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Effectiveness of furosemide in patients on peritoneal dialysis.

Abstract

Background

Residual renal function (RRF) is a marker for a good index of health and is associated with improved survival for individuals with end stage renal disease on peritoneal dialysis. As RRF declines with time on dialysis, fluid balance is more difficult to achieve. Urine output plays a vital role in fluid removal and it has been postulated that loop diuretics improve diuresis in peritoneal dialysis (PD) patients. The aim of this study is to evaluate our use of furosemide and its effect on diuresis in a home peritoneal dialysis program.

Methods

Sixty-one patients met inclusion criteria of having been on PD continuously for one year from their start date with complete 24-hour urine kinetics. Twenty patients were on furosemide and 41 patients were in the control group. Data for urine volume (UV), serum creatinine (SCr), total and residual creatinine clearance (Cr[Cl.sub.total] and Cr[Cl.sub.residual]), total and residual urea clearance (Kt/[V.sub.total] and Kt/[V.sub.residual]), and dry body weight were collected at baseline, six months and one year. The average change in UV, Cr[Cl.sub.total], and Kt/[V.sub.total] from baseline at six and 12 months and the proportion of patients who developed anuria at one year were determined.

Results

UV declined in the furosemide and control groups at six months by an average of 78.00 [+ or -] 445.2 mL/day and 105.5 [+ or -] 401.8 mL/day (p=0.8) and at 12 months by 85.00 [+ or -] 481.7 mL/day and 110.7 [+ or -] 455.4 mL/day (p=0.8), respectively. CrCl declined in the furosemide and control groups at six months by an average of 5.55 [+ or -] 20.4 mL/min and 4.52 [+ or -] 29.0 mL (p=0.9), and at 12 months by 3.95 [+ or -] 35.5 mL/min and 9.05 [+ or -] 28.4 mL/min (p=0.5) respectively. Kt/V increased by 0.0850 [+ or -] 0.890 in the furosemide group and declined by 0.0456 [+ or -] 0.614 in the control group at six months (p=0.5), but after 12 months, Kt/V declined in both the furosemide and control groups by 0.00400 [+ or -] 0.565 and 0.162 [+ or -] 0.558 (p=0.5) respectively. Only one patient (five per cent) in the furosemide group developed anuria after one year on PD, whereas nine patients (22%) in the control group became anuric (p = 0.1).

Conclusion

Furosemide did not have a statistically significant effect in either improving UV or preserving RRF in patients on PD for one year, but this study was not adequately powered to show an association. Although not statistically significant, fewer patients were anuric at one year in the furosemide group (five per cent versus 22%). Furosemide was not shown to be detrimental to either RRF or UV.

Key words: furosemide, residual renal function, peritoneal dialysis,

urine volume

Background

Residual renal function (RRF) is a good indicator of health for patients with end stage renal disease (ESRD). Although RRF progressively declines with time for both PD and hemodialysis (HD) patients, patients on PD have a 65% lower risk of RRF loss than those on HD (Moist et al., 2000). Presence of RRF has been strongly correlated with survival, but peritoneal clearance has not. Analysis of the CANUSA study showed that every 0.5 mL/min/1.73 [m.sup.2] increase in glomerular filtration rate (GFR) was associated with a 9% lower risk of death (RR=0.91) (Bargman, Thorpe, & Churchill, 2001). In another prospective cohort study, the NECOSAD Study Group examined the relative contribution of RRF and peritoneal clearance to patient survival (Termorshuizen et al., 2003). They determined that for each mL/min/1.73 [m.sup.2] increase in GFR, patients had a 12% reduction in mortality (RR=0.88, p=0.039).

