Hyperphosphatemia: a factor that provokes severe experimental acute renal failure.
The purpose of this study was to determine whether pre-existent hyperphosphatemia potentiates the severity of evolving ARF. Normal rats were subjected to graded phosphate infusions (0 to 0.07 mmol/kg/hr) in order to induce differing degrees of hyperphosphatemia (6.8 to 10.3 mg/dl). After a 40 min control period, ARF was induced either by HgCl2 administration (12 mg/kg) or by bilateral renal pedicle cross-clamping (25 min). GFRs before and after renal injury were determined by measuring the Cioth. 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 less than 0.001). In addition, 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 calcium/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 to 19.1 mg/dl. Phosphate-infused control rats had stable GFRs and normal renal histology.


CONCLUSIONS
Hyperphosphatemia may significantly exacerbate the functional and histologic correlates of acute renal failure. The pathogenesis of this response remains unknown.
D058186:Acute Kidney Injury / Q000097:blood* / Q000209:etiology / Q000473:pathology; D000818:Animals; D002118:Calcium / Q000097:blood; D005260:Female; D007511:Ischemia / Q000150:complications; D007687:Kidney Tubules, Proximal / Q000473:pathology; D008627:Mercuric Chloride; D008628:Mercury; D010710:Phosphates / Q000097:blood*; D051381:Rats; D011919:Rats, Inbred Strains
D010710:Phosphates; D008627:Mercuric Chloride; D008628:Mercury; D002118:Calcium