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• W2019019895 abstract "Although water is essential for life, its use for medicinal purposes is not universally accepted. We performed a comprehensive review of the literature to determine where the evolving state of knowledge lies regarding the benefits of water as a therapy for renal diseases. In the past two decades, water has emerged as a potential therapeutic agent in nephrolithiasis, chronic kidney disease (CKD), and polycystic kidney disease (PKD) in particular. In nephrolithiasis, the benefit of drinking water beyond that demanded by thirst is a cornerstone of therapy for both primary and secondary disease. In CKD, recent observational studies suggest a strong, direct association between preservation of renal function and fluid intake. In PKD, increased water intake slows renal cyst growth in animals via direct vasopressin suppression, and pharmacologic blockade of renal vasopressin-V2 receptors has recently been shown to be efficacious in retarding cyst growth in PKD patients. Although evidence is lacking to support increased water intake in the general population, available evidence indicates that individuals who are at risk for nephrolithiasis as well as those with CKD and PKD may benefit from 3 to 4l of urine output each day, a level of excretion that is likely to be safe. Although water is essential for life, its use for medicinal purposes is not universally accepted. We performed a comprehensive review of the literature to determine where the evolving state of knowledge lies regarding the benefits of water as a therapy for renal diseases. In the past two decades, water has emerged as a potential therapeutic agent in nephrolithiasis, chronic kidney disease (CKD), and polycystic kidney disease (PKD) in particular. In nephrolithiasis, the benefit of drinking water beyond that demanded by thirst is a cornerstone of therapy for both primary and secondary disease. In CKD, recent observational studies suggest a strong, direct association between preservation of renal function and fluid intake. In PKD, increased water intake slows renal cyst growth in animals via direct vasopressin suppression, and pharmacologic blockade of renal vasopressin-V2 receptors has recently been shown to be efficacious in retarding cyst growth in PKD patients. Although evidence is lacking to support increased water intake in the general population, available evidence indicates that individuals who are at risk for nephrolithiasis as well as those with CKD and PKD may benefit from 3 to 4l of urine output each day, a level of excretion that is likely to be safe. Water is essential to life itself, and since ancient times has been recognized as such. Thales of Miletus, one of the seven sages of ancient Greece, declared (c. 585 BCE) that water is ‘the principle, or the element, of things’, while Shizhen-Li, a Chinese physician of the Ming Dynasty, wrote in the Compendium of Materia Medica (1578) that ‘water is the best medicine’. Thus, in cultural traditions as varied as those of classical Greece and late Imperial China, the therapeutic benefits of water were heralded, even as its mechanism of therapeutic action remained to be determined. In the modern era, the earliest commonly accepted therapeutic benefit of water was in the treatment of nephrolithiasis, a development which had its roots in the 1930s. Since then, ecologic studies as well as work with large patient databases have suggested benefits in non-renal conditions as disparate as bladder cancer,1.Jones P.A. Ross R.K. Prevention of bladder cancer.N Engl J Med. 1999; 340: 1424-1426Crossref PubMed Scopus (31) Google Scholar colorectal cancer2.Lubin F. Rozen P. Arieli B. et al.Nutritional and lifestyle habits and water-fiber interaction in colorectal adenoma etiology.Cancer Epidemiol Biomarkers Prev. 1997; 6: 79-85PubMed Google Scholar and, potentially, coronary artery disease.3.Chan J. Knutsen S.F. Blix G.G. et al.Water, other fluids, and fatal coronary heart disease: the Adventist Health Study.Am J Epidemiol. 