In addition to mortality benefits, RRF has been shown to improve dialysis requirements, fluid balance, nutritional status, middle molecule clearance and quality of life (QoL) (Canada-USA [CANUSA] Peritoneal Dialysis Study Group, 1996). Patients with RRF require less dialysis per day, reducing their exposure to hyperosmolar glucose dialysate. Glucose degradation products (GDP) found in peritoneal dialysate are thought to be toxic to the peritoneal membrane, limiting the time a patient may remain on PD (Witowski et al., 2003). More frequent exchanges with higher concentrations of glucose dialysate also result in weight gain, hyperlipidemia, induction of diabetes in non-diabetic patients, and increased insulin and oral hypoglycemic requirements in diabetic patients (Bargman, Thorpe, & Churchill, 2001).

Residual renal function aids in fluid balance. Fluid balance is an important predictor of survival and QoL in patients with ESRD (CANUSA Peritoneal Dialysis Study Group, 1996). With more urine output, patients are able to have a more liberal fluid intake. This is important as persistent fluid overload contributes to left ventricular hypertrophy (LVH) and hypertension. Cardiovascular disease is the leading cause of death in patients with ESRD and, since 60% of patients have LVH at dialysis initiation, fluid balance is extremely important (Ozkahya et al., 2002). Studies have confirmed that as RRF declines nutritional status also declines, therefore, having some RRF also improves dietary parameters in PD patients (CANUSA Peritoneal Dialysis Study Group, 1996).

RRF is also important in maintaining endocrine functions of the kidney such as erythropoietin production and calcium, phosphorous, and vitamin D homeostasis (Bargman, Thorpe, & Churchill, 2001). Peritoneal dialysis (PD) patients benefit significantly from having RRF for removal of middle molecules that are not adequately removed by peritoneal clearance alone (CANUSA Peritoneal Dialysis Study Group, 1996).

Any intervention that slows the decline of RRF in patients on PD would be expected to be beneficial. Significant predictors that are associated with loss of RRF include: female gender, non-white race, history of diabetes, history of congestive heart failure (CHF), and lower baseline GFR (Moist et al., 2000). Strategies to preserve RRF should be employed in all patients. These include angiotensin-converting enzyme inhibitors (ACEIs) (Li, Chow, Wong, Leung, & Szeto, 2003), angiotensin receptor blockers (ARBs) (Suzuki, Kanno, Sugahara, Okada, & Nakamoto, 2004), calcium channel blockers, and avoiding nephrotoxic agents such as non-steroidal anti-inflammatory drugs (NSAIDs) and aminoglycosides (Moist et al., 2000).

The role of diuretics in preserving RRF is unclear. Previous short-term studies have shown that furosemide was effective in producing diuresis even in patients with a low GFR. In one small study comparing 16 patients (10 HD, six PD) with matched controls, Bandiani, Camaiora, Nicolini and Perotta (1985) concluded that muzolimine (a loop diuretic similar to furosemide) at 90 mg orally per day for one year preserved RRF. A second prospective, randomized, open-label study of 60 new PD patients found that CrCl declined at a constant rate in both groups and was unaffected by administration of furosemide 250 mg orally daily as compared to placebo.

[FIGURE 1 OMITTED]

Diuretics may be effective in preserving urine output. Maintaining diuresis reduces dialysis requirements and exposure to hyperosmolar glucose dialysate, which can help to prevent glucose toxicity. Both Bandiani, Camaiora, Nicolini and Perotta (1985) and Medcalf, Harris and Walls (2001) noted a greater diuresis in the diuretic group again, which potentially supports the role for diuretics in these patients.

The aim of this study was to evaluate the use and efficacy of furosemide in maintaining diuresis in our PD population. Since the evidence to date for diuretics in the preservation of RRF is not robust, it was also of interest to look at the effect of furosemide on RRF. Prescribing practices differ within our institution, making it possible to compare patients who received furosemide and patients who did not.

