Your activity: 18353 p.v.
your limit has been reached. plz Donate us to allow your ip full access, Email: [email protected]

Urine output and residual kidney function in kidney failure

Urine output and residual kidney function in kidney failure
Author:
Anthony Bleyer, MD, MS
Section Editor:
Jeffrey S Berns, MD
Deputy Editor:
Albert Q Lam, MD
Literature review current through: Feb 2022. | This topic last updated: Jul 09, 2020.

INTRODUCTION — Many patients starting dialysis have significant residual kidney function. Only 20 percent of individuals starting dialysis in 2016 had an estimated glomerular filtration rate (eGFR) <5 mL/min/1.73 m2 [1].

Preservation of this residual kidney function has been associated with improved outcomes, and nephrologists should try to preserve this residual kidney function as long as possible.

Even when the GFR is very low, the urine output is variable, ranging from oliguria to normal or even above normal levels. These findings are related to the fact that the urine output is determined not by the GFR alone, but also by the difference between the GFR and the rate of tubular reabsorption. If, for example, a patient with advanced acute or chronic kidney failure has a GFR of 5 L/day (versus the normal of 140 to 180 L/day), the daily urine output will still be 1.5 L if only 3.5 L of the filtrate is reabsorbed.

It had been thought that tubular damage impaired the ability to reabsorb sodium and water, thereby contributing to the maintenance of an adequate urine output in this setting. However, it seems more likely that volume expansion (due to initial sodium retention) and a urea osmotic diuresis (as the daily urea load is excreted by fewer functioning nephrons), due in part to solute intake, play a more important role in the persistent urine output [2-4].

In comparison, water intake (which usually determines the urine output via changes in the secretion of antidiuretic hormone [ADH]) plays relatively little role in regulating the urine output in advanced kidney disease. These patients can neither dilute nor concentrate the urine normally; the range of urine osmolality that can be achieved in the typical patient with advanced chronic kidney disease varies from a minimum of 200 mosmol/kg to a maximum of 300 mosmol/kg compared with 50 to 1200 mosmol/kg in normal subjects [4,5]. The net effect of this ADH resistance is that variations in ADH release in response to changes in water intake have relatively little effect on the urine output [5].

CLINICAL IMPORTANCE OF RESIDUAL KIDNEY FUNCTION — The loss of residual kidney function in patients with end-stage kidney disease (ESKD) has important clinical manifestations. This includes adverse effects upon volume control and patient survival [6-8]. There are two essential components to residual kidney function: renal clearance of uremic toxins and urinary volume. Urinary volume is being seen as increasingly important.

Although the remaining glomerular filtration rate (GFR) may only be 4 to 5 mL/min in patients begun on maintenance dialysis, this is sufficient to make a significant contribution to the removal of potential uremic toxins since filtration is continuous, as opposed to the 12 hours per week that the patient is undergoing hemodialysis [9]. In addition, residual kidney function allows for the clearance of larger molecules, such as beta-2 microglobulin, that dialysis filters cannot remove. Thus, this residual function encompasses more than the urea clearance that can be calculated as a contribution to dialysis dose. Even in patients with residual kidney function less than 1.5 mL/min, patients who were not anuric had significantly lower levels of non-urea solutes such as indoxyl sulfate and asymmetric dimethylarginine than patients on dialysis [10].

Continued urine output also facilitates the regulation of fluid and electrolyte balance and may enhance nutritional status and survival [8,11-14].

Fluid removal is an essential function of the kidney and the one most identifiable by patients. The amount of urine output in dialysis patients equates to fluid that does not need to be removed with dialysis (either peritoneal or hemodialysis). In hemodialysis, decreasing fluid removal with each dialysis treatment decreases the possibility of intradialytic hypotension, which can lead to myocardial stunning, ischemia, and increased mortality [15]. (See "Intradialytic hypotension in an otherwise stable patient", section on 'Outcomes'.)

In peritoneal dialysis, the need to remove less fluid allows for the use of dialysate with a lower glucose concentration, decreasing the caloric intake from peritoneal dialysis and also decreasing the toxicity of glucose and glucose intermediates to the peritoneal membrane [16]. (See "Peritoneal dialysis solutions", section on 'Low-molecular-weight agents'.)

Survival — Among peritoneal dialysis and hemodialysis patients, the beneficial effect of continued residual kidney function on survival is clear, as shown in the CANUSA study, a large study of Canadian and United States peritoneal dialysis patients [17]; the Netherlands Cooperative Study of the Adequacy of Dialysis (NECOSAD), a study of 1800 hemodialysis and peritoneal dialysis patients; and others. This is discussed separately. (See "Prescribing peritoneal dialysis" and "Prescribing and assessing adequate hemodialysis".)

In one study of 1946 patients from Korea, after adjustment for potential confounders, urine volume was significantly associated with survival, with GFR losing significance when urine volume was in the model [18].

In an analysis of the CANUSA study of incident peritoneal dialysis patients, there was a 36 percent reduction in relative risk of death with increased urine volume; residual GFR was not associated with improved mortality [17].

Therefore, one should adopt measures aimed at preserving residual kidney function among peritoneal dialysis and hemodialysis patients and improving endogenous fluid removal through increased urine volume. Even if urea clearance is small, the urinary volume is beneficial.

EFFECT OF DIALYSIS MODALITIES — Both volume expansion and the high urea load per nephron are rapidly reversed by dialysis (of any form), which removes sodium, water, and urea. Therefore, it is not surprising that many patients have a marked reduction in, or even cessation of, urine output when dialysis is instituted [2]. This observation has raised the question of whether dialysis itself worsens or delays recovery of residual kidney function in patients with chronic kidney failure. This issue is unresolved in acute kidney failure. (See "Dialysis-related factors that may influence recovery of kidney function in acute kidney injury (acute renal failure)".)

Peritoneal and hemodialysis may have different effects on residual kidney function. This is discussed in the following sections.