2002; 155: 827-833Crossref PubMed Scopus (124) Google Scholar However, it is in renal disorders, such as nephrolithiasis, chronic kidney disease (CKD) and, most recently, autosomal dominant polycystic kidney disease (ADPKD), that the putative therapeutic effects of water have been particularly well studied. Indeed, recent exciting observations are consistent with the view that higher levels of water intake are associated with slower progression of CKD4.Clark W.F. Sontrop J.M. Macnab J.J. et al.Urine volume and change in estimated GFR in a community-based cohort study.Clin J Am Soc Nephrol. 2011; 6: 2634-2641Crossref PubMed Scopus (138) Google Scholar,5.Strippoli G.F. Craig J.C. Rochtchina E. et al.Fluid and nutrient intake and risk of chronic kidney disease.Nephrology (Carlton). 2011; 16: 326-334Crossref PubMed Scopus (143) Google Scholar and with reduced cyst growth rate in ADPKD.6.Higashihara E. Torres V.E. Chapman A.B. et al.Tolvaptan in autosomal dominant polycystic kidney disease: three years' experience.Clin J Am Soc Nephrol. 2011; 6: 2499-2507Crossref PubMed Scopus (126) Google Scholar,7.Nagao S. Nishii K. Katsuyama M. et al.Increased water intake decreases progression of polycystic kidney disease in the PCK rat.J Am Soc Nephrol. 2006; 17: 2220-2227Crossref PubMed Scopus (193) Google Scholar In the present review, we evaluate the evidence supporting the medicinal use of water in these three conditions and offer guidance about how much water patients with established renal disease can safely drink. Understanding the linkage between solute and water excretion is important in evaluating potential medicinal uses of water (Figure 1). The water content of the human body is regulated by the kidneys, which adjust excretion according to the variable intakes of water and solute, as well as variable losses of water and solutes by the lungs, the skin, and the gastrointestinal tract. Although the kidneys can normally eliminate more water than any human would care to drink in a 24-h period, the minimum amount of water that must be excreted depends upon the amount of solute that must be eliminated to maintain the body’s solute content a steady state, albeit conditioned by the maximal extent to which the kidneys can concentrate urinary solutes. Most textbooks cite a maximum concentrating capacity of 1200mosm/kg H2O in those with normal renal function. The obligatory urine volume (V) can be determined for individuals by dividing the daily osmolar excretion (mosm/day) by the maximal urine osmolality (Uosm max): Obligatory V (ml)=daily osmolar excretion (mosm)÷Uosm max (mosm/kg H2O) Table 1 lists the amounts of water that must be excreted to ‘cover’ the osmoles in a hypothetical 24-h sample of urine for individuals who can achieve a maximal osmolality of 1000, 500, or 285mosm/kg H2O (thresholds which can be viewed as maximal urine osmolalities in mild, moderate, and severe renal disease, respectively), and clearly shows how the requirements for urinary water are increased as the solute load is increased. Thus, the failing kidneys lose the capacity to concentrate the urine maximally, meaning that they must excrete more water to eliminate the solutes acquired in the diet. As a consequence, patients are forced by thirst to drink more water to cover the loss linked to solute excretion. This is shown in Figure 1, which illustrates how, as an individual ages and CKD progresses, mean concentrating ability of the kidneys falls. While men, on average, demonstrate higher Uosm than women, the relationship between Uosm and renal function is evident in both men and women.Table 1Obligatory urine volume required to achieve different mean osmolalities in 24-h collectionsTotal daily urine osmolar excretion (mosm/day)Obligatory urine volume (l/day)Uosm max 1000 mosm/kg H2OUosm max 500 mosm/kg H2OUosm max 285 mosm/kg H2O2000.20.40.74000.40.81.46000.61.22.18000.81.62.811001.12.23.7Abbreviations: max, maximum; Uosm, urinary osmolality. Open table in a new tab Abbreviations: max, maximum; Uosm, urinary osmolality. Among renal disorders, nephrolithiasis is the condition for which water as a therapy is firmly