Methods

Patients

This retrospective chart review was approved by the University of Western Ontario's Health Sciences Research Ethics Board over a one-year period. The chief investigator screened 107 charts of patients starting on PD at our institution between June 2000 and April 2003. Our peritoneal dialysis program operates out of an academic tertiary care hospital and cares for approximately 120 patients from a large geographic region. Sixty-one patients met our inclusion criteria of having been on PD uninterrupted for at least one year from their start date on PD. Patients were excluded if they were not on PD continuously for one year (i.e., patients who were transplanted, changed to HD, or died during the one-year period), if they did not have urea kinetics completed, or if they started on PD before urea kinetics were routinely done. The majority of patients received automated PD (APD) as outpatients.

Study design

A list of all new start PD patients was screened by the chief investigator for inclusion in the study (see Figure One). Patient demographics including age, sex, cause of ESRD, date PD was initiated, history of diabetes and/or CHF, ACEI or ARB use, use of nephrotoxic drugs such as aminoglycosides or NSAIDs, and dose of furosemide used were collected at baseline. Urea kinetics were performed using patients' 24-hour urine collections. Dietary assistants performed the calculations required to obtain residual (renal) and total (peritoneal and renal) clearance in order to determine if a patient's current PD prescription was adequate. We collected data for urine volume (UV), creatinine clearance (Cr[Cl.sub.total] and Cr[Cl.sub.residual]), Kt/[V.sub.total], Kt/[V.sub.residual], and dry body weight at baseline (defined as the month PD initiated), six months, and one year. From these data, the average change ([+ or -]SD) in UV, Cr[Cl.sub.total], and Kt/[V.sub.total] from baseline at six and 12 months in each were determined. Of the 61 patients who met the inclusion criteria, 20 patients were prescribed furosemide for the one year of follow-up and formed the "furosemide group", while the remaining 41 patients were never prescribed furosemide for the one year of follow-up and formed the "control group".

Statistics

Our sample size was limited, as urea kinetics had only been routinely performed at our institution since June 2000. The primary outcome measure was change in UV at six months and one year. Secondary outcomes included change in CrCl, and Kt/V at six months and one year, and the number of patients who developed anuria at one year. Continuous data are expressed as mean ([+ or -] standard deviation). Outcome measures UV, CrCl and Kt/V were analyzed using unpaired t-tests, and anuria at one year was analyzed using a Fisher's exact test. Statistical significance was defined as p<0.05.

Results

Baseline characteristics are shown in Table One. The mean age at the start of PD was slightly higher in the control group and mean weight was greater in the furosemide group (not statistically significant). There were more men in the furosemide group, but an even distribution of both sexes in the control group. The most common causes of ESRD in both groups were diabetic nephropathy, glomerulonephritis, and nephrosclerosis. There were significantly more diabetics in the furosemide group (55% versus 37%), and ACEI/ARB use was not statistically significantly different between groups. The average daily dose of furosemide was 171.5 mg (range 40 to 250 mg) daily.

The mean UV at baseline in the furosemide group was almost double that of the control group (806.5 [+ or -] 494.8 mL/day versus 426.1 [+ or -] 479.2 mL/day). Change in UV from baseline at six months and one year is shown in Table Two. After six months on PD, UV declined by an average of 78.00 [+ or -] 445.2 mL/day and 105.5 [+ or -] 401.8 mL/day in the furosemide and control groups respectively (p=0.8). After one year on PD, UV declined by an average of 85.00 [+ or -] 481.7 mL/day in the furosemide group as compared to 110.7 [+ or -] 455.4 mL/day in the control group, but these findings did not reach statistical significance (p=0.8).

Mean CrCl (renal + peritoneal) was 84.1 [+ or -] 31.3 mL/min in the furosemide group and 73.2 [+ or -] 29.5 mL/min in the control group. Change in CrCl from baseline at six months and one year is shown in Table Two. After six months on PD, CrCl declined by an average of 5.6 [+ or -] 20.4 mL/min in the furosemide group and 4.5 [+ or -] 29.0 mL/min in the control group (p=0.9). After one year on PD, CrCl declined by an average of 4.0 [+ or -] 35.5 mL/min in the furosemide group whereas, in the control group it declined by 9.1 [+ or -] 28.4 mL/min (p=0.5).

