Aim. Up to now, an appropriate salt intake in renal insufficiency has not been clearly determined. We hypothesize that even a moderate decrease in salt intake may affect functional and morphologic response of the rat remnant kidney after 5/6 nephrectomy. Methods. Subtotal nephrectomy was performed in 77 inbred 12 week-old-female AVN Wistar rats. The two groups of rats were fed either a standard or a low salt diet. Median of salt intake was 14.6 and 10.4？mg/100？g/24？h in the two groups. Results. Ten weeks after ablation, the remnant kidney parenchyma wet weight was 0.66 ± 0.16？g/100？g of body weight and 0.56 ± 0.11？g/100？g of body weight () in rats with a standard and low salt diet, respectively. In these two groups, systolic blood pressure was 151 ± 29 versus 126 ± 21？mmHg (), serum creatinine levels were 164 ± 84 versus 106 ± 29？μmol/L (), proteinuria was 84 ± 37 versus 83 ± 40？mg/100？g/24？h (N.S.), and the glomerular injury score was 2.06 ± 0.49 versus 1.43 ± 0.62 (), respectively. Conclusion. Moderately decreased salt intake slowed down the development of ablation nephropathy in AVN inbred strain of rats. 1. Introduction Ablation of 5/6 (83%) of renal parenchyma in rats is an experimental model of chronic renal failure. Remnant “intact” nephrons respond by increasing single nephron filtration rate and with an impaired regulation of inflammatory mediators production. Later, the systemic hypertension and proteinuria develop. The final fatal consequence is the remnant glomeruli sclerosis, tubular atrophy and interstitial sclerosis (i.e., ablation nephropathy), and renal failure. This process can be reduced by a low protein diet and/or angiotensin converting enzyme inhibitors administration [1] or by the early kidney transplantation [2]. It is well known that low salt intake decreases systemic blood pressure in experimental animals and men [3–7] as well as the incidence of cardiovascular accidents [8]. Low salt intake suppresses asymmetric dimethylarginine (ADMA) formation and therefore nitric oxide (NO) production and downregulates the activity of platelet-derived growth factor (PDGF), interleukin-1 (IL-1), and other proinflammatory cytokines. Consequently, the endothelial function may be modified [8–11] and therefore atherosclerosis and cardiovascular and renal damages reduced [7]. Low salt intake also decreases proximal tubular epithelia hypertrophy [12–14]. In hemodialyzed patients with severe hypertension, low salt intake (5？g/24？h) caused a decrease in blood pressure due to the decrease in total peripheral resistance [7]. The normotension persisted
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