Bacterial growth in the urinary tract is usually prevented by host factors including bacterial eradication by urinary and mucus flow, urothelial bactericidal activity, urinary secretory IgA, and blood group antigens in secretions which interfere with bacterial adherence. Bacterial eradication from the urinary tract is partially dependent on urine flow and voiding frequency. Therefore, it seems logical to postulate a connection between fluid intake and the risk of urinary tract infections (UTIs). However, experimental and clinical data on this subject are conflicting. Experimental studies concerning the effect of water intake on susceptibility and course of UTIs were predominantly performed in the 60 s and 70 s. Despite many open questions, there has been no continuous research in this field.
Only few clinical studies producing contradictory results are available on the influence of fluid intake concerning the risk of UTI. One explanation for the inconsistency between the data might be the uncertainty about the exact amounts of fluid intake, which was mostly recorded in questionnaires. So far, there is no definitive evidence that the susceptibility for UTI is dependent on fluid intake. Nevertheless, adequate hydration is important and may improve the results of antimicrobial therapy in UTI. Results of experimental and clinical studies concerning urinary hydrodynamics are the basis for advice given by expert committees to patients with UTI to drink large volumes of fluid, void frequently, and completely empty the bladder. The combination of the behaviourally determined aspects of host defence and not simply increasing fluid intake is important in therapy and prophylaxis of UTI.
The urinary tract is a common site of infection. While 1% of male and 3% of female infants and children develop a urinary tract infection (UTI), 20% of females will have at least one UTI during lifetime (Mullholland & Bruun, 1973; Winberg et al, 1974). Bacteria periodically enter the female urinary bladder from the urethra in small numbers. They are able to bind, multiply, colonize, and invade the urinary tract in sequential order. Whether infection ensues depends on the virulence and inoculum size of the microorganism and the adequacy of host defence mechanisms (Roberts, 1996).
If bacteria enter the bladder, they may ascend up to the kidneys and cause an acute inflammation of the renal parenchyma. At worst, this may lead to renal scars. In this way, urinary tract infections may not only cause acute morbidity but may also result in long-term problems, including hypertension and reduced renal function.
In the therapy and prophylaxis of urinary tract infections, forcing fluids has always been advocated. A water diuresis serves to ‘flush’ the urinary tract of infecting organisms, and frequent voiding reduces bacterial multiplication in the bladder (Denman & Burton, 1992). In addition, a reduction in bacterial counts in the urine by hydration would enhance the effect of factors otherwise overwhelmed by large numbers of bacteria (eg, bladder mucosal defences or the effect of relatively low concentrations of antimicrobial drugs) (Sobel & Kaye, 1990).
Indeed, fluid intake exerts an influence on the composition of urine, on urine volume, on micturition frequency on renal perfusion, and on the osmolality of the renal medulla. The question is if and in which way all these factors contribute to the host defence against bacterial colonization and infection, and the results of their complex interaction.
Fluid intake and the composition of urine
Although urine is generally considered to be a good culture medium for most bacteria (Cox & Hinman, 1961), it does possess antibacterial activity. It has been shown that extremes of osmolality, high urea concentration, and low pH levels in urine are inhibitory for the growth of some uropathogenic bacteria.
Effect of urine osmolality and urea concentration
There is a high and positive correlation between osmolality and antibacterial activity of urine (Asscher et al, 1966; Kaye, 1968). Animal experiments suggest a protective effect of highly concentrated urine attained during dehydration. In an experiment carried out on Wistar rats, Prat et al (1976) compared two groups of animals after inoculation of Escherichia coli into the urinary bladder. One group received only a small amount of tap water (‘hydropenia’). The second group had free access to 5% glucose solution. In the hydropenic rats, urine osmolality was over 2000 mosmol/kg, and in rats with water diuresis between 47 and 181 mosmol/kg. A fortnight after infection, the mean log number of bacteria in the bladder urine from hydropenic rats was significantly lower than the corresponding number in diuretic rats. Additionally, the animals with hydropenia showed a significantly lower degree of renal infection.