Mean Kt/V was comparable at baseline in the two groups, 2.2 [+ or -] 0.57 in the furosemide group and 2.3 [+ or -] 0.56 in the control group. Adequate PD in our institution was defined as Kt/V > 1.7. Change in Kt/V from baseline at six months and one year is also shown in Table Two. After six months on PD, Kt/V increased by an average of 0.085 [+ or -] 0.89 in the furosemide group and declined by an average of 0.046 [+ or -] 0.61 in the control group (p=0.5). After one year on PD, Kt/V declined by an average of 0.0040 [+ or -] 0.57 in the furosemide group, and by 0.16 [+ or -] 0.56 in the control group (p=0.5).

Only one patient (five per cent) in the furosemide group developed anuria after one year on PD, whereas nine patients (22%) in the control group became anuric (p=0.1) (see Figure Two).

Since diabetes has been associated with increased risk of RRF loss, we wanted to look at the effect of furosemide in this sub-group of patients. There were 11 (55%) patients with diabetes in the furosemide group and 15 (37%) in the control group. The mean UV at baseline in patients with diabetes was 705.9 [+ or -] 509.7 mL/day in the furosemide group and 451.3 [+ or -] 444.7 mL/day in the control group. After six months on PD, UV declined by an average of 219.1 [+ or -] 495.9 mL/day in the furosemide group and 212.7 [+ or -] 414.5 mL/day in the control group (p=1.0). After one year on PD, UV declined by 218.2 + 497.7 mL/day from baseline in the furosemide group, and in the control group by 230.7 [+ or -] 490.3 mL/day (p=0.9). The mean CrCl in patients with diabetes at baseline was 83.2 [+ or -] 37.5 and 74.2 [+ or -] 34.0 mL/min in the furosemide and control groups respectively. After six months on PD, CrCl declined by an average of 4.8 [+ or -] 25.0 mL/min in the furosemide group and 1.4 [+ or -] 42.0 mL/min in the control group (p=0.7). After one year on PD, CrCl declined by an average of 14.1 [+ or -] 25.5 mL/min in the furosemide group and 10.1 [+ or -] 36.6 mL/min in the control group (p=0.5).

[FIGURE 2 OMITTED]

ACEIs and ARBs have been shown to preserve RRF in patients on PD, so it was of interest to see if there was an effect on UV and/or CrCl in patients on ACEIs and ARBs with and without a diuretic. There were 13 patients (65%) on such therapy in the furosemide group and 22 (54%) in the control group. The mean UV at baseline in this sub-group was 915.0 [+ or -] 536.7 mL/day in the furosemide group and 433.7 [+ or -] 491.2 mL/day in the control group. After six months on PD, UV declined by an average of 198.1 [+ or -] 457.3 mL/day in the furosemide group and 166.0 [+ or -] 369.6 mL/day in the control group (p=0.8). After one year on PD, UV declined by 131.2 [+ or -] 569.8 mL/day from baseline in the furosemide group, and 28.7 [+ or -] 484.1 mL/day in the control group (p=0.5). The mean CrCl in patients on an ACEI or ARB at baseline was 85.41 [+ or -] 32.54 and 74.24 [+ or -] 30.25 mL/min in the furosemide and control groups respectively. After six months on PD, CrCl declined by an average of 5.6 [+ or -] 23.1 mL/min in the furosemide group and 0.54 [+ or -] 30.5 mL/min in the control group (p=0.5). After one year on PD, CrCl declined by an average of 5.5 [+ or -] 44.2 mL/min from baseline in the furosemide group, and in the control group it declined by 3.8 [+ or -] 27.0 mL/min (p=0.9).

Discussion

In our study, there was no statistically significant difference detected in the decline of CrCl or Kt/V between patients who received diuretics and those who did not. Patients treated with furosemide had a similar decline in UV compared to the control group, 78.0 and 105.5 mL at six months, and 85.0 and 110.7 mL at one year, respectively. Only one patient (five per cent) in the furosemide group became anuric following one year of PD, whereas nine patients (22%) in the control group lost urine output. While not statistically significant, this difference may be clinically important.

