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Acid-Base Profile in Patients on PD

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Acid-Base Profile in Patients on PD View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Elsevier - Publisher Connector Kidney International, Vol. 64, Supplement 88 (2003), pp. S26–S36 Acid-base profile in patients on PD SALIM MUJAIS Renal Division, Baxter Healthcare Corporation, McGaw Park, Illinois Acid-base profile in patients on PD. Secular trends in dialy- successes. Changes in buffer sources have been under- sis dose in peritoneal dialysis (PD) and modes of dialysis de- taken in both HD (from acetate to bicarbonate) and in livery [automated PD (APD) versus continuous ambulatory PD (from acetate to lactate, and to bicarbonate alone or PD (CAPD)] require a reexamination of acid-base status in patients treated with these renal replacement modalities. We supplemented with lactate) [1, 3, 6–10, 12]. Furthermore, explored steady-state acid-base profile and its determinants in changes in dialysis dose (increasing in both HD and PD) 175 patients on CAPD and 77 patients on APD. The major- [21–28], dialysis frequency (shorter times in in-center HD ity (62% to 70%) of patients had serum bicarbonate levels and the emergence of short daily and nocturnal HD), and in the normal range, and a minority (17% to 27%) had val- modifications in dialysis delivery modes (an increasing ues just above 28 mEq/L. Only a small percentage (10% to 12%) of patients in either the CAPD or the APD groups had a use of APD), may have an impact on the correction of serum HCO3 less than 22 mEq/L, an indication of the successful uremic acidosis. It is the aim of the present paper to exam- correction of acidosis in most patients. The anion gap was ele- ine the status of acidosis correction in patients on PD and vated (>16 mEq/L) in the majority of patients on CAPD and compare the effects of CAPD, APD, and patient factors APD and bore an inverse relationship to serum HCO3 and a that may modulate response to alkali therapy delivered direct relationship to serum albumin and serum phosphate. In CAPD patients, but not APD patients, a significant inverse re- by dialysis. lationship was observed between the anion gap and peritoneal permeability as assessed by four-hour D/Pcreatinine. The correc- tion of acidosis in PD appears to be predominantly achieved METHODS by the continuous supplementation of alkali via dialysis, with residual renal function not differentiating the degree of cor- The present analysis is based on cohorts of patients rection. Steady-state serum bicarbonate in patients on CAPD originally recruited to participate in a randomized con- appeared to be responsive to the underlying peritoneal mem- trolled trial for the evaluation of a new dialysis solu- brane permeability characteristics of the patient that govern tion [29, 30]. Only measurements obtained at baseline alkali loss and gain, but the higher dialysate volumes in APD while patients were on standard dialysis regimen and appear to override this effect. Higher albumin, blood urea ni- solution are considered herein. The criteria for patient trogen (BUN), and phosphate in patients with lower HCO3 suggest a discrepancy between daily acid load and dialysis selection, and hence, inclusion in the current analysis, dose. were as follows: (1) Patients who had given written in- formed consent; (2) patients who were at least 18 years old; (3) patients who were treated with PD for at least Acidosis is one of the cardinal manifestations of re- 90 days before the screening visit; and (4) patients whose nal failure and its correction is one of the elementary standard prescription was stable for at least 30 days prior and obvious goals of renal replacement therapy. A vari- to the screening visit. ety of studies have examined the correction of acidosis The following patients were excluded from the study and the relevance of such corrections on the health of pa- and hence the present analysis: (1) Patients who had an tients on dialysis [1–20]. While these contributions have acute or chronic exit site or tunnel infection; (2) patients greatly advanced our understanding of mechanisms of who required antibiotics for the treatment of an episode generation and correction of acidosis [13, 14], the ongoing of peritonitis in the 30 days prior to the screening visit; changes in dialysis technology as to delivery modes and (3) patients who were known to be HIV positive; (4) pa- changing buffer use in both hemodialysis (HD) and peri- tients who had other serious disease such as active ma- toneal dialysis (PD) require that examination of contem- lignancy, or, if