Protein catabolic rate (PCR), dietary protein intake (DPI) and metabolic acidosis

A. Grzegorzewska

K. Marcinkowski University of Medical Sciences, Department of Nephrology, Al. Przybyszewskiego 49, Poznan, Poland

Sir,

I have read with great interest the article by Movilli et al. [1] and a comment of Iorio et al. [2], concerning the relationships between PCR, DPI and metabolic acidosis. With the aim of adding further information on this issue, I would like to present the results of PCR, DPI and blood gas parameters obtained in continuous ambulatory peritoneal dialysis (CAPD) patients.

In our uraemic patients (n=55; Female, 16 and Male, 39; age 45±12 years) treated with CAPD through 1–27 (19±11) months, values of PCR and DPI, daily energy intake (DEI), blood acid–base parameters and nitrogen balance were evaluated every 3 months. PCR was calculated according to Randerson et al. [3] and normalized to total body mass (TBM), ideal body mass (IBM), TBW/0.58 (TBW, total body water) and lean body mass (LBM) estimated according to three methods: (i) from creatinine kinetics using the method of Keshaviah et al. [4]—LBMcr; (ii) from anthropometric measurements—LBManthr; and (iii) from the relationship LBM=TBW/0.73. Values of DPI and DEI were obtained on the basis of diet histories taken by an experienced dietetician and checked against coloured pictures of individual foods and meals for accuracy. DPI and DEI were calculated using the computer program FOOD version 1.0 (The Institute of Nutrition and Food, Poland, licence 017). DPI was normalized as aforementioned for PCR. TBW was estimated according to the method of Watson et al. [5]. Parameters of acid–base balance were obtained from arterialized capillary blood using Blood Gas Analyzer Compact 1 (Austria). Daily nitrogen balance was calculated as the difference between nitrogen intake and nitrogen loss. Nitrogen intake was calculated as DPI/6.25 (g/day). Nitrogen loss was calculated as a sum of total nitrogen removal in dialysate and urine, basing on the nitrogen determinations performed by the modified Kjeldahl method [6]. A fixed amount of 1.824 g was taken into consideration accounting for nitrogen from protein (1.504 g) and amino acids (0.32 g) lost through the gastrointestinal tract and skin daily [7,8]. This fixed amount of nitrogen was also subtracted from values of nitrogen intake. Positive values of nitrogen balance indicate uptake of nitrogen (anabolic processes), negative values of nitrogen balance mean a loss of nitrogen (catabolic processes). Total DEI was calculated as oral DEI taken from diet record analysis plus DEI from glucose absorbed from the peritoneal cavity minus energy from glucose lost with daily urine. Total DEI was normalized to TBM.

Our earlier analyses revealed no significant differences in respective values of PCR, DPI and concentrations of H+ and HCO3- in the course of CAPD [9,10]. In the current study, mean result of each parameter was obtained in every patient as representative for her/his entire CAPD course, then mean±SD for all respective parameters were calculated for the entire group. The correlation analysis was performed using Spearman method. The P value <0.05 was defined as significant.

Results (mean±SD) of PCR and DPI are presented in Table 1Go. Mean blood gas parameters in the course of CAPD were as follows: H+ concentration 42.7±3.5 µmol/l; partial pressure of CO2 (pCO2) 38.6±2.8 mmHg; HCO3- concentration 21.9±2.2 mmol/l. HCO3- concentration <22 mmol/l was shown in 28 patients, including 32% uraemics with HCO3-<19.9 mmol/l. Metabolic alkalosis (HCO3- concentration >26 mmol/l) occurred in 7% of patients. Significant correlations between examined parameters are expressed in Table 2Go. PCR (g/day) negatively correlated with DPI normalized to LBM. When both PCR and DPI were normalized to LBMcr, a positive relationship was shown, however, a mathematical coupling cannot be excluded. PCR negatively correlated with HCO3- concentration. There were no significant correlations between DPI and blood gas parameters. Nitrogen balance in the course of CAPD was 5.14±3.48 g/day. Total DEI was 35.8±11.5 kcal/kg TBM/day.