The only other large study (n=61) found no statistically significant difference in CrCl between the control and diuretic group, but did show a statistically significant decline in UV at 12 months in the control group (733 [+ or -] 124 mL/24 hours versus 1070 [+ or -] 193 mL/24 hours) (Medcalf, Harris & Walls, 2001).

There are a few possibilities as to why our study did not show statistical significance: the study was underpowered, the dose of furosemide was too low to increase diuresis in these patients, or there simply was no association between furosemide and improving UV. It is suspected that our study was indeed underpowered to show a significant change between the two groups and that the doses of furosemide used were too low.

There were other limitations to our study. First, the study was retrospective in nature and performed at a single centre. Second, the sample size was small, making it underpowered to detect statistically significant changes in UV or CrCl. Our sample size was limited, as urea kinetics have only been routinely performed at our institution since June 2000. Many patients were also excluded when they were temporarily switched to HD due to illness. Third, some patients' 24-hour urine collections for urea kinetic modelling were inaccurate. During data collection, it was noted that a few 24-hour collections were incomplete, which may have resulted in erroneous urea kinetics and inaccurate urine collection volumes. Fourth, patients in both groups had high baseline CrCl values possibly making it more difficult to detect a difference between the two groups. Fifth, two patients in the control group were on low-dose metolazone (a diuretic) possibly influencing the results. As well, the majority of patients were on a sub-therapeutic dose of furosemide (mean 171.5 mg daily [dose range 40 to 250 mg]). Approximately 85% of patients were on less than 250 mg of furosemide daily. Most diuretics have no effect if urine output is less than 100 mL/day with the exception of furosemide and metolazone that can be used with the low GFR of patients with ESRD (Wilcox, 2002). Doses of furosemide studied in dialysis patients are between 250 to 2000 mg (Bandiani, Camaiora, Nicolini & Perotta, 1985; Medcalf, Harris & Walls, 2001; van Olden, Guchelaar, Struijk, Krediet & Arisz, 2003). It is expected that if patients had been given adequate doses of furosemide, a larger effect on UV may have been detected.

This study also gave us an opportunity to observe other parameters in our PD patient population. Body weight increased in both groups at one year from baseline by an average of 3.4 kg in the furosemide group and 1.2 kg in the control group. It should be noted, however, that there was a significantly higher proportion of patients with diabetes in the furosemide group (55% versus 37%), and this weight gain is most likely actual weight gain and not excess body water. Both ACEIs and ARBs have been associated with preserving RRF in PD patients and should be used in all patients where possible. Only 57% of patients in this study were taking an ACEI or ARB. Cardiovascular disease is the leading cause of death in this population, yet only 41% were taking daily ASA for primary or secondary cardioprotection. Almost all ESRD patients would benefit from ASA use. The literature reports of a higher incidence of LVH in this patient population than that found in this study. Only 29% of patients in our study had documented congestive heart failure (CHF). The incidence is likely under-reported since echocardiograms are not done routinely on all new PD patients and, if they are, results are not always transcribed into dialysis charts.

Although we were not able to obtain information regarding adverse effects due to furosemide, it was expected that the incidence would be low. The most serious adverse effect of furosemide is ototoxicity, but is extremely rare. Doses of up to 2000 mg daily have been used safely in patients on PD with no reports of ototoxicity. Other, less serious adverse effects of furosemide include hypokalemia, hypomagnesemia, photosensitivity, and the precipitation of gouty attacks.

Conclusion

Furosemide did not have a statistically significant effect in improving UV or preserving RRF in patients on PD for one year. Fewer patients were anuric at one year in the furosemide group than in the control group (5% versus 22% respectively). A prospective, randomized controlled trial is needed to determine whether trends identified in this study are statistically significant. Important factors to control for when designing such a study would include the accuracy of 24-hour urine collection, the dose of furosemide used, and adherence to therapy.

