This study investigates the effect in rats of acute CdCl₂ (5µM) intoxication on renal function and characterizes the transport of Ca²⁺, Cd²⁺ and Zn²⁺ in the proximal tubule (PT), loop of Henle (LH) and terminal segments of the nephron (DT) using whole kidney clearance and nephron microinjection techniques. Acute Cd²⁺ injection resulted in renal losses of Na⁺, K⁺, Ca²⁺, Mg²⁺, PO₄^2- and water, but glomerular filtration remained stable. ⁴⁵Ca microinjections showed that Ca²⁺ permeability in the DT was strongly inhibited by Cd²⁺ (20µM), Gd³⁺ (100µM) and La³⁺ (1mM), whereas nifedipine (20µM) had no effect. ¹⁰⁹Cd and ⁶⁵Zn microinjections showed that each segment of nephron was permeable to these metals. 95% of injected amounts of ¹⁰⁹Cd were taken up in the PT. ¹⁰⁹Cd fluxes were inhibited by Gd³⁺ (90µM), Co²⁺ (100µM) and Fe²⁺ (100µM) in all nephron segments. Bumetanide (50µM) only inhibited ¹⁰⁹Cd fluxes in LH; Zn²⁺ (50µM and 500µM) inhibited transport of ¹⁰⁹Cd in DT. In conclusion, these results indicate that 1) the renal effects of acute Cd²⁺ intoxication are suggestive of proximal tubulopathy; 2) Cd²⁺ inhibits Ca²⁺ reabsorption possibly occurs through ECaC in the DT and this blockade could account for the hypercalciuria associated with Cd²⁺ intoxication; 3) the PT is the major site of Cd²⁺ reabsorption; 4) the paracellular pathway and DMT1 could be involved in Cd²⁺ reabsorption along the LH; 5) DMT1 may be one of the major transporters of Cd²⁺ in the DT; 6) Zn²⁺ is taken up along each part of the nephron and its transport in the terminal segments could occur via DMT1.