Hemodialysis versus peritoneal dialysis — For reasons that are incompletely understood, the loss of residual kidney function appears to occur more rapidly with hemodialysis than with peritoneal dialysis [9,19-22]. As examples:

In a prospective study of 279 hemodialysis and 243 peritoneal dialysis patients, loss of residual kidney function was greater in hemodialysis patients than peritoneal dialysis patients, with peritoneal dialysis patients on average having a 30 percent higher residual glomerular filtration rate (GFR) than hemodialysis patients [22].

In a retrospective study of 811 hemodialysis and 1032 peritoneal dialysis patients, peritoneal dialysis patients had a 65 percent lower risk of oliguria (self-reported urine volume <200 mL/day) at one year of follow-up compared with hemodialysis patients [20].

However, it is important to note that many of the studies addressing this issue are older, and, at the time, modern hemodialytic techniques such as volumetric control, ultrapure water, and biocompatible membranes were not in use. Residual kidney function has also been studied extensively in the peritoneal dialysis population, but there have been few studies in the hemodialysis population.

Potential reasons for differences in loss of residual kidney function with hemodialysis include intermittent hypotension and activation of nephrotoxic inflammatory mediators during treatments [22-24]. In one study of 522 patients initiating either peritoneal dialysis or hemodialysis, predictors of the rate of decline in residual kidney function at baseline included a higher diastolic blood pressure and increased proteinuria [22]. Over time, decreases in residual kidney function were associated with hypotension with hemodialysis and dehydration episodes with peritoneal dialysis. Relatively higher kidney function was consistently observed with peritoneal dialysis, which increased over time. (See "Intradialytic hypotension in an otherwise stable patient".)

Another possible explanation for the different effect upon residual kidney function is that volume expansion with continuous peritoneal dialysis may help to preserve kidney function [22,23,25]. In one study that examined volume control versus the use of antihypertensive agents for control of hypertension in hemodialysis patients with a baseline urine production of approximately 1600 mL/day, urine output dropped by only 12 percent during treatment with antihypertensive medications, but, with the use of volume removal, urine output decreased to <200 mL/day in all patients [25]. Blood pressure control improved, and left ventricular mass decreased significantly with volume removal.

As mentioned above, newer hemodialytic techniques may result in a slower rate of decline of residual kidney function. In one study, the loss of residual kidney function was similar in a comparison of 175 patients receiving continuous ambulatory peritoneal dialysis (CAPD) versus 300 patients dialyzed with ultrapure water, bicarbonate buffer, and high-flux polysulphone membranes [24].

The loss of residual kidney function may be more rapid in hemodialysis versus peritoneal dialysis patients. However, most of the studies that have examined this issue are older, and the data are inconclusive (see "Dialysis modality and patient outcome", section on 'Selection of dialysis modality'). It is reasonable to mention to patients who are preparing for dialysis that residual kidney function is likely better preserved using peritoneal dialysis rather than hemodialysis. However, survival with either modality appears to be equivalent, and lifestyle preferences should remain the predominant factor when choosing dialysis modality. (See "Dialysis modality and patient outcome".)

Hemodialysis — There is suggestive evidence that the institution of maintenance hemodialysis alone may accelerate nephronal injury in the few nephrons that are still functioning at the onset of dialysis [26], resulting in a progressive fall in the residual GFR [9,19-22].

The characteristics of the hemodialysis procedure may affect the rate of loss of function:

Hemodialysis with biocompatible membranes may better preserve residual kidney function compared with bioincompatible membranes [27-29]. (See "Clinical consequences of hemodialysis membrane biocompatibility".)

Most of the studies in this area have suffered from methodologic flaws or small sample sizes. In a prospective, multicenter, randomized study of 159 incident hemodialysis patients who were assigned to dialysis with high-flux membranes or low-flux bioincompatible membranes, there was no statistical difference in the rate of change of kidney function, although the residual kidney function at the start of the study was quite low (approximately 1 mL/min in the bioincompatible membrane group and 0.7 mL/min in the control group) [30].

In a prospective, randomized study of 20 dialysis patients who were dialyzed with either cellulose or polysulfone membranes, there was better preservation of residual kidney function in the polysulfone group at one year [31].

The possible role of the hemodialysis dialysate was addressed in a study in which 30 patients initiating hemodialysis were randomly assigned to dialysis using either conventional or ultrapure dialysate [32]. Residual kidney function in the ultrapure group was significantly higher at 24 months (4.3 versus 2.5 mL/min). Markers of inflammation, such as C-reactive protein, were also significantly lower among these patients. (See "Ultrapure dialysis fluid".)

As mentioned above, the loss of residual kidney function was similar in a comparison of 175 patients receiving CAPD versus 300 patients dialyzed with ultrapure water, bicarbonate buffer, and high-flux polysulphone membranes [24].

More frequent hemodialysis may accelerate the loss of residual kidney function. One study evaluated residual kidney function in participants of the Frequent Hemodialysis Network (FHN) Daily and Nocturnal trials [33]. Patients assigned to frequent nocturnal dialysis (six times per week) had significantly lower urine volume and urea clearance at 4 and 12 months compared with conventional nocturnal dialysis (three times per week). There was no significant difference in loss of urine volume or residual kidney function in patients who did frequent versus conventional daily dialysis, although there was likely not enough statistical power to identify a difference.

In a retrospective review of patients who initiated dialysis in a large dialysis organization in the US, among 351 individuals who started hemodialysis with fewer than three treatments per week, both renal urea clearance and urine volume declined more slowly over time compared with a matched cohort of 8065 patients who dialyzed thrice weekly [34]. The median renal urea clearance and urine volume were 4.8 mL/min/1.73 m2 and 1150 mL in the less frequent dialysis group versus 3.04 mL/min/1.73 m2 and 800 mL in the conventional dialysis group. There was no difference in survival between the two groups. However, in a sub-analysis among patients who had a baseline renal urea clearance <3 mL/min/1.73 m2, those who started twice-weekly hemodialysis experienced higher mortality compared with the conventional hemodialysis.