However, the data of rat experiments are not representative for man. Rodents generally show a much higher concentrated urine with osmolalities in the range of 1000–2000 mosmol/kg than man, in whom urine osmolality rarely exceeds 800 mosmol/kg (Kunin, 1987). Moreover, some uropathogenic bacteria, for instance E. coli, possess a protective mechanism against osmotic shock. This mechanism involves the uptake of osmoprotective substances such as glycine, glutamine, choline, proline, and betaine that are secreted by the kidney in the tubular fluid (Chambers & Kunin, 1987). Thus, some authors suggest antibacterial activity of human urine being rather a function of urea content than of osmolality (Schlegel et al, 1961; Kaye, 1975).
There is an impressive day and night rhythm of urine volume and osmolality, regulated by antidiuretic hormone excretion (Rittig et al, 1995). Cicmanec et al (1985) compared the growth of E. coli 06 in concentrated urine samples from first morning voids in 15 males and 15 females, and in dilute urine samples, by adding one part of concentrated urine to three parts of distilled water. In concentrated urine, 90% of the initial inoculum died during the lag phase and the surviving bacteria had a long lag period before growth commenced. Once growth began, the maximum growth yield was achieved after 55 h. In dilute urine, 75% of the same bacteria survived the lag phase; once growth began, they reached the maximum growth yield in 13 h. Considering poor bacterial growth in concentrated urine, the authors assumed a natural host defence mechanism. However, as urine is not ordinarily voided at night, this mechanism may be offset by the prolonged incubation time.
In conclusion, highly concentrated urine, as produced in states of dehydration, may contribute to a decrease in multiplication of uropathogenic bacteria after invasion into the bladder.
Fluid intake and the bladder defence mechanism
In the mid-20th century, the mechanical effect of urine flow in diluting and removing bacteria from the urinary tract has been touched upon by several workers. The ‘bladder defence mechanism’ is the result of two factors: vesical emptying and destruction of bacteria by an antibacterial action of the bladder mucosa (Cox & Hinman, 1961).
Voiding alone cannot mechanically free the bladder from organisms, since, at the very least, a film of infected urine remains on the bladder wall (O'Grady & Cattell, 1966a). Without some bladder defence mechanism, the remaining bacteria would be expected to multiply to high titers during long periods, without voiding such as during sleep. One most effective bladder defence mechanism lies in the bladder mucosa itself. Independent from urine flow, contact with the bladder mucosa inhibited the growth of adhering and nonadhering pathogenic E. coli strains (Schlager et al, 1993; Mannhardt et al, 1996).
Harrison et al (1988) evaluated the contributions of different host defence mechanisms to bacterial clearance in rats infected with E. coli. Bacterial clearance from the urinary bladder was divided into two phases, primary (0–4 h) and secondary (4–24 h). In all, 99% of E. coli was cleared during the primary phase from normal, dehydrated, and polyuric animals, and 93% from anuric animals. Clearance was shown to be dependent on the presence of viable tissue. Bacterial numbers continued to decrease during the secondary phase in normal and dehydrated animals, but increased in polyuric and anuric groups. In the last two groups, ultrastructural changes of the bladder associated with impaired antibacterial properties were found. The study showed that the clearance of microorganisms from the bladder was not associated with the voided volume, but with the antibacterial activity of the mucosal surface.
Nevertheless, diuresis and voiding frequency affect the high antibacterial competence of ‘intrinsic hydrokinetic clearance mechanisms’ (Cattell et al, 1970). In female patients with proven UTI, Roberts et al (1967) showed that both diuresis and the time of day when the specimen is taken may considerably affect the bacterial colony count. Urinary diuresis greatly reduced the colony count of infected urine. It was interesting, however, that in all patients investigated the level of infection invariably returned overnight to prediuresis levels, irrespective of whether a daytime diuresis had been induced or not (Roberts et al, 1967). In fact, the importance of the overnight period must be emphasized in that if water diuresis and frequent bladder emptying are not maintained, the washout effect will be transient (Cattell et al, 1970).