established. For the purpose of this review, primary nephrolithiasis refers to the first episode of a kidney stone, whereas secondary nephrolithiasis refers to disease recurrence. Four studies drawn from two large prospective cohorts convincingly addressed the utility of medicinal water in primary stone prevention (Table 2).8.Curhan G.C. Willett W.C. Speizer F.E. et al.Comparison of dietary calcium with supplemental calcium and other nutrients as factors affecting the risk for kidney stones in women.Ann Intern Med. 1997; 126: 497-504Crossref PubMed Scopus (551) Google Scholar, 9.Taylor E.N. Stampfer M.J. Curhan G.C. Dietary factors and the risk of incident kidney stones in men: new insights after 14 years of follow-up.J Am Soc Nephrol. 2004; 15: 3225-3232Crossref PubMed Scopus (361) Google Scholar, 10.Curhan G.C. Willett W.C. Knight E.L. et al.Dietary factors and the risk of incident kidney stones in younger women: Nurses' Health Study II.Arch Int Med. 2004; 164: 885-891Crossref PubMed Scopus (368) Google Scholar, 11.Curhan G.C. Willett W.C. Rimm E.B. et al.Family history and risk of kidney stones.J Am Soc Nephrol. 1997; 8: 1568-1573PubMed Google Scholar The National Health Professionals cohort, which included >90,000 men aged 44–69 years, and the National Nurse Association cohort, which included>20,000 women aged 33–60 years, originally created to study causes of mortality on a population-wide basis were utilized to assess the relationship between water intake and stone formation. The mean follow-up ranged from 8 (ref. 10.Curhan G.C. Willett W.C. Knight E.L. et al.Dietary factors and the risk of incident kidney stones in younger women: Nurses' Health Study II.Arch Int Med. 2004; 164: 885-891Crossref PubMed Scopus (368) Google Scholar, 11.Curhan G.C. Willett W.C. Rimm E.B. et al.Family history and risk of kidney stones.J Am Soc Nephrol. 1997; 8: 1568-1573PubMed Google Scholar) to 14 (ref. 8.Curhan G.C. Willett W.C. Speizer F.E. et al.Comparison of dietary calcium with supplemental calcium and other nutrients as factors affecting the risk for kidney stones in women.Ann Intern Med. 1997; 126: 497-504Crossref PubMed Scopus (551) Google Scholar, 9.Taylor E.N. Stampfer M.J. Curhan G.C. Dietary factors and the risk of incident kidney stones in men: new insights after 14 years of follow-up.J Am Soc Nephrol. 2004; 15: 3225-3232Crossref PubMed Scopus (361) Google Scholar) years and demonstrated an association of high urine volumes with a reduced risk of first stone formation. This association was strengthened by finding an inverse relationship between the amount of urine excreted and the risk of developing a renal stone. In two studies using data from the National Health Professionals cohort, men with the highest urine volume (mean, 2.5l/day), compared with men with the lowest urine volume (1.2l/day), had a significant reduction in the relative risk of stone formation to 0.58 (95% confidence intervals, 0.42–0.79) at 8 years of follow-up and to 0.71 (95% confidence interval, 0.59–0.85) at 14 years. Similar findings were also demonstrated in two studies of women from the National Nurse Association cohort.Table 2Primary prevention studies of nephrolithiasisReferenceStudy designNumber of participantsAge at baselineYears of follow-upUrine volume, lowest quintile (l/day)Urine volume, highest quintile (l/day)Relative risk (95% CI)Curhan11.Curhan G.C. Willett W.C. Rimm E.B. et al.Family history and risk of kidney stones.J Am Soc Nephrol. 1997; 8: 1568-1573PubMed Google ScholarProspective37,99955aMean.8<1.3>2.50.58 (0.42–0.79)Taylor9.Taylor E.N. Stampfer M.J. Curhan G.C. Dietary factors and the risk of incident kidney stones in men: new insights after 14 years of follow-up.J Am Soc Nephrol. 