Taken together, these findings suggest that the use of biocompatible membranes (which is already in place in most dialysis centers) and the use of ultrapure water may decrease the risk of loss of residual kidney function, though definitive data in this area is lacking. Avoiding hypotension during hemodialysis treatments appears beneficial in preserving residual kidney function. More frequent dialysis may have an adverse effect on residual function.

Peritoneal dialysis — Although earlier studies suggested that automated forms of peritoneal dialysis (APD) might be associated with a more rapid decline in residual kidney function, more recent studies have found minimal effect of peritoneal dialysis modality on the loss of residual kidney function.

One prospective, nonrandomized study evaluated residual kidney function after six months of dialysis among 18 patients treated with nightly intermittent peritoneal dialysis (NIPD), continuous cycler peritoneal dialysis (CCPD), or CAPD [35]. The average renal clearance prior to the initiation of dialysis among patients in each group was approximately 4 mL/min/1.73 m2. The loss of residual kidney function was significantly less among patients treated with CAPD (+0.01 mL/min per month) than among those treated with NIPD or CCPD (-0.29 and -0.34 mL/min per month, respectively).

A second prospective study assessed the loss of kidney function at six months and one year among 18 patients beginning treatment with CAPD and 18 starting intermittent dialysis (12 treated with CCPD and 6 with NIPD) [36]. The loss of function was significantly higher in the group undergoing intermittent dialysis compared with the continuous dialysis group: -0.28 versus -0.10 mL/min at six months and -0.26 versus -0.13 mL/min at one year, respectively.

In a single-center retrospective study of 70 CAPD and 114 APD patients, modality choice did not affect change in residual kidney function over time [37].

A Cochrane Database systematic review, published in 2007, showed no association between modality and loss of residual kidney function [38]. However, this study only analyzed two early trials.

In a prospective study of 647 dialysis patients (505 CAPD and 78 APD), APD was associated with a nearly twofold higher risk of losing residual kidney function during the first year, which persisted after adjusting for multiple variables. This study did not adjust for the multiple comparisons performed in the analysis [39].

In a retrospective study of 179 CAPD and 441 APD patients from the United States, with mean survival on therapy of 1407 days in CAPD patients and 1616 days in APD patients, there was no significant difference in residual kidney function decline over time [40].

One study [41] analyzed the effect of weight gain on residual kidney function among 148 peritoneal dialysis patients. In a multivariate model, patients with a weight increase greater than 2.3 kg had a 4.17 increased risk of loss of residual kidney function. Other variables in the model that predicted faster loss of kidney function included diabetes mellitus, proteinuria, elevated C-reactive protein, and elevated systolic blood pressure.

In another study of peritoneal dialysis patients (the balANZ trial), better preservation of residual kidney function was associated with male gender, higher baseline residual kidney function, higher systolic blood pressure, biocompatible fluids, lower peritoneal ultrafiltration, and lower dialysate glucose exposure [42].

Other risk factors for developing anuria among peritoneal dialysis patients include serum bicarbonate <24 mEq/L [43] and development of peritonitis [44].

In summary, studies are conflicting and show that different peritoneal dialysis modalities likely have limited effect on the decline in residual kidney function over time. Modality choice at this time should not be determined by risk of loss of residual kidney function according to a particular peritoneal dialysis modality. Although confirmatory studies are needed, preventing weight gain and normalizing the serum bicarbonate may preserve residual kidney function.

FACTORS THAT MAY AFFECT RESIDUAL KIDNEY FUNCTION

Intradialytic hypotension — It is important to avoid hypotension with or after dialysis. Hypotension during dialysis not only causes myocardial, cerebrovascular, and mesenteric ischemia but can also lead to decreased renal perfusion and loss of kidney function.

Hypotension may result from attempts to challenge the target weight (ie, reduce the target weight) in an effort to achieve euvolemia in patients who are just starting dialysis. Among patients who start dialysis with reasonable residual kidney function, attempts to aggressively remove fluid may result in low blood pressures that can cause progressive loss of kidney function, even in the absence of symptoms such as cramping or presyncope [45].

Diuretics — Unless urine output is negligible, diuretics should be continued in patients who initiate dialysis. Loop diuretics increase urine and sodium excretion (though do not affect residual kidney function) [46] and decrease the need for volume removal with dialysis [8]. In a study of 61 peritoneal dialysis patients randomly assigned to either furosemide (250 mg/day) or no furosemide, urine volume was significantly higher in the group receiving the diuretic at 6 and 12 months, although clearance of creatinine and urea had declined at a similar rate in both groups [46].

There are no evidence-based guidelines or safety data for chronic dosing of furosemide in hemodialysis or peritoneal dialysis patients. In one study, chronic daily administration of 250 to 2000 mg of furosemide resulted in sun-induced bullous dermatosis in 3 of 10 patients without evidence of ototoxicity [47]. While furosemide has been associated with deafness, there are no reported cases of deafness from furosemide in patients with end-stage kidney disease (ESKD) receiving furosemide. In the author's experience, doses of furosemide up to 120 mg orally each day with 5 mg metolazone are in general well tolerated. While these agents confer significant benefit in terms of increased urinary volume, the lack of clinical safety data, benefits, risks, and alternatives should be discussed with the patient. It is important that these agents be stopped when urine output becomes negligible and patients be monitored for hearing loss and skin changes.

Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers — The preservation of residual kidney function among those undergoing peritoneal dialysis may be enhanced by the administration of an angiotensin-converting enzyme (ACE) inhibitor or an angiotensin receptor blocker (ARB). In a 2014 Cochrane review of six non-blinded trials and 257 patients, the decline in eGFR was modestly smaller at 12 months among patients who were treated with an ACE inhibitor or an ARB [48]. Among hemodialysis patients, results from small trials of ACE inhibitors or ARBs compared with placebo for preservation of residual kidney function are conflicting [49,50].

