Tubular injury resulting from obstructive nephropathy impairs renal sodium conservation. Tubular atrophy, in turn, may be due in part to apoptosis of tubular epithelial cells. To determine whether renal apoptosis due to UUO is modulated by dietary sodium, 5 adult Sprague-Dawley rats were fed low sodium(LS) diet (2.9±0.2 umol/g BW), and 5 rats were pair-fed a normal sodium(NS) diet (17.3±0.9 umol/g BW). After 2 weeks, the fraction of apoptotic and necrotic cells in each kidney was measured by flow cytometry after propidium iodide labeling. In 6 additional rats, renal apoptotic cells were identified by the TUNEL technique, and tubular diameter was measured. Compared to the intact kidney (3.9±0.5%), UUO nearly doubled the fraction of apoptotic cells in the NS group (7.0±1.5%, p<0.05). In the LS group, compared to the intact kidney (4.2±1.4%), UUO nearly tripled the fraction of apoptotic cells (11.4±2.0%, p<0.05) which was greater than that of the obstructed kidney in the NS group (p<0.05). In contrast, neither UUO nor dietary sodium affected the fraction of necrotic cells. Whereas the diameter of apoptotic tubules was increased by UUO regardless of dietary sodium, the diameter of non-apoptotic tubules was increased only in NS, and not LS obstructed kidneys. We conclude that sodium deprivation enhances renal apoptosis in tubules dilated by ipsilateral UUO. By promoting apoptosis in patients with obstructive nephropathy, renal“sodium wasting” may therefore accelerate the progression of tubular atrophy.