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Table 1. Daily values of PCR and DPI obtained in uraemic patients (n=55) in the course of CAPD
 

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Table 2. Significant correlations between daily PCR, daily DPI and blood gas parameters shown in uraemic patients treated with CAPD
 
Our studies indicate a relationship between DPI, PCR and acid–base parameters in the course of CAPD. However, it is not easy to show direct correlation between DPI and PCR; according to the current study the results of correlation analysis depend on the method of normalization of both DPI and PCR values. When among patients with similar DPI (g/day) there are those with higher LBM, the correlation analysis indicates that such patients have a smaller catabolism expressed by PCR (g/day). Suggestion that PCR should be normalized to LBM was previously made by Keshaviah et al. [11]. On the other hand, there is evidence that PCR reflects DPI when patients are neither catabolic nor anabolic [12]. In this study nitrogen balance varied widely in individual patients from +14.6 to -2.04 g/day, thus, it also does not indicate stable protein metabolism, that can enhance difficulties in obtaining significant correlation between DPI and PCR. Di Iorio et al. [13] emphasize that protein intake in chronic haemodialysed patients may be influenced by clinical, social, economics and pharmacology factors. These factors obviously act also in CAPD patients and contribute to PCR changes. In our study, differences in DPI did not influence directly acid–base parameters and, inversely, H+ and HCO3- concentrations did not affect DPI. It is worthwhile to note that mentioned data were obtained with adequate mean total DEI of 35.8 kcal/kg TBM/day, thus dietary protein could be properly metabolised.

In conclusion, our studies support the idea that PCR is influenced by acid–base status. PCR reflects DPI poorly under conditions of unbalanced nitrogen turnover.

References

  1. Movilli E, Bossini N, Viola F et al. Evidence for an independent role of metabolic acidosis on nutritional status in haemodialysis patients. Nephrol Dial Transplant 1998; 13: 674–678[Abstract]
  2. Di Iorio B, Terracciano V, Gaudiano G, Bellizzi. Daily variations of protein intake in haemodialysed patients. Nephrol Dial Transplant 1998; 13: 2977–2978[Free Full Text]
  3. Randerson DH, Chapman GV, Farrell PC. Amino acid and dietary status in long-term CAPD patients. In: Atkins RC, Farrell PC, Thomson N (eds). Peritoneal dialysis. Churchill Livingstone, Edinburgh; 1981: 171–191
  4. Keshaviah PR, Nolph KD, Collins AJ. Lean body mass (LBM) estimation from creatinine kinetics. J Am Soc Nephrol 1991; 2: 332 [Abstract]
  5. Watson PE, Watson ID, Hatt RD. Total body water volumes for adult males and females estimated from simple anthropometric measurements. Am J Clin Nutr 1980; 33: 27–39[Abstract]
  6. Jankiewicz M. Zestaw do oznaczania zawartosci azotu w materiale biologicznym zmodyfikowana metoda Kjeldahla. Rocz Wyzszej Szkoly Rolniczej 1962; 13: 291–298
  7. Kopple JD, Blumenkrantz MJ, Jones MR et al. Plasma amino acid levels and amino acid losses during continuous ambulatory peritoneal dialysis. Am J Clin Nutr 1982; 36: 395–402[Abstract]
  8. Sargent J, Gotch F, Borah M et al. Urea kinetics, a guide to nutritional management of renal failure. Am J Clin Nutr 1978; 31: 1606–1702
  9. Grzegorzewska AE, Chmurak A, Dobrowolska-Zachwieja A. Nutrition of uremic patients in the course of CAPD treatment. Adv Perit Dial 1996; 12: 293–297[Medline]
  10. Grzegorzewska AE, Mariak I. Parameters of blood acid-base balance and adequacy of continuous ambulatory peritoneal dialysis as well as dietary intake. Pol Merkuriusz Lek 1999; 6: 176–181[Medline]
  11. Keshaviah PR, Nolph KD, Prowant B et al. Defining adequacy of CAPD with urea kinetics. Adv Perit Dial 1990; 6: 173–177[Medline]
  12. Krediet T. Physicians are urged to be wary of using `PCR' to modify dialysis dose. Perit Dial Today 1996; 2: 10
  13. Di Iorio B, Terracciano V, Gaudiano G, Altieri C. Factors affecting nPCR in haemodialysed patients. Int J Artif Organs 1995; 18: 131–140




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