In part, these findings led the 2006 Kidney Disease Outcomes Quality Initiative (KDOQI) work group for peritoneal dialysis adequacy to recommend the use of ACE inhibitors or ARBs to help preserve residual kidney function in those who require antihypertensive medications [51,52]. They suggest that such agents should also be considered for nephroprotection among normotensive peritoneal dialysis patients. However, at present, there is not enough evidence to recommend the use of these agents in normotensive patients, unless they have other specific indications for these medications (such as heart failure).

Peritoneal dialysis solutions — Some [53,54], but not all [55-58], studies have suggested that more biocompatible peritoneal dialysis solutions, specifically those with low glucose degradation products and a neutral pH, preserve residual kidney function. In a 2015 meta-analysis of six trials, patients who underwent peritoneal dialysis with these biocompatible solutions had a slower rate of decline of residual kidney function, a higher achieved Kt/V, and a higher urine volume compared with patients who were treated with conventional peritoneal dialysis solutions [59].

Icodextrin solution has also been compared with biocompatible peritoneal dialysis solutions. In one trial, there was no difference in residual kidney function between groups at one year [60]. However, patients using icodextrin had a slower decline in urine volume compared with patients using biocompatible solutions.

Aminoglycosides — Given that aminoglycosides are nephrotoxic, it is generally believed that aminoglycosides should be used with caution to preserve residual kidney function. (See "Manifestations of and risk factors for aminoglycoside nephrotoxicity" and "Pathogenesis and prevention of aminoglycoside nephrotoxicity and ototoxicity".)

However, a number of studies have found no effect of aminoglycoside use on the decline of residual kidney function. As an example, residual kidney function was determined at baseline and at follow-up in 70 peritoneal dialysis patients who received cefazolin and gentamicin for peritonitis, 61 individuals with peritonitis who received vancomycin and ciprofloxacin, and 74 control patients without peritonitis [61]. There was no significant difference in the rate of kidney function decline between groups. The lack of effect of aminoglycosides was also observed in a retrospective analysis of 1412 patients [62]. The change in residual kidney function over time was similar in 1075 patients who received empiric aminoglycosides for peritonitis as compared with 339 who did not.

Another study of 102 patients who received either cefazolin and netilmicin or cefazolin and ceftazidime showed no differences in residual kidney function between groups [63].

Thus, limited data suggest that the risk of loss of residual kidney function from short-term use of aminoglycosides for peritonitis is low.

Iodinated radiocontrast agents — Iodinated radiocontrast agents can cause acute tubular necrosis, possibly leading to the loss of residual kidney function. (See "Contrast-associated and contrast-induced acute kidney injury: Clinical features, diagnosis, and management".)

However, three studies that prospectively evaluated the effect of contrast on residual kidney function found no loss of function:

In one study, residual kidney function was evaluated at baseline and two weeks after contrast administration in 36 peritoneal dialysis patients [64]. Thirty-six control patients also underwent determination of residual kidney function two weeks apart. Studies were performed with adequate prehydration and minimal contrast usage (mean urinary volume 104 mL). No differences were found between baseline and follow-up residual kidney function and urine volume in those receiving contrast, and results were not statistically different from controls.

In a second study of 10 peritoneal dialysis patients who received nonionic hypo-osmolar contrast media, residual kidney function was measured on days 1 through 7, day 10, and day 30 [65]. There was a mild decline in mean renal clearance on day 6, but clearance subsequently increased back to baseline by day 30.

One study showed no difference in the rate of loss of residual kidney function at six months in 42 patients who were given approximately 100 mL of iodixanol contrast compared with 45 patients who did not receive contrast [66].

Despite these studies, it is prudent to avoid radiocontrast agents in dialysis patients, if possible. The primary alternative to iodinated radiocontrast media is imaging with gadolinium-based magnetic resonance imaging (MRI) or the use of noncontrast imaging studies. However, among patients with moderate to advanced kidney failure (dialysis-dependent or estimated GFR [eGFR] <30 mL/min), the administration of gadolinium has been associated with nephrogenic systemic fibrosis. In such patients, gadolinium-based imaging should be avoided. (See "Nephrogenic systemic fibrosis/nephrogenic fibrosing dermopathy in advanced kidney disease".)

N-acetylcysteine — The administration of N-acetylcysteine may help to preserve residual kidney function. This was suggested by a pilot study in which oral N-acetylcysteine was administered at a dose of 1200 mg twice daily for four weeks to 10 peritoneal dialysis patients [67]. There was a trend toward improvement from baseline in residual kidney function, with an increase in mean urea and creatinine clearance, urine volume, and residual renal Kt/V. These results are interesting, but the study is limited by the lack of a control group and small patient numbers.

Other factors — Other factors may affect residual kidney function. These include:

Cardiac disease [37]

Elevated baseline uric acid levels [68]

Repeated episodes of peritonitis [69,70], although this was not confirmed in all studies [61]

Peripheral vascular disease [70]

Larger body mass index (BMI) [71]

Diabetes [71]

Increasing age [72]

Higher baseline GFR [72]

Hypertension [72]

Proteinuria [72]

Initiation of dialysis after kidney transplant failure [73]

MANAGEMENT OF KIDNEY ALLOGRAFT FAILURE IN PATIENTS STARTING HEMODIALYSIS OR PERITONEAL DIALYSIS — The withdrawal of immunosuppression in patients with kidney transplant failure is a complex management issue since prolonged immunosuppression increases the risk of infection and sepsis posttransplant, but overly rapid withdrawal of immunosuppression can lead to symptomatic acute rejection and rapid worsening of kidney function. This issue is discussed elsewhere. (See "Kidney transplantation in adults: Management of the patient with a failed kidney transplant".)