Many experimental studies and mathematical models demonstrated that an increase of voiding frequency might reduce the risk of UTI. This is not consistently supported by clinical studies. Hunt and Waller (1992) did not find a significant difference in the frequency of urination between female patients with urinary tract infection and healthy controls. In normal female volunteers, in whom the introital flora was closely observed during a 5-day period, those subjects who previously were not colonized with pathogens became colonized with increased frequency of voiding (Seddon et al, 1976). In a further study, 19 patients with a history of documented recurrent urinary tract infection showed a significantly increased frequency of voiding compared to controls (Seddon et al, 1980). It was hypothesized that during micturition the introitus and perineal areas are soiled with urine, allowing transfer of faecal organisms to the introital area.
In conclusion, the mechanical factors of the bladder defence mechanism are at least, in part, dependent on urine output. It is well recognized that, in patients with bacteriuria, a high fluid intake with frequent micturition may result in a marked reduction in the concentration of organisms recovered on culture of specimens of urine. Mild dehydration leads to a decrease in urine output and an increase in bladder dwelling times. Under normal conditions, this state is given at night during sleep, without any consequences concerning the susceptibility for UTI. This may be a sign for the effectiveness of other specific bladder defence mechanisms contributed by the bladder mucosa and by antibacterial effects of the urine itself.
Fluid intake and infection of the upper urinary tract
The hydrokinetics of the upper urinary tract are somewhat different from those of the bladder and urethra. Two factors govern persistence of bacteria in the upper urinary tract (Kunin, 1987): The bacterial multiplication rate: the maximum doubling time for enteric bacteria in urine is about 20 min. This may be altered depending on the character of the urine (pH, osmolality, and other factors). The perfusion volume ratio: the number of bacteria in the urine also depends on the rate of urine flow divided by the volume in a given fluid space (the perfusion volume ratio).
The concentration of organisms will remain steady if the rate of addition of fresh urine is just fast enough to halve the concentration of bacteria at each doubling time (critical perfusion/volume ratio).
O'Grady and Cattell (1966b) examined the effect of different perfusion/volume ratios on the ability of bacterial populations to achieve full growth (climax) or become sterile over time. They calculated the critical perfusion/volume ratio in the upper urinary tract, which is required in order to allow a bacterial population to reach a steady state. This turns out to be at about the normal physiologic rates of urine flow (assuming that the average volume of the urinary tract is 10 ml and urine flow is 0.69 ml/min or about 1 l/day). Higher rates of flow will tend to raise the ratio and gradually eliminate bacteria from the system. Lower rates of flow, as occur overnight or in states of mild dehydration, would tend to increase the bacterial population.
Fluid intake and renal parenchymal infection
Early studies concerned with the pathogenesis of pyelonephritis have demonstrated that the medulla of the kidney is much more susceptible to infection than the cortex. This vulnerability may be due to anatomical location, relatively poor circulation, high concentration of ammonia, and habitual hypertonicity of the renal medulla. Blood and interstitial fluids of the medulla are hypertonic when the urine is concentrated, but approach isotonicity with a moderate water diuresis.
In 1966, Andriole studied the inflammatory response to thermal injury in the medulla and cortex of control rats and rats undergoing a chronic water diuresis by serial histological study. Water diuresis enhanced the inflammatory response, for example, the mobilization of granulocytes into the renal medulla. In contrast, the inflammatory response was delayed and diminished during antidiuresis. The results of this study suggested that an isotonic or nearly isotonic environment may be necessary for prompt leukocyte migration into the medulla of the kidney and that the speed of granulocyte mobilization may have some bearing on the protective effect of water diuresis in preventing renal infection.
Andriole and Epstein (1965) demonstrated that, in rats, haematogenic candida and staphylococcal renal parenchymal infection could be prevented by water diuresis, and suggested that staphylococcal renal infection could be cured by decreasing the normally hypertonic environment of the renal medulla through sustained water diuresis.
