Short-term effects of low protein-normal sodium diet on renal function in chronic renal failure

Cianciaruso, Bruno; Bellizzi, Vincenzo; Capuano, Alfredo; Bovi, Giuseppe; Nastasi, A; Conte, Giuseppe; Nicola, Luca De

doi:10.1038/ki.1994.112

Cited by 14 publications

(6 citation statements)

References 34 publications

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“…On the other hand, a previous study by our group indicates that the isolated restriction of protein intake, that is, in the presence of constantly normal salt intake, does not induce any change of mean BP values in CKD patients. 30 Overall, these data identify the moderate reduction of salt intake, with the dependent partial correction of extracellular volume expansion, as a relevant determinant of BP decrease during VLPD. In addition, other authors have evidenced that moderate dietary sodium restriction rapidly normalizes BP in patients with systolic hypertension also by improving large elastic artery compliance.…”

Section: Discussionmentioning

confidence: 67%

Very low protein diet supplemented with ketoanalogs improves blood pressure control in chronic kidney disease

Bellizzi

Iorio

Nicola

et al. 2007

Kidney International

121

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Blood pressure (BP) is hardly controlled in chronic kidney disease (CKD). We compared the effect of very low protein diet (VLPD) supplemented with ketoanalogs of essential amino acids (0.35 g/kg/day), low protein diet (LPD, 0.60 g/kg/day), and free diet (FD) on BP in patients with CKD stages 4 and 5. Vegetable proteins were higher in VLPD (66%) than in LPD (48%). LPD was prescribed to 110 consecutive patients; after run-in, they were invited to start VLPD. Thirty subjects accepted; 57 decided to continue LPD; 23 refused either diet (FD group). At baseline, protein intake (g/kg/day) was 0.79+/-0.09 in VLPD, 0.78+/-0.11 in LPD, and 1.11+/-0.18 in FD (P<0.0001). After 6 months, protein intake was lower in VLPD than LPD and FD (0.54+/-0.11, 0.78+/-0.10, and 1.04+/-0.21 g/kg/day, respectively; P<0.0001). BP diminished only in VLPD, from 143+/-19/84+/-10 to 128+/-16/78+/-7 mm Hg (P<0.0001), despite reduction of antihypertensive drugs (from 2.6+/-1.1 to 1.8+/-1.2; P<0.001). Urinary urea excretion directly correlated with urinary sodium excretion, which diminished in VLPD (from 181+/-32 to 131+/-36 mEq/day; P<0.001). At multiple regression analysis (R2=0.270, P<0.0001), BP results independently related to urinary sodium excretion (P=0.023) and VLPD prescription (P=0.003), but not to the level of protein intake. Thus, in moderate to advanced CKD, VLPD has an antihypertensive effect likely due to reduction of salt intake, type of proteins, and ketoanalogs supplementation, independent of actual protein intake.

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Section: Discussionmentioning

confidence: 67%

Very low protein diet supplemented with ketoanalogs improves blood pressure control in chronic kidney disease

Bellizzi

Iorio

Nicola

et al. 2007

Kidney International

121

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show abstract

“…Recent data from our group actually confute this hypothesis. We have demonstrated that in patients with moderate CRF, renal hemodynamics do not change when a LPD is started while maintaining a constant salt intake [19]; conversely, a decrease of renal perfusion and GFR becomes evident if patients undergo salt restriction in the presence of a constant protein intake [20].…”

Section: Discussionmentioning

confidence: 99%

Salt Intake and Renal Outcome in Patients with Progressive Renal Disease

Cianciaruso¹,

Bellizzi²,

Minutolo³

et al. 1998

Mineral Electrolyte Metab

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133

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Experimental studies suggest that salt intake plays a critical role in the progressive glomerular filtration rate (GFR) loss of established renal disease; however, this issue has never been addressed in humans. To this aim, we have retrospectively analyzed the clinical data of patients with chronic renal failure (CRF), in whom a low-protein diet was prescribed, over a period of about 3 years. On the basis of the daily urinary sodium output, the patients were divided into two groups: a group of patients constantly ingesting >200 mEq NaCl/day (high sodium intake, HSD, n = 30) and a group in which salt intake was <100 mEq/day (low sodium intake, LSD, n = 27). Patients taking diuretics or ACE inhibitors were excluded. At baseline, the LSD group, as compared to the HSD group, was characterized by significantly lower creatinine clearance (24 ± 2 vs. 28 ± 2 ml/min) and higher proteinuria (2.9 ± 0.3 vs. 1.5 ± 0.2 g/day). Despite the presence of these risk factors for progression, and a similar control of blood pressure (the average of the mean arterial pressure during follow-up was 111 ± 2 mm Hg in LSD and 107 ± 2 mm Hg in HSD), the LSD patients showed a better renal outcome: in this group, as compared to HSD, the GFR decline was lower (0.25 ± 0.07 vs. 0.51 ± 0.09 ml/min/month, p < 0.05), and proteinuria did not change while it markedly increased in HSD. During follow-up, LSD patients also ingested a significantly lower amount of protein. This study therefore suggests that efficacious salt restriction in CRF patients improves the outcome of renal disease independent from its antihypertensive effects.

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“…It is possible that a longer follow-up would have been required to reach statistical significance. Interestingly, with regards to the acute GFR response to a low-protein diet, we have previously demonstrated by means of inulin and PAH clearance studies that, in CKD patients (basal GFR around 40 mL/min), reduced protein intake per se does not translate in acute decline in GFR if salt intake is kept constant [ 60 ]. In contrast, low salt intake in the presence of constant protein intake is associated with a GFR reduction of 6 mL/min on average related to reductions in ECV and BP [ 61 ].…”

Section: The Check-mark Sign: Not Only Sglt2imentioning

confidence: 99%

Nephroprotection by SGLT2 Inhibition: Back to the Future?

Nicola

Gabbai

Garofalo

et al. 2020

JCM

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The introduction of sodium/glucose cotransporter 2 inhibitors (SGLT2i) has opened new perspectives for the management of diabetic population at risk of or with chronic kidney disease (CKD). More important, recent, large real-world studies have repositioned the nephroprotective efficacy of SGLT2i emerged from randomized trials within the frame of effectiveness. Furthermore, the salutary effects of these agents may extend to the nondiabetic population according to the positive results of current studies. Nevertheless, the clear benefits of these agents on the prevention of organ damage contrast with their unexpected, limited use in clinical practice. One potential barrier is the acute decline in glomerular filtration rate (GFR) commonly observed at the beginning of treatment. This phenomenon is reminiscent of the early response to the traditional nephroprotective interventions, namely blood pressure lowering, dietary protein and salt restriction and the inhibition of the renin–angiotensin system. Under this perspective, the “check-mark” sign observed in the GFR trajectory over the first weeks of SGT2i therapy should renew interest on the very basic goal of CKD treatment, i.e., alleviate hyperfiltration in viable nephrons in order to prolong their function.

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Short-term effects of low protein-normal sodium diet on renal function in chronic renal failure

Cited by 14 publications

References 34 publications

Very low protein diet supplemented with ketoanalogs improves blood pressure control in chronic kidney disease

Very low protein diet supplemented with ketoanalogs improves blood pressure control in chronic kidney disease

Salt Intake and Renal Outcome in Patients with Progressive Renal Disease

Nephroprotection by SGLT2 Inhibition: Back to the Future?

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