SUMMARY AND RECOMMENDATIONS

The loss of residual kidney function in patients with end-stage kidney disease (ESKD) has important clinical manifestations. This includes adverse effects upon volume control and patient survival. Among both peritoneal dialysis and hemodialysis patients, continued residual kidney function is associated with improved survival. We therefore suggest the adoption of measures aimed at preserving residual kidney function among peritoneal dialysis patients (Grade 2B) and hemodialysis patients (Grade 2C). (See 'Survival' above and "Prescribing peritoneal dialysis" and "Prescribing and assessing adequate hemodialysis".)

Both volume expansion and the high urea load per nephron are rapidly reversed by dialysis of any form. Therefore, many patients have a marked reduction in, or even cessation of, urine output when dialysis is instituted. (See 'Effect of dialysis modalities' above.)

Measures to preserve residual kidney function include avoiding hypotension during and after dialysis, avoiding nephrotoxins as much as possible, and using angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs) in hypertensive patients.

We also maintain patients on diuretics to increase urine volume, although this does not affect residual kidney function. It is preferable to maintain euvolemia with diuretics rather than increased ultrafiltration. (See 'Factors that may affect residual kidney function' above.)

Residual kidney function may be better maintained in patients on peritoneal dialysis compared with hemodialysis. However, comparison studies may not account for modern techniques in hemodialysis (such as biocompatible membranes, ultrapure dialysate, and volumetric control) that may result in preservation of kidney function. (See 'Hemodialysis versus peritoneal dialysis' above.)

