratory and Clinical Medicine 100(2): 230-239
1982
ISSN/ISBN: 0022-2143 PMID: 6212619 Document Number: 186899
Whether preexistent hyperphosphatemia potentiates the severity of evolving ARF . The percent decrease of GFR after renal injury strongly correlated with the degree of phosphate loading (r = 0.71, HgCl2; r = 0.82, ischemia) (P < 0.001). Phosphate-treated ARF rats showed striking histologic changes not seen in their non-phosphate-treated counterparts, i.e., marked vacuolization of the proximal tubules and variable degrees of glomerular capillary collapse. Renal Ca/phosphate deposition could not be demonstrated in any kidney by the Von Kossa or the alizarin red histochemical techniques. Terminal serum phosphate concentrations ranged from 7.5-19.1 mg/dl. Phosphate-infused control rats had stable GFR and normal renal histology. Hyperphosphatemia may significantly exacerbate the functional and histologic correlates of acute renal failure. The pathogenesis of this response remains unknown.