In 1970, Andriole demonstrated that E. coli pyelonephritis can be induced in the nonobstructed, nonmanipulated normal kidney of the rat, simply by increasing the osmolality of medullary tissue through a decrease in daily water intake (Andriole, 1970). E. coli were applied intravenously to water-restricted rats with an urine osmolality of over 2000 mosm/kg, and in rats of a control group which were allowed access to tap water ad lib. At 8 days after bacterial challenge, pyelonephritis was observed in 19 of 30 water-restricted animals and in only five of 38 control rats.
Another controlled animal study showed that enterococcal pyelonephritis in rats could be cured by a sustained water diuresis for 7–14 days without antimicrobial therapy (Andriole & Checko, 1968). The eradication of infection was associated with the infiltration of polymorphonuclear leukeocytes in the renal medulla.
Several mechanisms might explain the profound influence of water intake on the susceptibility or resistance of the renal medulla to bacterial infection. Water restriction decreased blood flow to the medulla and increased urine concentration and medullary osmolality. Furthermore, granulocyte mobilization and phagocytosis are inhibited in highly concentrated urine (Chernew & Braude, 1962; Andriole, 1966) and superoxide production, degranulation, phagocytosis, and killing by neutrophils are decreased in hypertonic environments (Hampton et al, 1994). Rising urine pH and reducing urine osmolality by water loading increase the bactericidal activity of neutrophils (Gargan and Hamilton-Miller, 1994).
In conclusion, the data of animal experiments show that upper urinary hydrodynamics and the environment of the renal medulla are important factors in the pathogenesis of pyelonephritis. These findings could provide a rationale for the practice of ‘forcing fluids’ in the prevention and treatment of upper UTI. In lower UTI, the situation may be quite different.
Effect of hydration on bacteriuria
The influence of oliguria on the symptomatology of urinary tract infection in male patients with transurethral catheters due to prostatic hyperplasia/carcinoma or with urolithiasis was studied by Ziesche (1966). After thirsting for 24 h, 26% of the patients with transurethral catheters and 36% with urolithiasis, in whom bacteriuria had been detected, developed an increased axillary temperature. The author concluded that this temperature reaction was a sign of an exacerbation of a ‘latent inflammatory process’, induced by oliguria. This conclusion is, however, highly speculative.
Most studies investigated the effect of ‘forcing fluids’ on bacteriuria. Therefore, only indirect conclusions can be drawn concerning the effects of dehydration on the initiation and course of UTI in man (Table 1).
Catell et al (1970) studied the influence of diuresis and frequent micturition on the bacterial content of infected urine in 30 adult patients. The change in bacterial counts in clean catch midstream urine specimens broadly varied between patients. In some patients, the bacterial counts in their urine were reduced to levels of less than 103 organisms/ml, whereas in other patients there was no significant change. The authors suggested that this variability might be due to undetectable abnormalities of the urinary tract and/or residual urine in the bladder, compromising the competence of the ‘hydrokinetic clearance mechanism’.
Borzone et al (1988) used alkaline bicarbonate water in an amount of at least 2 l/day for the duration of 5 days in 10 middle-aged patients to treat an asymptomatic bacteriuria after surgical intervention for gallbladder stones. In seven of the 10 patients, complete eradication of the bacteria was observed. In 10 similar cases receiving conventional antibiotic therapy, eight got rid of the bacteriuria during 5 days treatment. The author concluded that high water intake is a useful, harmless and cheap therapy for asymptomatic UTI for outpatients. However, there was no control group without treatment.
In another uncontrolled study in five nursing home residents with bacteriuria (>105 colony counts), a transurethral catheter was inserted into the bladder in the morning after restricting overnight fluid intake and voiding (Friedman & Gladstone, 1970). Urine samples were taken after one further hour of fluid restriction and during subsequent water diuresis with water intake ad libitum. Bacterial concentration decreased from five- to 77-fold. As the decreases in colony count were proportionally greater than the increases in urine flow, the authors assumed that the decrease was not only due to dilution of bacteria including a constant rate of new bacteria, but also due to the activity of host defence mechanisms.