REFERENCES

  1. United States Renal Data System. 2017 USRDS annual data report: Atlas of chronic kidney disease and end-stage renal disease in the United States. National Institutes of Health; National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, MD 2017.
  2. Yeh BP, Tomko DJ, Stacy WK, et al. Factors influencing sodium and water excretion in uremic man. Kidney Int 1975; 7:103.
  3. Danovitch GM, Bourgoignie J, Bricker NS. Reversibility of the "salt-losing" tendency of chronic renal failure. N Engl J Med 1977; 296:14.
  4. Feinfeld DA, Danovitch GM. Factors affecting urine volume in chronic renal failure. Am J Kidney Dis 1987; 10:231.
  5. Tannen RL, Regal EM, Dunn MJ, Schrier RW. Vasopressin-resistant hyposthenuria in advanced chronic renal disease. N Engl J Med 1969; 280:1135.
  6. Bargman JM, Golper TA. The importance of residual renal function for patients on dialysis. Nephrol Dial Transplant 2005; 20:671.
  7. Wang AY, Lai KN. The importance of residual renal function in dialysis patients. Kidney Int 2006; 69:1726.
  8. Bragg-Gresham JL, Fissell RB, Mason NA, et al. Diuretic use, residual renal function, and mortality among hemodialysis patients in the Dialysis Outcomes and Practice Pattern Study (DOPPS). Am J Kidney Dis 2007; 49:426.
  9. Rottembourg J. Residual renal function and recovery of renal function in patients treated by CAPD. Kidney Int Suppl 1993; 40:S106.
  10. Toth-Manikowski SM, Sirich TL, Hostetter TH, et al. HEMO study results suggest that "clinically negligible" residual kidney function is a significant contributor to uremic solute clearance [Abstract]. J Am Soc Nephrol 2017; 28:FRPO894.
  11. Suda T, Hiroshige K, Ohta T, et al. The contribution of residual renal function to overall nutritional status in chronic haemodialysis patients. Nephrol Dial Transplant 2000; 15:396.
  12. Shemin D, Bostom AG, Laliberty P, Dworkin LD. Residual renal function and mortality risk in hemodialysis patients. Am J Kidney Dis 2001; 38:85.
  13. Termorshuizen F, Dekker FW, van Manen JG, et al. Relative contribution of residual renal function and different measures of adequacy to survival in hemodialysis patients: an analysis of the Netherlands Cooperative Study on the Adequacy of Dialysis (NECOSAD)-2. J Am Soc Nephrol 2004; 15:1061.
  14. Szeto CC, Wong TY, Chow KM, et al. Are peritoneal dialysis patients with and without residual renal function equivalent for survival study? Insight from a retrospective review of the cause of death. Nephrol Dial Transplant 2003; 18:977.
  15. Burton JO, Jefferies HJ, Selby NM, McIntyre CW. Hemodialysis-induced cardiac injury: determinants and associated outcomes. Clin J Am Soc Nephrol 2009; 4:914.
  16. Krediet RT, Zweers MM, van Westrhenen R, et al. What can we do to preserve the peritoneum? Perit Dial Int 2003; 23 Suppl 2:S14.
  17. Bargman JM, Thorpe KE, Churchill DN, CANUSA Peritoneal Dialysis Study Group. Relative contribution of residual renal function and peritoneal clearance to adequacy of dialysis: a reanalysis of the CANUSA study. J Am Soc Nephrol 2001; 12:2158.
  18. Lee MJ, Park JT, Park KS, et al. Prognostic Value of Residual Urine Volume, GFR by 24-hour Urine Collection, and eGFR in Patients Receiving Dialysis. Clin J Am Soc Nephrol 2017; 12:426.
  19. Lysaght MJ, Vonesh EF, Gotch F, et al. The influence of dialysis treatment modality on the decline of remaining renal function. ASAIO Trans 1991; 37:598.
  20. Moist LM, Port FK, Orzol SM, et al. Predictors of loss of residual renal function among new dialysis patients. J Am Soc Nephrol 2000; 11:556.
  21. Misra M, Vonesh E, Van Stone JC, et al. Effect of cause and time of dropout on the residual GFR: a comparative analysis of the decline of GFR on dialysis. Kidney Int 2001; 59:754.
  22. Jansen MA, Hart AA, Korevaar JC, et al. Predictors of the rate of decline of residual renal function in incident dialysis patients. Kidney Int 2002; 62:1046.
  23. Lameire N, Van Biesen W. The impact of residual renal function on the adequacy of peritoneal dialysis. Perit Dial Int 1997; 17 Suppl 2:S102.
  24. McKane W, Chandna SM, Tattersall JE, et al. Identical decline of residual renal function in high-flux biocompatible hemodialysis and CAPD. Kidney Int 2002; 61:256.
  25. Gunal AI, Kirciman E, Guler M, et al. Should the preservation of residual renal function cost volume overload and its consequence left ventricular hypertrophy in new hemodialysis patients? Ren Fail 2004; 26:405.
  26. Ogata K. Clinicopathological study of kidneys from patients on chronic dialysis. Kidney Int 1990; 37:1333.
  27. McCarthy JT, Jenson BM, Squillace DP, Williams AW. Improved preservation of residual renal function in chronic hemodialysis patients using polysulfone dialyzers. Am J Kidney Dis 1997; 29:576.
  28. Caramelo C, Alcázar R, Gallar P, et al. Choice of dialysis membrane does not influence the outcome of residual renal function in haemodialysis patients. Nephrol Dial Transplant 1994; 9:675.
  29. Lang SM, Bergner A, Töpfer M, Schiffl H. Preservation of residual renal function in dialysis patients: effects of dialysis-technique-related factors. Perit Dial Int 2001; 21:52.
  30. Hakim RM, Wingard RL, Husni L, et al. The effect of membrane biocompatibility on plasma beta 2-microglobulin levels in chronic hemodialysis patients. J Am Soc Nephrol 1996; 7:472.
  31. Hartmann J, Fricke H, Schiffl H. Biocompatible membranes preserve residual renal function in patients undergoing regular hemodialysis. Am J Kidney Dis 1997; 30:366.
  32. Schiffl H, Lang SM, Fischer R. Ultrapure dialysis fluid slows loss of residual renal function in new dialysis patients. Nephrol Dial Transplant 2002; 17:1814.
  33. Daugirdas JT, Greene T, Rocco MV, et al. Effect of frequent hemodialysis on residual kidney function. Kidney Int 2013; 83:949.
  34. Obi Y, Streja E, Rhee CM, et al. Incremental Hemodialysis, Residual Kidney Function, and Mortality Risk in Incident Dialysis Patients: A Cohort Study. Am J Kidney Dis 2016; 68:256.
  35. Hiroshige K, Yuu K, Soejima M, et al. Rapid decline of residual renal function in patients on automated peritoneal dialysis. Perit Dial Int 1996; 16:307.
  36. Hufnagel G, Michel C, Queffeulou G, et al. The influence of automated peritoneal dialysis on the decrease in residual renal function. Nephrol Dial Transplant 1999; 14:1224.
  37. Holley JL, Aslam N, Bernardini J, et al. The influence of demographic factors and modality on loss of residual renal function in incident peritoneal dialysis patients. Perit Dial Int 2001; 21:302.
  38. Rabindranath KS, Adams J, Ali TZ, et al. Continuous ambulatory peritoneal dialysis versus automated peritoneal dialysis for end-stage renal disease. Cochrane Database Syst Rev 2007; :CD006515.
  39. Michels WM, Verduijn M, Grootendorst DC, et al. Decline in residual renal function in automated compared with continuous ambulatory peritoneal dialysis. Clin J Am Soc Nephrol 2011; 6:537.
  40. Cnossen TT, Usvyat L, Kotanko P, et al. Comparison of outcomes on continuous ambulatory peritoneal dialysis versus automated peritoneal dialysis: results from a USA database. Perit Dial Int 2011; 31:679.
  41. Kim JK, Kim YS, Song YR, et al. Excessive Weight Gain during the First Year of Peritoneal Dialysis Is Associated with Inflammation, Diabetes Mellitus, and a Rapid Decrease in Residual Renal Function. PLoS One 2015; 10:e0139033.
  42. Htay H, Cho Y, Pascoe EM, et al. Predictors of Residual Renal Function Decline in Peritoneal Dialysis Patients: The balANZ Trial. Perit Dial Int 2017; 37:283.
  43. Chang TI, Kang EW, Kim HW, et al. Low Serum Bicarbonate Predicts Residual Renal Function Loss in Peritoneal Dialysis Patients. Medicine (Baltimore) 2015; 94:e1276.
  44. Szeto CC, Kwan BC, Chow KM, et al. Predictors of residual renal function decline in patients undergoing continuous ambulatory peritoneal dialysis. Perit Dial Int 2015; 35:180.
  45. Marants R, Grant C, Lee T, McIntyre CW. Renal perfusion falls during hemodialysis: An explanation for the loss of residual renal function in dialysis patients [Abstract]. J Am Soc Nephrol 2016; 27:327A.
  46. Medcalf JF, Harris KP, Walls J. Role of diuretics in the preservation of residual renal function in patients on continuous ambulatory peritoneal dialysis. Kidney Int 2001; 59:1128.
  47. van Olden RW, van Meyel JJ, Gerlag PG. Acute and long-term effects of therapy with high-dose furosemide in chronic hemodialysis patients. Am J Nephrol 1992; 12:351.
  48. Zhang L, Zeng X, Fu P, Wu HM. Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers for preserving residual kidney function in peritoneal dialysis patients. Cochrane Database Syst Rev 2014; :CD009120.
  49. Kjaergaard KD, Peters CD, Jespersen B, et al. Angiotensin blockade and progressive loss of kidney function in hemodialysis patients: a randomized controlled trial. Am J Kidney Dis 2014; 64:892.
  50. Xydakis D, Papadogiannakis A, Sfakianaki M, et al. Residual renal function in hemodialysis patients: the role of Angiotensin-converting enzyme inhibitor in its preservation. ISRN Nephrol 2013; 2013:184527.
  51. K/DOQI Clinical Practice Guidelines for Peritoneal Dialysis Adequacy. Am J Kidney Dis 2006; 47(Supp 4):S1.
  52. Hemodialysis Adequacy 2006 Work Group. Clinical practice guidelines for hemodialysis adequacy, update 2006. Am J Kidney Dis 2006; 48 Suppl 1:S2.
  53. Kim S, Oh J, Kim S, et al. Benefits of biocompatible PD fluid for preservation of residual renal function in incident CAPD patients: a 1-year study. Nephrol Dial Transplant 2009; 24:2899.
  54. Kim S, Oh KH, Oh J, et al. Biocompatible peritoneal dialysis solution preserves residual renal function. Am J Nephrol 2012; 36:305.
  55. Ha IS, Yap HK, Munarriz RL, et al. Risk factors for loss of residual renal function in children treated with chronic peritoneal dialysis. Kidney Int 2015; 88:605.
  56. Fan SL, Pile T, Punzalan S, et al. Randomized controlled study of biocompatible peritoneal dialysis solutions: effect on residual renal function. Kidney Int 2008; 73:200.
  57. Szeto CC, Chow KM, Lam CW, et al. Clinical biocompatibility of a neutral peritoneal dialysis solution with minimal glucose-degradation products--a 1-year randomized control trial. Nephrol Dial Transplant 2007; 22:552.
  58. Johnson DW, Brown FG, Clarke M, et al. Effects of biocompatible versus standard fluid on peritoneal dialysis outcomes. J Am Soc Nephrol 2012; 23:1097.
  59. Wang J, Zhu N, Yuan W. Effect of neutral pH and low-glucose degradation product-containing peritoneal dialysis solution on residual renal function in peritoneal dialysis patients: a meta-analysis. Nephron 2015; 129:155.
  60. Chang TI, Ryu DR, Yoo TH, et al. Effect of Icodextrin Solution on the Preservation of Residual Renal Function in Peritoneal Dialysis Patients: A Randomized Controlled Study. Medicine (Baltimore) 2016; 95:e2991.
  61. Baker RJ, Senior H, Clemenger M, Brown EA. Empirical aminoglycosides for peritonitis do not affect residual renal function. Am J Kidney Dis 2003; 41:670.
  62. Badve SV, Hawley CM, McDonald SP, et al. Use of aminoglycosides for peritoneal dialysis-associated peritonitis does not affect residual renal function. Nephrol Dial Transplant 2012; 27:381.
  63. Lui SL, Cheng SW, Ng F, et al. Cefazolin plus netilmicin versus cefazolin plus ceftazidime for treating CAPD peritonitis: effect on residual renal function. Kidney Int 2005; 68:2375.
  64. Moranne O, Willoteaux S, Pagniez D, et al. Effect of iodinated contrast agents on residual renal function in PD patients. Nephrol Dial Transplant 2006; 21:1040.
  65. Dittrich E, Puttinger H, Schillinger M, et al. Effect of radio contrast media on residual renal function in peritoneal dialysis patients--a prospective study. Nephrol Dial Transplant 2006; 21:1334.
  66. Janousek R, Krajina A, Peregrin JH, et al. Effect of intravascular iodinated contrast media on natural course of end-stage renal disease progression in hemodialysis patients: a prospective study. Cardiovasc Intervent Radiol 2010; 33:61.
  67. Feldman L, Shani M, Efrati S, et al. N-acetylcysteine improves residual renal function in peritoneal dialysis patients: a pilot study. Perit Dial Int 2011; 31:545.
  68. Park JT, Kim DK, Chang TI, et al. Uric acid is associated with the rate of residual renal function decline in peritoneal dialysis patients. Nephrol Dial Transplant 2009; 24:3520.
  69. Shin SK, Noh H, Kang SW, et al. Risk factors influencing the decline of residual renal function in continuous ambulatory peritoneal dialysis patients. Perit Dial Int 1999; 19:138.
  70. Tian SL, Tian XK, Han QF, et al. Presence of peripheral arterial disease predicts loss of residual renal function in incident CAPD patients. Perit Dial Int 2012; 32:67.
  71. Singhal MK, Bhaskaran S, Vidgen E, et al. Rate of decline of residual renal function in patients on continuous peritoneal dialysis and factors affecting it. Perit Dial Int 2000; 20:429.
  72. Perl J, Bargman JM. The importance of residual kidney function for patients on dialysis: a critical review. Am J Kidney Dis 2009; 53:1068.
  73. Madar H, Korzets A, Ori Y, et al. Residual renal function in peritoneal dialysis after renal transplant failure. Perit Dial Int 2010; 30:470.
Topic 1941 Version 24.0