Acknowledgements

The authors would like to thank Ms. Helen Zok, unit clerk on SS4W, for compiling the lists of PD patients for chart review. We would also like to thank Ms. Laura Fairbairn, RD, for sharing her expertise in urea kinetic modelling.

References

Bandiani, G., Camaiora, E., Nicolini, M.A., & Perotta, U. (1985). Muzolimine in patients on chronic hemodialysis (HD) and continuous ambulatory peritoneal dialysis (CAPD). Zeitschrift fur Kardiologie, 74, 84-87.

Bargman, J.M., Thorpe, K.E., & Churchill, D.N. (2001). Relative contribution of residual renal function and peritoneal clearance to adequacy of dialysis: A re-analysis of the CANUSA study. Journal of the American Society of Nephrology, 12, 2158-2162.

Canada-USA (CANUSA) Peritoneal Dialysis Study Group. (1996). Adequacy of dialysis and nutrition in continuous peritoneal dialysis associated with clinical outcomes. Journal of the American Society of Nephrology, 7, 198-207.

Li, P.K.T., Chow, K.M., Wong, T.Y.H., Leung, C.B., & Szeto, C.C. (2003). Effects of an angiotensin-converting enzyme on residual renal function in patients receiving peritoneal dialysis. Annals of Internal Medicine, 139, 105-112.

Medcalf, J.F., Harris, K.P, & Walls, J. (2001). Role of diuretics in the preservation of residual renal function in patients on continuous peritoneal dialysis. Kidney International, 59, 1128-1133.

Moist, L.M., Port, F.K., Orzol, S.M., Young, E.W., Ostbye, T., Wolfe, R.A., Hulbert-Shearon, T., Jones, C.A., & Bloembergen, W.E. (2000). Predictors of loss of renal function among new dialysis patients. Journal of the American Society Nephrology, 11, 556-564.

Ozkahya, M., Toz, H., Qzerkan, F., Duman, S., Ok, E., Basci, A., & Mees, E.J. (2002). Impact of volume control on left ventricular hypertrophy in dialysis patients. Journal of Nephrology, 15(6), 655-660.

Suzuki, H., Kanno, Y., Sugahara, S., Okada, H., & Nakamoto, H. (2004). Effects of an angiotensin II receptor blocker, valsartan, on residual renal function in patients on CAPD. American Journal of Kidney Diseases, 43, 1056-1064.

Termorshuizen, F., Korevaar, J.C., Dekker, F.W., van Manen, J.G., Boeschoten, E.W., & Krediet, R.T. (2003). The relative importance of residual renal function compared with peritoneal clearance for patient survival and quality of life: Analysis of the Netherland Cooperative Study on the Adequacy of Dialysis (NECOSAD)-2. American Journal of Kidney Diseases, 41, 1293-1302.

van Olden, R.W., Guchelaar, H.J., Struijk, D.G., Krediet, R.T., & Arisz, L. (2003). Acute effects of high-dose furosemide on residual renal function in CAPD patients. Peritoneal Dialysis International, 23, 339-347.

Wilcox, C.S. (2002). New insights into diuretic use in patients with chronic renal disease. Journal of the American Society of Nephrology, 13, 798-805.

Witowski, J., Bender, T.O., Wisniewska-Elnur, J., Ksiazek, K., Passlick-Deetjen, J., Breborowicz, A., & Jorres, A. (2003). Mesothelial toxicity of peritoneal dialysis fluids is related primarily to glucose degradation products, not to glucose per se. Peritoneal Dialysis International, 23(4), 381-390.

By Amy Flinn, BSc, BScPharm, ACPR, Seadna Ledger, BScPharm, ACPR, and Peter Blake, MD, MB FRCCP

Amy Flinn, BSc, BscPharm, ACPR, is a Pharmacist, Acute Care of the Elderly, London Health Sciences Centre, London, Ontario.