The clinical studies cited above support the empiric experience of many patients, especially women, that hydration status alone may be able to influence the duration of bacteriuria. However, based on the presented data, the evidence is far from consistent.
Influence of hydration on the susceptibility to UTI
In a case–control study, Remis et al (1987) investigated the possible influence of behavioural factors on the risk of UTI. In all, 43 women with culture-confirmed UTI were compared with women with upper respiratory infection and women visiting a gynaecology clinic (controls). There was no association between susceptibility to UTI and the volume of fluids consumed (Table 2).
Adatto et al (1979) studied the voiding habits of 84 female university students with a history of recurrent urinary infection, and compared the data with those of a control group. There was no difference in the estimated daily fluid intake of patients and controls, and little difference in the total number of micturitions. However, voluntary retention of urine for more than an hour after experiencing the urge to urinate was present in 61% of the patients and in only 11% of the controls.
Other studies demonstrated an influence of hydration on the susceptibility to UTI. Pitt (1989) compared the fluid intake of 107 adult females and males who where visiting their general practitioner with symptoms of UTI, with that of a control group using a questionnaire for self completion. The mean fluid intake of the infected group was two glasses a day compared with four glasses a day in the noninfected group.
Nygaard and Linder (1997) checked the impact of voiding habits at work and voluntary fluid restriction at work on UTI in 791 female teachers. Voluntary fluid restriction was common (about 50%) to avoid the way to the toilet. Women with voluntary fluid restriction drank less and had a 2.21-fold higher risk of UTI than women without restriction after controlling for being pregnant, infrequent voiding, and urge incontinence.
Ervine et al (1980) prospectively studied self-care behaviour and fluid intake in 23 women with symptoms of dysuria, frequency or urgency, and more than 105 colonies per ml of a single pathogenic organism in a midstream urine specimen. The patients with UTI drank significantly less water and urinated significantly less frequently than 64 ambulatory patients, who were seeking care for problems unrelated to UTI. The question is whether low voiding frequency rather than low fluid intake was the main factor predisposing to UTI in this study. Low voiding frequency is a well-known risk factor for UTI in girls or young women. The ‘infrequent voiding syndrome’ may result in muscular decompensation of the bladder, development of a large bladder unable to contract, residual urine, and recurrent UTIs.
Nielsen and Walter (1979) sent a questionnaire, concerning micturition habits, to women living in the county of Northern Jutland. In all, 11.3% of the more than 1000 women had experience of UTI and 2.0% had three or more infections per year. The frequency of UTI was significantly higher among women with three or less voidings per day than among those with four or more voidings per day.
Lapides et al (1968) carried out a complete urological evaluation on 112 women with documented recurrent UTI. Infrequent voiding habits (ie urination once in 5–10 h) were noted in more than 60% (70/112) of cases; most of them exhibited bladder capacities of more than 500 ml. UTI could be prevented by voiding every 2 h during the day and once or twice at night. Therefore, the authors advised their patients to void frequently, but they did not instruct them to increase fluid intake.
Prophylactic approaches using hydration to avoid bacterial colonization are rare. Eckford et al (1995) used a simple hydration monitoring to encourage adequate hydration and reduce urinary osmolality. In total, 17 premenopausal women who had at least two idiopathic UTIs in the previous 6 months were followed over 8 months. Urinary osmolality was assessed by the patients at each void by a hand-held conductivity meter. The subjects were randomly assigned to a group, who used the instrument for 4 months, followed by 4 months with no use and by another group who did the reverse. Advice to maintain a high fluid intake and to void frequently and completely was reiterated at the start of and throughout the study; the patients were told to reach a specific urine gravity <1015. Six women developed UTIs during the study; two had UTIs both when using and not using the conductivity meter and four had UTIs when not using the instrument, but were sterile when using it. The decrease in UTIs during the 4-month period of use was significant (P=0.046). The authors concluded that encouraging ‘adequate’ hydration was able to reduce urinary osmolality and incidence of UTIs.
