ASN's Mission

To create a world without kidney diseases, the ASN Alliance for Kidney Health elevates care by educating and informing, driving breakthroughs and innovation, and advocating for policies that create transformative changes in kidney medicine throughout the world.

learn more

Contact ASN

1401 H St, NW, Ste 900, Washington, DC 20005

email@asn-online.org

202-640-4660

The Latest on X

Kidney Week

Abstract: SA-PO0884

Metabolic Effects and Nutritional Safety of a Low-Protein Diet in Advanced CKD: Preliminary Prospective Findings

Session Information

Category: Health Maintenance, Nutrition, and Metabolism

  • 1500 Health Maintenance, Nutrition, and Metabolism

Authors

  • Tanzarella, Elena, Universita Vita Salute San Raffaele, Milan, Lombardy, Italy
  • Brambilla Pisoni, Matteo, IRCCS Ospedale San Raffaele, Milan, Lombardy, Italy
  • Lanzani, Chiara, IRCCS Ospedale San Raffaele, Milan, Lombardy, Italy
  • Vezzoli, Giuseppe, IRCCS Ospedale San Raffaele, Milan, Lombardy, Italy
  • Sciarrone Alibrandi, Maria Teresa, IRCCS Ospedale San Raffaele, Milan, Lombardy, Italy
  • Simonini, Marco, IRCCS Ospedale San Raffaele, Milan, Lombardy, Italy
Background

Nutritional therapy is a cornerstone of conservative management in advanced chronic kidney disease (CKD). Low-protein diets (LPD, 0.55–0.60 g/kg/day) are recommended to reduce uremic toxin production and slow disease progression; however, concerns persist regarding long-term nutritional safety, in particularly the risk of protein-energy wasting (PEW) and sarcopenia. In diabetic patients, the high carbohydrate content of low-protein food products raises additional concerns about glycemic control.

Methods

Prospective observational study enrolling 84 pre-dialysis patients with CKD stage IIIB–V (34 diabetic, 50 non-diabetic), followed in a nephrology outpatient clinic with scheduled visits every 4 months (± 2 weeks). Baseline assessment included biochemical parameters, a Food Frequency Questionnaire, and the Malnutrition Inflammation Score (MIS). Body composition was evaluated by bioelectrical impedance analysis (BIA); functional status by hand grip strength (HGS), chair stand test, and SARC-F questionnaire.

Results

At longitudinal analysis, LPD was associated with a significant reduction in serum urea (Δ = −37 mg/dL, p<0.001 across all CKD stages) and serum phosphate in advanced stages (p=0.001), without changes in phosphate binder therapy. Creatinine and eGFR remained stable throughout follow-up. Nutritional markers (albumin, pre-albumin, BMI, and transferrin) showed no clinically relevant decline. BIA-derived phase angle improved (p=0.018) and appendicular skeletal muscle mass index (ASMMI) showed a favorable trend (p=0.05). HGS and chair stand test performance remained stable. In diabetic patients, HbA1c did not deteriorate, confirming glycemic safety.

Conclusion

These preliminary findings suggest that LPD, implemented within a structured multidimensional nutritional monitoring program, effectively reduces uremic metabolic burden without inducing measurable deterioration in nutritional status or physical function in advanced CKD. The favorable safety profile, including in the diabetic subgroup, supports LPD as a first-line conservative tool, pending validation in larger cohorts with extended follow-up.