previously treated, residual malignancy porary patient groups be undertaken to delineate current or systemic infection; (5) patients who had active liver disease such as cirrhosis of the liver, active hepatitis, or other active liver disease; (6) patients who had an ill- Key words: peritoneal dialysis, acidosis, residual renal function, creati- ness or injury requiring hospitalization during the 30 days nine clearance. preceding the screening visit; and (7) patients who were C 2003 by the International Society of Nephrology pregnant or lactating. It is recognized that any and each S-26 Mujais: Acid-base profile in patients on PD S-27 Table 1. Overall demographic profile Table 3. Overall renal and dialytic profile Parameter CAPD APD P value Parameter CAPD APD N 175 77 N 175 77 Age 55.29 ± 1.05 52.68 ± 1.66 NS Urine volume mL/24 hr 718 ± 56 510 ± 61 Height 165.2 ± 0.9 170.1 ± 1.1 0.002 CrCl mL/min 5.23 ± .45 2.22 ± .48 Weight 76.0 ± 1.2 81.2 ± 1.8 0.018 Urea Cl mL/min 2.53 ± .20 .96 ± .19 M:F 60:115 49:28 RRF mL/min 3.88 ± .31 1.59 ± .31 Duration of dialysis years 2.15 ± 0.16 3.96 ± 0.54 0.001 Dialysis volume mL/24 hr 9356 ± 112 14172 ± 314 4-hour D/Pcreatinine .67 ± .01 .69 ± .01 Data are mean ± SE. D4/D0glucose .38 ± .01 .39 ± .02 4-hour D/Purea .89 ± .01 .90 ± .01 PET-UF mL/4 hr 436 ± 16 352 ± 26 Table 2. Overall biochemical profile LD-UF mL 294 ± 27 303 ± 45 Parameter CAPD APD Data are mean ± SE. Abbreviations are: CrCl, creatinine clearance; urea Cl, urea clearance; RRF, average of creatinine and urea clearances; N 175 77 4-hour D/P , ratio of dialysate creatinine at 4 hours of dwell to serum ± ± creatinine BUN mg/dL 51.08 1.24 50.12 1.92 creatinine; D4/D0glucose, ratio of 4-hour dialysate glucose to 0 hour dialysate Creatinine mg/dL 9.67 ± .28 10.96 ± .49 glucose; 4-hour D/Purea, ratio of dialysate urea at 4 hours of dwell to BUN; Na mEq/L 137.71 ± .27 138.40 ± .44 PET-UF, net ultrafiltration during a 4-hour PET with 2.5% dextrose solution; K mEq/L 3.91 ± .05 3.84 ± .07 LD-UF,net ultrafiltration during an overnight dwell with 2.5% dextrose solution. Cl mEq/L 95.07 ± .33 95.45 ± .46 HCO3 mEq/L 25.30 ± .24 25.73 ± .36 AGAP mEq/L 21.23 ± .30 20.97 ± .515 Ca mg/dL 9.44 ± .06 9.29 ± .10 70%) of patients had serum bicarbonate levels in the nor- ± ± PO4 mg/dL 5.07 .11 5.21 .19 mal range, and a small group (17% to 27%) had values Albumin g/dL 3.21 ± .04 3.27 ± .0521 Cholesterol mg/dL 206.36 ± 3.72 200.12 ± 4.84 just above 28 mEq/L (Fig. 1). The anion gap was ele- vated (>16 mEq/L) in the majority of patients on CAPD Data are mean ± SE. Abbreviations are: BUN, blood urea nitrogen; Na, sodium; K, potassium; Cl, chloride; HCO3, bicarbonate; AGAP, anion gap; Ca, and APD (Fig. 2) and bore an inverse relationship to calcium; PO4, phosphate. serum HCO3 (Fig. 3) and a direct relationship to serum albumin (Fig. 4) and serum phosphate (Fig. 5). In CAPD patients, but not APD patients, a significant inverse rela- of the above exclusion conditions can have an effect on tionship was observed between the anion gap and peri- patient acid-base balance. toneal permeability as assessed by four-hour D/Pcreatinine As part of their baseline evaluation, all patients de- (Fig. 6). The correlation between the anion gap and albu- scribed had standard blood chemistry and hematology min in CAPD patients (r = 0.403, P < 0.001) was reduced measures, as well as a standard peritoneal equilibra- when it was controlled for phosphate levels (r = 0.363, tion test (PET). All patients, who had urine output P < 0.001), but remained significant and was further re- >100 mL/24 hours, collected their 24-hour urine output duced when controlled for both phosphate and four-hour = < during the 24 hours preceding baseline. Urea nitrogen D/Pcreatinine (r 0.276, P 0.001). In APD patients, how- and creatinine were used to determine the residual renal ever, the correlation between albumin and the anion gap function (RRF). RRF was calculated as the average of re- (r = 0.543, P < 0.001) was minimally affected by control- nal creatinine clearance (CrCl) and renal urea nitrogen ling for phosphate (r = 0.528, P < 0.001) or both phos- = < clearance (Ucl) by standard formulas. phate and four-hour D/Pcreatinine (r 0.516, P 0.001). In CAPD patients, the correlation between the anion = < RESULTS gap and four-hour D/Pcreatinine (r −0.319, P 0.001) General characteristics of the population was reduced but remained significant when it was con- trolled for phosphate (r = −0.269, P < 0.001). Controlling The overall profile of the study population is illustrated for albumin, however, abolished the correlation between in Tables 1–3.
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