Lumsden and Hyner (1985) prospectively investigated the effect of health education on the recurrence rate of UTIs in female outpatients. In all, 34 volunteers were randomly assigned to either an experimental education group or a control group. Controls were offered routine patient information provided by practitioners at the outpatient clinic. Members of the experimental group participated in an educational session which addressed UTIs, its risk factors, and behavioural changes which might reduce its recurrence. At follow-up 3 months after the educational session, the experimental group had a significant (P<0.05) reduction in the recurrence of UTIs.
In conclusion, voiding dysfunction and defects of the uroepithial bactericidal competence have been proved to be important host factors in the pathogenesis of UTIs. Clinical data concerning low fluid intake as a main pathogenetic factor of UTI are, however, conflicting (Spach et al, 1993). One explanation for the differences between the data might be the uncertainty about the exact amounts of fluid intake per day. In fact, most studies used a questionnaire to estimate fluid intake. Hunt and Waller (1994) noted significant errors in estimating fluid intake when compared with diary recordings in the same patients. In questionnaires the levels of fluid consumption were consistently underestimated. The same is true for subjectively estimated urinary frequency compared with chart-determined urinary frequency (McCormack et al, 1992). Considering these methodic biases, the low number of studies, and the small patient groups, the results of the available clinical studies do not prove a significant effect of hydration status on the susceptibility to UTI.
Based on empirical data and personal experience, many infectiologists, nephrologists, and urologists recommend high fluid intake to prevent UTIs. Kunin (1987) stated that ‘instruction to patients to drink ample fluids and void frequently appears to be justifiable except when the patient is being treated for infection with agents that need to be concentrated in the urine’. Some physicians establish a routine forced hydration programme for their patients as a means of prophylaxis. Bailey (1994) states that many women with recurrent UTIs are helped by ensuring that they have a fluid intake of at least 2 l daily. Some paediatric urologists make ‘an attempt to increase the child's urine volume to improve mechanical aspects of bacterial elimination by recommending to the parents that a 1-l jug of water with the child's name on it be placed in the refrigerator to be consumed each day’ (Piercy et al, 1993). Smellie et al (1988) consider measures like adequate fluid intake together with regular frequent complete voiding and correction of constipation as important as prescribing prophylactic drugs.
Most studies concerning the effect of water intake on susceptibility and course of UTIs directly or indirectly were performed in the 60 s and 70 s. Despite many open questions, work in this field of research has not be continued persistently enough to find acceptable answers. For example, no sufficient clinical data exist concerning the effects of dehydration or forced fluid intake on the susceptibility for UTI. Behavioural studies are limited and neither extensive nor sophisticated. There have been no studies on the outcome of therapy in patients undergoing water diuresis compared with patients on a normal fluid intake or on mild dehydration. Controlled prospective randomized clinical studies are needed to answer the questions whether mild dehydration has any deleterious effect and whether high fluid intake might be efficacious in the prevention of UTI in man.
Adatto K, Doebele KG, Galland L & Granowetter L (1979): Behavioural factors and urinary tract infection. JAMA 241, 2525–2526.
Andriole VT (1966): Acceleration of the inflammatory response of the renal medulla by water diuresis. J. Clin. Invest. 45, 847–854.
Andriole VT (1970): Water, acidosis, and experimental pyelonephritis. J. Clin. Invest. 49, 21–30.
Andriole VT & Checko PJ (1968): Effect of water diuresis on chronic pyelonephritis. J. Lab. Clin. Med. 71, 1–16.
Andriole VT & Epstein FH (1965): Prevention of pyelonephritis by water diuresis: evidence for the role of medullary hypertonicity in promoting renal infection. J. Clin. Invest. 44, 73–79.
Asscher AW, Sussman M, Waters WE, Davis RH & Chick S (1966): Urine as a medium for bacterial growth. Lancet 2, 1037–1041.
Bailey RR (1994): Management of uncomplicated urinary tract infections. Int. J. Antimicrob. Agents 4, 95–100.