References

1 : United States Renal Data System. 2017 USRDS annual data report: Atlas of chronic kidney disease and end-stage renal disease in the United States. National Institutes of Health; National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, MD 2017.

2 : Factors influencing sodium and water excretion in uremic man.

3 : Reversibility of the "salt-losing" tendency of chronic renal failure.

4 : Factors affecting urine volume in chronic renal failure.

5 : Vasopressin-resistant hyposthenuria in advanced chronic renal disease.

6 : The importance of residual renal function for patients on dialysis.

7 : The importance of residual renal function in dialysis patients.

8 : Diuretic use, residual renal function, and mortality among hemodialysis patients in the Dialysis Outcomes and Practice Pattern Study (DOPPS).

9 : Residual renal function and recovery of renal function in patients treated by CAPD.

10 : HEMO study results suggest that "clinically negligible" residual kidney function is a significant contributor to uremic solute clearance [Abstract]

11 : The contribution of residual renal function to overall nutritional status in chronic haemodialysis patients.

12 : Residual renal function and mortality risk in hemodialysis patients.

13 : Relative contribution of residual renal function and different measures of adequacy to survival in hemodialysis patients: an analysis of the Netherlands Cooperative Study on the Adequacy of Dialysis (NECOSAD)-2.

14 : Are peritoneal dialysis patients with and without residual renal function equivalent for survival study? Insight from a retrospective review of the cause of death.

15 : Hemodialysis-induced cardiac injury: determinants and associated outcomes.

