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Special Features |


* Department of Medicine, Division of Nephrology, University Hospital Hamburg-Eppendorf, Hamburg, Germany;
The Ohio State University, Columbus, Ohio; and
Outpatient Clinic for Nephrology and Dialysis Schlankreye, Hamburg, Germany
Address correspondence to: Dr. Ulrich O. Wenzel, University Hospital of Hamburg-Eppendorf, Department of Medicine, Division of Nephrology, Martinistrasse 52, Hamburg, 20246 Germany. Phone: +49-40-42803-3908; Fax: +49-40-42803-5186; E-mail: wenzel{at}uke.uni-hamburg.de
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"My wife forgot to ask whether it is really necessary to keep a fluid intake of 4.5 L daily. This was the advice of her primary care physician. Perhaps 3 L would be better for her BP and sufficient for her kidney." The husband of the patient raised this question at the end of her consultation visit at our University Hospital Clinic. The patient was seen for a second opinion regarding the management of her chronic kidney disease (CKD) manifested by a serum creatinine of 3.0 mg/dl and non-nephrotic proteinuria. The husband, who is an oncologist, was mainly concerned because his wife was losing sleep at night because of her many nocturnal trips to the bathroom. If the oncologist and his wife were an isolated case, then we would not be writing this article. However, over the years, we have encountered numerous such examples in our nephrology consultative practice. We suggest further that the patients who have CKD and complain about the instruction to drink large amounts of fluid may represent only the "tip of the iceberg." Likely, there are many more patients who have CKD and whom we nephrologists never hear about because they silently accept their watery fate. Without complaint, they follow the advice of their primary care physician, which is reinforced by the lay press ("drink at least 8 glasses of water a day") and by well-meaning friends who urge the patient with CKD to "push fluids" to clear the waste from their system. In light of the above, the purpose of this article is to place in modern perspective the widely held but incorrect notion that high fluid intake is a good thing in those with CKD.
Patients with CKD commonly are advised by primary care physicians or lay people to maintain a generous fluid intake. Moreover, in daily practice, there even seems to exist a direct correlation between serum creatinine and prescribed daily fluid intake. The higher the serum creatinine, the higher the prescribed fluid intake, the upper limit in our experience being approximately 4 L/d. Indeed, two recent authoritative publications recommended "increased" fluid intake in the management of CKD (2,3). The reason that physiciansin almost all cases, non-nephrologiststend to recommend such an increased fluid intake is difficult to understand. An increased fluid intake is not supported from modern evidenced-based medicine. The origin of this peculiar medical behavior seems to be merely historic. In the early years of renal physiology, it was shown that urinary urea clearance was sharply increased as urine flow rates increased from 1 to 2 ml/min (4). Lower blood urea nitrogen from chronic high fluid intake seems to be the basis for the historic recommendation to maintain urine volumes up to 4 L in chronic kidney insufficiency. Contemporary evidence of a beneficial effect of a high fluid intake in chronic kidney insufficiency is provided only by studies in rats. Increasing fluid intake suppressed maladaptive renal hypertrophy and interstitial fibrosis (5). Studies by Bankir et al. (6) in animal models of kidney disease showed that water restriction that results in high antidiuretic hormone levels promotes progression of kidney disease in part because antidiuretic hormone induces glomerular hyperfiltration. However, as mentioned by Bankir herself, marked species differences exist in the osmotic work that is required to concentrate urine. Rats concentrate their urine much more than humans because rats have more nephrons with long loops of Henle than humans. This may explicate why high fluid intake is beneficial in rats, whereas data in humans are lacking (7). What is the treating physician aiming at when he recommends a high fluid intake? Three historic misconceptions can be extracted from daily practice.
Misconception 1. An expanded plasma volume raises renal perfusion, which increases urine production, facilitating enhanced excretion of creatinine and urea. This assumption is valid only in the case of prerenal kidney failure caused by dehydration. Overuse of diuretics, fluid loss as a result of diarrhea or high fever, and inadequate hydration are examples. The decrease in kidney function is functional and fully reversible after administration of fluids. In euvolemic patients, high fluid intake may lead to volume expansion and arterial hypertension, especially when accompanied by high salt intake.
Misconception 2. The kidney needs a moist environment to work well, and a high urine output indicates a better kidney function. The second misconception engages all patients with CKD. Does a scientific reason exist for this group to improve kidney function by an increased intake of fluid? The kidney needs only a surprisingly small amount of fluid intake to work well. The daily solute load that needs to be excreted by the kidney averages 800 mOsmol. The working range of a healthy kidney is from 50 (maximal diluted urine) to 1200 (maximal concentrated urine) mOsmol/kg. Therefore, the healthy kidney needs a urine output of 670 ml to excrete 800 mOsmol of waste. A kidney with a 50% reduction in the concentrating ability will require a daily urine output of 1340 ml (Table 1). However, not all of this excreted fluid comes from drinking. Our daily fluid balance consists of (1) fluid intake as drink and that contained in food and (2) water generated in the metabolism. In addition to daily urine output, fluid is lost from the body as insensible losses (skin and airways) and a small amount via the stools. Accordingly, the person with the healthy kidney in our example would require a daily fluid intake of only 470 ml to maintain fluid balance (8,9). The patient who has CKD and a maximal concentrating capacity of 600 mOsmol/kg would need only 1140 ml of free fluid drinking (Table 1). However, humans usually drink more than this minimum requirement for social and cultural reasons.
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There are a few clinical entities that need an increased fluid intake. A list to identify who requires high fluid intake and who does not is shown in Table 2. Patients who need an increased fluid intake can be separated into three categories: (1) Those who need high fluid intake to prevent disease such as nephrolithiasis; (2) those who need a high fluid intake to compensate for a underlying disease, such as renal or central diabetes insipidus or salt-wasting nephropathy; and (3) those who have conditions such as polydipsia or salt gluttony (12), where the underlying disease should be treated.
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This does not mean that it is beneficial for the kidney to restrict fluid intake. However, we advocate that there is no advantage to increasing the daily fluid intake above what the thirst sensation tells you. The thirst mechanism is one of the most delicately regulated body systems and works very predictably. However, it should be noted that age-related changes in thirst sensation increase the susceptibility for dehydration in the elderly (17), particularly in the female elderly (18).
In this context, it is of interest that it was reported recently that excessive consumption of fluids can cause hyponatremia in marathon runners (19). In fact, many organizations are beginning to revise their recommendations that fixed, large volumes of dilute fluids be consumed during athletic competition. It is now suggested that athletes use thirst as their guide for fluid replacement. This is a major change in guidelines (from "stay ahead of your thirst" to "replace sweat loss") (20).
Conclusion
Patients with CKD should not "push fluids." Normal thirst-guided intake should determine water intake, unless there is a specific reason to increase fluid intake (Table 2). There is no evidence of a beneficial effect of a high fluid intake. Indeed, there is evidence that it could cause harm by promoting progression of kidney disease.
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This article has been cited by other articles:
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C.-y. Hsu, C. Iribarren, C. E. McCulloch, J. Darbinian, and A. S. Go Risk Factors for End-Stage Renal Disease: 25-Year Follow-up Arch Intern Med, February 23, 2009; 169(4): 342 - 350. [Abstract] [Full Text] [PDF] |
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