Borzone A, Iannace C, Vulpio C & Castiglioni GC (1988): Asymptomatic urinary hospital infections: choice of treatment with drinking water. Clin. Ter. 124, 183–186.
Catell WR, Fry IK, Spiro FI, Sardeson JM, Sutcliffe MB, O'Grady F & Path MRC (1970): Effect of diuresis and frequent micturition on the bacterial count of infected urine: a measure of competence of intrinsic hydrokinetic clearance mechanisms. Br. J. Urol. 42, 290–295.
Chambers ST & Kunin CM (1987): Isolation of glycine betaine and proline betaine from human urine: assessment of their role as osmoprotective agents for bacteria and the kidney. J. Clin. Invest. 79, 731–737.
Chernew I & Braude AI (1962): Depression of phagocytosis by solutes in concentrations found in the kidney and urine. J. Clin. Invest. 41, 1945–1953.
Cicmanec JF, Shank RA & Evans AT (1985): Overnight concentration of urine. Natural defence mechanism against urinary tract infection. Urology 26, 157–159.
Cox CE & Hinman F (1961): Experiments with induced bacteriuria, vesical emptying and bacterial growth on the mechanism of bladder defence to infection. J. Urol. 6, 739–748.
Denman SJ & Burton JR (1992): Fluid intake and urinary tract infection in the elderly. JAMA 267, 2245–2246.
Eckford SD, Keane DP, Lamond E, Jackson SR & Abrams P (1995): Hydration monitoring in the prevention of recurrent idiopathic urinary tract infections in pre-menopausal women. Br. J. Urol. 76, 90–93.
Ervine C, Komaroff AL & Pass TM (1980): Behavioural factors and urinary tract infection. JAMA 243, 330–331.
Friedman SA & Gladstone JL (1970): The effects of hydration and bladder incubation time on urine colony counts. J. Urol. 105, 428–432.
Gargan RA & Hamilton-Miller JMT (1994): Opsonophagocytosis in infected urine: relation to pH and osmolality. J. Urol. 152, 1615–1618.
Hampton MB, Chambers ST, Vissers MCM & Winterbourn CC (1994): Bacterial killing by neutrophily in hypertonic environments. J. Infect. Dis. 169, 839–846.
Harrison G, Cornsih J, Vanderwee MA & Miller TE (1988): Host defence mechanisms in the bladder I. Role of mechanical factors. Br. J. Exp. Pathol. 69, 245–254.
Hunt J & Waller G (1992): Psychological factors in recurrent uncomplicated urinary tract infection. Br. J. Urol. 69, 460–464.
Hunt J & Waller G (1994): The reliability of self-report of behaviours associated with recurrent urinary tract infection. Br. J. Urol. 74, 300–310.
Kaye D (1968): Antibacterial activity of human urine. J. Clin. Invest. 47, 2374–2390.
Kaye D (1975): Host defence mechanisms in the urinary tract. Urol. Clin. North. Am. 2, 407–422.
Kunin C.M. (1987): Detection, Prevention and Management of Urinary Tract Infections. Philadelphia: Lea & Febiger.
Lapides J, Costello RT, Zierdt DK & Stone TE (1968): Primary cause and treatment of recurrent urinary infection in women: preliminary report. J. Urol. 100, 552–555.
Lumsden L & Hyner GC (1985): Effects of an educational intervention on the rate of recurrent urinary tract infections in selected female outpatients. Women Health 10, 79–86.
Mannhardt W, Becker A, Putzer M, Zepp F, Hacker J & Schulte-Wissermann H (1996): Host defence within the urinary tract. I. Bacterial adhesion initiates uroepithelial defence mechanism. Pediatr. Nephrol. 10, 568–572.
McCormack M, Infant-Rivard C & Schick E (1992): Agreement between clinical methods of measurement of urinary frequency and functional bladder capacity. Br. J. Urol. 69, 7–21.
Mullholland SG & Bruun A (1973): A study of urinary tract infection. J. Urol. 110, 245–248.
Nielsen AF & Walter S (1979): Epidemiology of infrequent voiding and associated symptoms. Scand. J. Urol. Nephrol. 157(Suppl), 49–53.
