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      Hypertension but Not Sodium Intake Determines Progression of Renal Failure in Experimentally Uremic Rats


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          Background/Aims: High sodium intake is implicated in contributing to progression of chronic renal failure. We studied the effect of high sodium consumption on progression of rat experimental renal failure while sodium-induced hypertension was pharmacologically controlled. Methods: 64 Sprague-Dawley rats underwent 5/6 nephrectomy. Subsequently, they were divided in three groups which were fed either low, normal, or high sodium diet. Only the high sodium-consuming group developed hypertension. This group was further divided in two subgroups in which hypertension was either untreated or titrated to normotension by hydralazine alone or with propranolol. Results: Sequential GFR values did not differ between the respective normotensive groups. Survival downslopes of all three normotensive groups (including the pharmacologically treated, high sodium-consuming subgroup) were also similar, extending over 10 weeks. By contrast, pharmacologically untreated animals exhibited severe hypertension and 100% mortality within 3 weeks. In all experimental groups, 24-hour urinary sodium excretion paralleled sodium intake. Proteinuria rose similarly and significantly in all animals on high sodium. A significant correlation between 24-hour sodium and proteinuria was evident throughout the experimental period. Conclusions: (1) In 5/6 nephrectomized rats, renal function deterioration was not affected by dietary sodium, provided hypertension was pharmacologically controlled. (2) Enhanced proteinuria secondary to high sodium consumption had no adverse effect on progression of renal failure in this model.

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          Most cited references19

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          Management of glomerular proteinuria: a commentary.

          It is widely accepted that proteinuria reduction is an appropriate therapeutic goal in chronic proteinuric kidney disease. Based on large randomized controlled clinical trials (RCT), ACE inhibitor (ACEI) and angiotensin receptor blocker (ARB) therapy have emerged as the most important antiproteinuric and renal protective interventions. However, there are numerous other interventions that have been shown to be antiproteinuric and, therefore, likely to be renoprotective. Unfortunately testing each of these antiproteinuric therapies in RCT is not feasible. The nephrologist has two choices: restrict antiproteinuric therapies to those shown to be effective in RCT or expand the use of antiproteinuric therapies to include those that, although unproven, are plausibly effective and prudent to use. The goal of this work is to provide the documentation needed for the nephrologist to choose between these strategies. This work describes 25 separate interventions that are either antiproteinuric or may block injurious mechanisms of proteinuria. Each intervention is assigned a level of recommendation (Level 1 is the highest; Level 3 is the lowest) according to the strength of the evidence supporting its antiproteinuric and renoprotective efficacy. Pathophysiologic mechanisms possibly involved are also discussed. The number of interventions at each level of recommendation are: Level 1, n = 7; Level 2, n = 9; Level 3, n = 9. Our experience indicates that we can achieve in most patients the majority of Level 1 and many of the Level 2 and 3 recommendations. We suggest that, until better information becomes available, a broad-based, multiple-risk factor intervention to reduce proteinuria can be justified in those with progressive nephropathies. This work is intended primarily for clinical nephrologists; therefore, each antiproteinuria intervention is described in practical detail.
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            Deleterious effects of calcium channel blockade on pressure transmission and glomerular injury in rat remnant kidneys.

            Hypertensive mechanisms are postulated to play a major role in the progressive glomerulosclerosis (GS) after renal mass reduction. But, in contrast to converting enzyme inhibitors, BP reduction by calcium channel blockers, has not provided consistent protection. Radiotelemetric BP monitoring for 7 wk was used to compare nifedipine (N) and enalapril (E) in the rat approximately 5/6 renal ablation model. After the first week, rats received N, E, or no treatment (C). The overall averaged systolic BP in C (173 +/- 7 mmHg) was reduced by both E and N (P < 0.001), but E was more effective (113 +/- 2 vs. 134 +/- 3 mmHg, P < 0.01). GS was prevented by E (2 +/- 1 vs. 26 +/- 5% in C) but not by N (25 +/- 6%). GS correlated well with the overall averaged BP in individual animals of all groups, but the slope of the relationship was significantly steeper in N compared with C+E rats (P < 0.02), suggesting greater pressure transmission to the glomeruli and GS for any given BP. Since autoregulatory mechanisms provide the primary protection against pressure transmission, renal autoregulation was examined at 3 wk in additional rats. Autoregulation was impaired in C rats, was not additionally altered by E, but was completely abolished by N. These data demonstrate the importance of autoregulatory mechanisms in the pathogenesis of hypertensive injury and suggest that calcium channel blockers which adversely affect pressure transmission may not provide protection despite significant BP reduction.
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              Low-potassium and glucose-free dialysis maintains urea but enhances potassium removal.

              The influence of potassium (K) removal on dialysis efficiency as measured by urea elimination is not clear. In this prospective, randomized, cross-over study we investigated the magnitude of K removal and its effect on urea (u) elimination during high-flux haemodialysis (HD).

                Author and article information

                Nephron Physiol
                Nephron Physiology
                S. Karger AG
                September 2004
                08 September 2004
                : 98
                : 1
                : p1-p7
                aNephrology Division, Departments of bInternal Medicine A and cInternal Medicine F, Assaf Harofeh Medical Center (affiliated to Sackler Faculty of Medicine, Tel Aviv University), Zerifin, Israel
                79931 Nephron Physiol 2004;98:p1–p7
                © 2004 S. Karger AG, Basel

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                Page count
                Figures: 4, Tables: 2, References: 34, Pages: 1
                Self URI (application/pdf): https://www.karger.com/Article/Pdf/79931
                Self URI (text/html): https://www.karger.com/Article/FullText/79931
                Self URI (journal page): https://www.karger.com/SubjectArea/Nephrology
                Original Paper

                Cardiovascular Medicine,Nephrology
                Hypertension, hemodynamics,Sodium intake,Chronic renal failure,Proteinuria,Glomerular filtration rate


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