Rate of Residual Kidney Function (RKF) Loss in Peritoneal Dialysis and Hemodialysis

Several reports have suggested that residual kidney function (RKF) is better preserved among patients treated with PD as compared to HD (1–5). Many of these observations are based on either single center uncontrolled studies or on theoretical considerations. Possible explanations for these effects of PD RKF may include:

Better control of arterial blood pressure due to more uniform and gradual ultrafiltration.

Rationale: More stable blood pressure may prevent intermittent glomerular ischemia during episodes of hypotension or glomerular capillary hypertension during periods of volume expansion and thus decrease the development of glomerular sclerosis.

More steady concentration of solutes in blood with avoidance of significant fluctuations in osmolality.

Rationale: Tubular and capillary injury from transient hyperosmolar states could contribute to loss of RKF.

Differences in protein intake between PD and HD patients.

Rationale: A lower protein intake has been associated with better preservation of RKF. Patients undergoing PD often have lower protein intakes, possibly related to a lower Kt/Vurea. A high and sustained intake of dietary protein has been proposed to increase renal blood flow and glomerular filtration rates, which require additional renal work, recruitment of reserve glomeruli and the eventual development of intra-renal hypertension leading to glomerular sclerosis and loss of renal function (6).

Protein losses.

Rationale: The continuous loss of protein through the peritoneal effluent may lessen the filtration load each nephron must handle among patients on PD and therefore slow development of glomerular sclerosis.

Higher nephrotoxicity in HD.

Rationale: The intermittent exposure of blood to hemodialyzers, tubing and other components of extracorporeal circuits has been associated with secretion of cytokines (IL-1, tumor necrotizing factor, etc.) and other mediators of inflammation known to accelerate loss of RKF. Much progress has been made in the development of more biocompatible HD components to minimize the production of undesirable cytokines, but this possibility is still an important consideration. Conversely, increased cytokine secretion has also been associated with the use of conventional PD solutions. The latter has stimulated research in the development of more physiological solutions and biocompatible materials for use in PD.

While most clinical reports strongly suggest better preservation of RKF in PD, other investigators have not been able to confirm this finding (7,8). Tattersall studied 100 patients undergoing HD and PD and performed an exponential regression of Krt/V against time (7). During the first year of treatment, RKF contributed the equivalent of Krt/V = 1.0. No significant difference in the rate of renal failure progression was noted among the groups. In a subsequent study, these same authors compared the decline of kidney residual urea clearance in a cohort of 475 incident ESKD patients who received treatment with CAPD (N=175) or hemodialysis (HD) utilizing high-flux polysulphone membranes, ultrapure water, and bicarbonate as the buffer (N=300) (8). There were no significant differences in the mean urea clearance in each group at dialysis initiation, or at any 6-month time point during the ensuing 48 months (~4.5 mL/min at initiation to 1 mL/min at 48 months); although the mean urea clearance was higher in HD vs. CAPD until the 36-month time point. This was true even after exclusion of patients who had died in the first year after initiation, those transferred to another dialysis modality, or those who had been transplanted. Only age and chronic interstitial disease predicted retention of urea clearance at one year. It seemed apparent that in hemodialysis using high-flux biocompatible membranes and ultrapure water, RKF declines at a rate indistinguishable from that in CAPD. This may have important implications, since preservation of RKF has major benefits and is a valid therapeutic goal.

The rate of loss of RKF is difficult to predict due to the aforementioned factors influencing renal function preservation and inter-patient differences. However, Gotch et al. have published the rate of fall in Krt/V from a randomized dialysis prescription and clinical outcomes study (9). The observed decline was 0.21 Krt/V ± 0.34/6 months or 0.035/month. A more recent study in 4911 incident HD patients (over 5 years) with a median baseline RKF of 2.2 mL/min/1.73 m2, reported a faster loss of eGFR in patients who initiated HD at higher GFRs (10). The reductions in urea clearance one year post-HD initiation were: 1.29, 1.17, 1.1, and 0.78 mL/min/1.73 m2 in patients with eGFRs of >10, 8–<10, 6–<8, and <6 mL/min/1.73 m2, respectively. Higher UFRs were also shown to be associated faster decline in RKF; with UFRs ≥13 mL/kg/h increasing the case-mix adjusted risk of decline by 93% (11).

Inter-patient variation in the progression of renal failure is well known. The specific disease entities and comorbid conditions responsible for ESRD also influence the rate of deterioration of RKF. These disease processes continue to progress after the initiation of dialysis. Diabetic patients with generalized vasculopathy, those presenting with vasculitis and certain forms of focal sclerosing glomerulonephropathy often show a rapid rate of progression, while certain patients with tubulointerstitial disease progress remarkably slowly. In addition, nephrotoxic insults may be more prone to play a role in some groups of patients. A classic example is radiographic contrast media. Two risk factors in the development of acute renal failure from contrast media are the severity of renal failure and the coexistence of diabetes mellitus (12). Diabetics are at high risk of developing coronary artery disease and other vascular complications. Many transplant programs recommend or require a thorough cardiac work-up, including coronary arteriograms, for diabetics. Therefore, the use of contrast media may potentially play an important role in the loss of RKF.


  1. Lysaght MJ, Vonesh EF, Gotch F, et al. The influence of dialysis treatment modality on the decline of remaining renal function. ASAIO Trans. 37(4):598-604. http://www.ncbi.nlm.nih.gov/pubmed/1768496. Accessed March 7, 2018.
  2. Rottembourg. Residual renal function and recovery of renal function in patients treated by CAPD – PubMed. Kidney Int Suppl. 1993;40:S106-S110. https://pubmed.ncbi.nlm.nih.gov/8445831/. Accessed March 12, 2021.
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  6. Brenner BM, Meyer TW, Hostetter TH. Dietary Protein Intake and the Progressive Nature of Kidney Disease: N Engl J Med. 1982;307(11):652-659. doi:10.1056/nejm198209093071104
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  8. McKane W, Chandna SM, Tattersall JE, Greenwood RN, Farrington K. Identical decline of residual renal function in high-flux biocompatible hemodialysis and CAPD. Kidney Int. 2002;61(1):256-265. doi:10.1046/j.1523-1755.2002.00098.x
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  11. Lee Y, Okuda Y, Sy J, et al. Ultrafiltration Rate Effects Declines in Residual Kidney Function in Hemodialysis Patients. Am J Nephrol. 2019;50(6):481-488. doi:10.1159/000503918
  12. Diaz Buxo JA, Wagoner RD, Hattery RR, Palumbo PJ. Acute renal failure after excretory urography in diabetic patients. Ann Intern Med. 1975;83(2):155-158. doi:10.7326/0003-4819-83-2-155

P/N 101799-01 Rev B 03/2021