Nygaard I & Linder M (1997): Thirst at work—an occupational hazard? Int. Urogynecol. J. Pelvic Floor Dysfunct. 8, 340–343.
O'Grady F & Cattell WR (1966a): Kinetics of urinary tract infection. II. The bladder. Br. J. Urol. 38, 156–162.
O'Grady F & Cattell WR (1966b): Kinetics of urinary tract infection. I. Upper urinary tract. Br. J. Urol. 38, 149–155.
Piercy KR, Khoury AE, McLorie GA & Churchill BM (1993): Diagnosis and management of pediatric urinary tract infection. Curr. Opin. Urol. 3, 25–29.
Pitt M (1989): Fluid intake and urinary tract infection. Nurs. Times 85, 36–38.
Prat V, Hatala M, Schuch O & Bohnslan V (1976): The influence of water diuresis on the course of experimental E. coli bacteriuria after unilateral nephrectomy in rats. Acta Biol. Med. Ger. 35, 1651–1656.
Remis RS, Gurwith MJ, Gurwith D, Hargrett-Bean NT & Layde PM (1987): Risk factors for urinary tract infection. Am. J. Epidemiol. 126, 686–694.
Rittig S, Matthiesen TB, Hunsballe JM, Pederson EB & Djurhuus JC (1995): Age-related changes in the circadian control of urine output. Scand. J. Urol. Nephrol. 173(Suppl), S71–S74.
Roberts AP, Robinson RE & Beard RW (1967): Some factors affecting bacterial colony counts in urinary infection. Br. Med. J. 1, 400–403.
Roberts JA (1996): Factors predisposing to urinary tract infections in children. Pediatr. Nephrol. 10, 517–522.
Schlager TA, Lohr JA & Hendley JO (1993): Antibacterial activity of the bladder mucosa. Urol. Res. 21, 313–317.
Schlegel JU, Cuellar J & O'Dell RM (1961): Bactericidal effect of urea. J. Urol. 86, 819–822.
Seddon JM, Bruce AW, Chadwick P & Carter D (1976): Introital bacterial flora—effect of increased frequency of micturition. Br. J. Urol. 48, 211–218.
Seddon JM, Bruce AW, Chadwick P & Willett WS (1980): Frequency of micturition and urinary tract infection. J. Urol. 123, 524–526.
Smellie JM, Grüneberg RN, Bantock HM & Prescod N (1988): Prophylactic co-trimoxazole and trimethoprim in the management of urinary tract infection in children. Pediatr. Nephrol. 2, 12–17.
Spach DH, Stapleton AE & Stamm W (1993): Behavioral and genetic factors related to urinary tract infection. Curr. Opin. Infect. Dis. 6, 31–35.
Sobel JD & Kaye D (1990): Urinary tract infections. In Principles and Practice of Infectious Diseases. (3rd Edition) eds GL Mandell, RG Douglas & JE Bennett. New York: Churchill Livingstone.
Winberg J, Anderson T, Bergstrom H, Larson H & Lincoln K (1974): Epidemiology of symptomatic urinary tract infection in childhood. Acta Paediatr. Scand (Suppl.) 252, 1–20.
Ziesche HW (1966): Oligurie und Harnwegsinfekt. Z. Urol. Nephrol. 5, 625–631.
About this article
Cite this article
Beetz, R. Mild dehydration: a risk factor of urinary tract infection?. Eur J Clin Nutr 57, S52–S58 (2003). https://doi.org/10.1038/sj.ejcn.1601902
- urinay tract infection
- fluid intake
- host factors
Der Urologe (2020)
Performative Compliance and the State–Corporate Structuring of Neglect in a Residential Care Home for Older People
Critical Criminology (2020)
International Urogynecology Journal (2020)
International Urology and Nephrology (2016)
Angiotensin-Converting Enzyme Inhibitor Treatment and the Development of Urinary Tract Infections: A Prescription Sequence Symmetry Analysis
Drug Safety (2013)