Seadna Ledger, BScPharm, ACPR, is the Advanced Practice Renal Pharmacist, London Health Sciences Centre, London, Ontario.

Peter Blake, MD, MB, FRCCP, is Chair, Division of Nephrology, London Health Sciences Centre, London, Ontario and Professor of Medicine, University of Western Ontario, London, Ontario.

Address correspondence to Amy Flinn, e-mail: amy.flinn@lhsc.on.ca

Submitted for publication: June 27, 2006.

Accepted for publication in revised form: August 13, 2006.
Table One. Baseline characteristics

Variable Furosemide group n=20

Women, n (%) 7 (35)
Mean age [+ or -] SD, yrs [range] 53.3 [+ or -] 16.5 [19-75]
Mean body weight [+ or -] SD, kg 78.9 [+ or -] 16.0
Cause of ESRD, n (%)
 Glomerulonephritis 2 (10)
 Diabetic nephropathy 8 (40)
 Nephrosclerosis 2 (10)
 Other or unknown 8 (40)
Patients with DM, n (%) 11 (55)
Patients with CHF, n (%) 5 (25)
Patients on ACEI or ARB, n (%) 13 (65)
Mean daily dose furosemide mean [range], mg 171.5 [40-250]
Mean UV [+ or -] SD, mL/day 806.5 [+ or -] 494.8
Mean CrCl (total) [+ or -] SD, mL/min 84.1 [+ or -] 31.3
Mean Kt/V (total) [+ or -] SD 2.23 [+ or -] 0.57

Variable Control group n=41

Women, n (%) 21 (51)
Mean age [+ or -] SD, yrs [range] 59.7 [+ or -] 16.7 [19-80]
Mean body weight [+ or -] SD, kg 71.2 [+ or -] 15.3
Cause of ESRD, n (%)
 Glomerulonephritis 6 (15)
 Diabetic nephropathy 12 (29)
 Nephrosclerosis 6 (15)
 Other or unknown 17 (41)
Patients with DM, n (%) 15 (37)
Patients with CHF, n (%) 7 (17)
Patients on ACEI or ARB, n (%) 22 (54)
Mean daily dose furosemide mean [range], mg --
Mean UV [+ or -] SD, mL/day 426.1 [+ or -] 479.2
Mean CrCl (total) [+ or -] SD, mL/min 73.2 [+ or -] 29.5
Mean Kt/V (total) [+ or -] SD 2.25 [+ or -] 0.56

SD = standard deviation; ESRD = end stage renal disease; DM = diabetes
mellitus; CHF = congestive heart failure; ACEI = angiotensin-converting
enzyme inhibitors; ARB = angiotensin receptor blockers; UV = urine
volume; CrCl = creatinine clearance

Table Two. Change in urine volume, creatinine clearance and Kt/V from
baseline at six months and at one year

 Furosemide group (n=20)
Change from baseline 6 months 12 months

Urine volume (mL/day) 78.0 [+ or -] 445.2 85.0 [+ or -] 481.7
Creatinine clearance 5.6 [+ or -] 20.4 4.0 [+ or -] 35.5
(mL/min)
Kt/V 0.085 [+ or -] 0.89 0.0040 [+ or -] 0.57

 Control group (n=41)
Change from baseline 6 months 12 months

Urine volume (mL/day) 105.5 [+ or -] 401.8 110.7 [+ or -] 455.4
Creatinine clearance 4.5 [+ or -] 29.0 9.1 [+ or -] 28.6
(mL/min)
Kt/V 0.046 [+ or -] 0.61 0.16 [+ or -] 0.56

 p-value
Change from baseline 6 months 12 months

Urine volume (mL/day) 0.8 0.8
Creatinine clearance 0.9 0.5
(mL/min)
Kt/V 0.5 0.3
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Author:Flinn, Amy; Ledger, Seadna; Blake, Peter
Publication:CANNT Journal
Geographic Code:1CANA
Date:Jul 1, 2006
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