16 : What can we do to preserve the peritoneum?

17 : Relative contribution of residual renal function and peritoneal clearance to adequacy of dialysis: a reanalysis of the CANUSA study.

18 : Prognostic Value of Residual Urine Volume, GFR by 24-hour Urine Collection, and eGFR in Patients Receiving Dialysis.

19 : The influence of dialysis treatment modality on the decline of remaining renal function.

20 : Predictors of loss of residual renal function among new dialysis patients.

21 : Effect of cause and time of dropout on the residual GFR: a comparative analysis of the decline of GFR on dialysis.

22 : Predictors of the rate of decline of residual renal function in incident dialysis patients.

23 : The impact of residual renal function on the adequacy of peritoneal dialysis.

24 : Identical decline of residual renal function in high-flux biocompatible hemodialysis and CAPD.

25 : Should the preservation of residual renal function cost volume overload and its consequence left ventricular hypertrophy in new hemodialysis patients?

26 : Clinicopathological study of kidneys from patients on chronic dialysis.

27 : Improved preservation of residual renal function in chronic hemodialysis patients using polysulfone dialyzers.

28 : Choice of dialysis membrane does not influence the outcome of residual renal function in haemodialysis patients.

29 : Preservation of residual renal function in dialysis patients: effects of dialysis-technique-related factors.

30 : The effect of membrane biocompatibility on plasma beta 2-microglobulin levels in chronic hemodialysis patients.

31 : Biocompatible membranes preserve residual renal function in patients undergoing regular hemodialysis.

32 : Ultrapure dialysis fluid slows loss of residual renal function in new dialysis patients.

33 : Effect of frequent hemodialysis on residual kidney function.

34 : Incremental Hemodialysis, Residual Kidney Function, and Mortality Risk in Incident Dialysis Patients: A Cohort Study.

35 : Rapid decline of residual renal function in patients on automated peritoneal dialysis.

36 : The influence of automated peritoneal dialysis on the decrease in residual renal function.

37 : The influence of demographic factors and modality on loss of residual renal function in incident peritoneal dialysis patients.

38 : Continuous ambulatory peritoneal dialysis versus automated peritoneal dialysis for end-stage renal disease.

39 : Decline in residual renal function in automated compared with continuous ambulatory peritoneal dialysis.

40 : Comparison of outcomes on continuous ambulatory peritoneal dialysis versus automated peritoneal dialysis: results from a USA database.

41 : Excessive Weight Gain during the First Year of Peritoneal Dialysis Is Associated with Inflammation, Diabetes Mellitus, and a Rapid Decrease in Residual Renal Function.

42 : Predictors of Residual Renal Function Decline in Peritoneal Dialysis Patients: The balANZ Trial.

43 : Low Serum Bicarbonate Predicts Residual Renal Function Loss in Peritoneal Dialysis Patients.

44 : Predictors of residual renal function decline in patients undergoing continuous ambulatory peritoneal dialysis.

45 : Renal perfusion falls during hemodialysis: An explanation for the loss of residual renal function in dialysis patients [Abstract]

46 : Role of diuretics in the preservation of residual renal function in patients on continuous ambulatory peritoneal dialysis.

47 : Acute and long-term effects of therapy with high-dose furosemide in chronic hemodialysis patients.

48 : Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers for preserving residual kidney function in peritoneal dialysis patients.

49 : Angiotensin blockade and progressive loss of kidney function in hemodialysis patients: a randomized controlled trial.

50 : Residual renal function in hemodialysis patients: the role of Angiotensin-converting enzyme inhibitor in its preservation.

51 : K/DOQI Clinical Practice Guidelines for Peritoneal Dialysis Adequacy

52 : Clinical practice guidelines for hemodialysis adequacy, update 2006.

53 : Benefits of biocompatible PD fluid for preservation of residual renal function in incident CAPD patients: a 1-year study.

54 : Biocompatible peritoneal dialysis solution preserves residual renal function.

55 : Risk factors for loss of residual renal function in children treated with chronic peritoneal dialysis.

56 : Randomized controlled study of biocompatible peritoneal dialysis solutions: effect on residual renal function.

57 : Clinical biocompatibility of a neutral peritoneal dialysis solution with minimal glucose-degradation products--a 1-year randomized control trial.

58 : Effects of biocompatible versus standard fluid on peritoneal dialysis outcomes.

59 : Effect of neutral pH and low-glucose degradation product-containing peritoneal dialysis solution on residual renal function in peritoneal dialysis patients: a meta-analysis.

60 : Effect of Icodextrin Solution on the Preservation of Residual Renal Function in Peritoneal Dialysis Patients: A Randomized Controlled Study.

61 : Empirical aminoglycosides for peritonitis do not affect residual renal function.

62 : Use of aminoglycosides for peritoneal dialysis-associated peritonitis does not affect residual renal function.

63 : Cefazolin plus netilmicin versus cefazolin plus ceftazidime for treating CAPD peritonitis: effect on residual renal function.

64 : Effect of iodinated contrast agents on residual renal function in PD patients.

65 : Effect of radio contrast media on residual renal function in peritoneal dialysis patients--a prospective study.

66 : Effect of intravascular iodinated contrast media on natural course of end-stage renal disease progression in hemodialysis patients: a prospective study.

67 : N-acetylcysteine improves residual renal function in peritoneal dialysis patients: a pilot study.

68 : Uric acid is associated with the rate of residual renal function decline in peritoneal dialysis patients.

69 : Risk factors influencing the decline of residual renal function in continuous ambulatory peritoneal dialysis patients.

70 : Presence of peripheral arterial disease predicts loss of residual renal function in incident CAPD patients.

71 : Rate of decline of residual renal function in patients on continuous peritoneal dialysis and factors affecting it.

72 : The importance of residual kidney function for patients on dialysis: a critical review.

73 : Residual renal function in peritoneal dialysis after renal transplant failure.