Glomerular and tubular dynamics in mercuric chloride-induced acute renal failure.

Mercuric chloride (HgCl2)-induced acute renal failure has received considerable investigative attention but little agreement as to its pathogenesis. A source of some disagreement has been the lack of direct glomerular dynamics measurements in this disorder. We examined glomerular dynamics, tubular integrity, and whole kidney function at 24 hours in Munich-Wistar rats given either HgCl2, 3.5 mg/kg, or a similar volume of 0.9% saline solution intramuscularly. Arterial blood pressure was elevated in HgCl2-injected rats, but renal blood flow and its distribution were similar to those of controls. Inulin clearance, however, was reduced by 89% in HgCl2-injected animals. Glomerular dynamics experiments demonstrated similar glomerular plasma flow (QA) and glomerular capillary and tubular pressures in control and HgCl2-injected animals but a higher net afferent ultrafiltration pressure and lower ultrafiltration coefficient (Kf) in the HgCl2-injected group. Single-nephron glomerular filtration rate (SNGFR), when measured from Bowman's space and HgCl2-injected rats, was similar to that measured from late proximal tubules in controls. However, SNGFR determined from the later proximal tubule in HgCl2-injected rats was only one third of that measured from Bowman's space. QA estimated from glomerular counting was similar to that calculated from Bowman's space SNGFR in HgCl2-injected rats. 3H-inulin microinjection experiments confirmed the presence of tubular fluid backleak suggested by the discrepancy in Bowman's space and late proximal tubular SNGFR measurements. It is concluded that at 24 hours in low-dose HgCl2-induced acute renal failure, tubular fluid backleak is the major pathogenetic factor, with a decline in Kf having a potential secondary role.