2004; 15: 3225-3232Crossref PubMed Scopus (361) Google ScholarProspective45,61940–75bRange.14<1.3>2.50.71 (0.59–0.85)Curhan10.Curhan G.C. Willett W.C. Knight E.L. et al.Dietary factors and the risk of incident kidney stones in younger women: Nurses' Health Study II.Arch Int Med. 2004; 164: 885-891Crossref PubMed Scopus (368) Google ScholarProspective96,24536aMean.8<1.4>2.80.68 (0.56–0.83)Curhan8.Curhan G.C. Willett W.C. Speizer F.E. et al.Comparison of dietary calcium with supplemental calcium and other nutrients as factors affecting the risk for kidney stones in women.Ann Intern Med. 1997; 126: 497-504Crossref PubMed Scopus (551) Google ScholarProspective91,73130–55bRange.12<1.4>2.60.61 (0.48–0.78)Abbreviation: CI, confidence interval.a Mean.b Range. Open table in a new tab Abbreviation: CI, confidence interval. A family history of nephrolithiasis in the National Health Professionals cohort received particular scrutiny by Curhan et al.11.Curhan G.C. Willett W.C. Rimm E.B. et al.Family history and risk of kidney stones.J Am Soc Nephrol. 1997; 8: 1568-1573PubMed Google Scholar A positive family history was an independent risk factor for nephrolithiasis that was not modified by increased fluid intake, suggesting that several different stone-forming phenotypes might exist. One phenotype is typified by patients in whom supersaturation-related spontaneous nucleation is the predominant mechanism of stone formation and is usually associated with low daily urine volumes and increased calcium ingestion;12.Kavanagh J.P. Calcium oxalate crystallization in vitro.in: Khan S.R. Calcium Oxalate in Biological Systems. CRC Press, Boca Raton, FL, USA1995Google Scholar water would be expected to be salutary in this group of patients. Another phenotype is characterized by specific alterations in renal tubule function, leading to increased calcium and oxalate excretion and may be less responsive to increased water intake. In the 1960s, it was recognized that living in a tropical climate13.Blacklock N.J. The pattern of urolithiasis in the Royal Navy.in: Nordin B.E.C. Hodgkinson A. Proceedings of the Renal Stone Research Symposium. Churchil, London, UK1969: 235Google Scholar or lacking access to water were associated with an increased risk of stone formation.14.Frank M. De Vries A. Atsmon A. et al.Epidemiological investigation of urolithiasis in Israel.J Urol. 1959; 81: 497-505Abstract Full Text PDF PubMed Scopus (40) Google Scholar Four key retrospective studies have addressed the use of water in the treatment of secondary nephrolithiasis (Table 3).15.Strauss A.L. Coe F.L. Deutsch L. et al.Factors that predict relapse of calcium nephrolithiasis during treatment: a prospective study.Am J Med. 1982; 72: 17-24Abstract Full Text PDF PubMed Scopus (87) Google Scholar, 16.Hosking D.H. Erickson S.B. Van den Berg C.J. et al.The stone clinic effect in patients with idiopathic calcium urolithiasis.J Urol. 1983; 130: 1115-1118Abstract Full Text PDF PubMed Scopus (160) Google Scholar, 17.Embon O.M. Rose G.A. Rosenbaum T. Chronic dehydration stone disease.Br J Urol. 1990; 66: 357-362Crossref PubMed Scopus (61) Google Scholar, 18.Daudon M. Hennequin C. Boujelben G. et al.Serial crystalluria determination and the risk of recurrence in calcium stone formers.Kidney Int. 2005; 67: 1934-1943Abstract Full Text Full Text PDF PubMed Scopus (103) Google Scholar Study sample sizes ranged from 108 to 256 patients and follow-up time ranged from 3.0 to 5.2 years. In each study, first-time stone formers were encouraged to drink more fluid, ranging from 1.9 to 3.0l/day. Upon follow-up, urine volumes were compared between those with and without stone recurrence. Baseline urine volumes were similar, but recurrent stone formers tended to have less daily increase in their urine output than individuals who had no recurrence (+0.25l vs. +0.50l, respectively), emphasizing the potential role of increased water intake in the prevention of stone recurrence.Table 3Secondary prevention studies of nephrolithiasisReferenceStudy designNumber of participantsAge at baseline (years)Years of follow-upWater prescription (l)Urine volume at baselineUrine volume at follow-upStone recurrence rate (%)Strauss15.Strauss A.L. Coe F.L. Deutsch L. et al.Factors that predict relapse of calcium nephrolithiasis during treatment: a prospective study.Am J Med. 1982; 72: 17-24Abstract Full Text PDF PubMed Scopus (87) Google ScholarRetrospective256434.3Drink 1Recurrence: 1.7No recurrence: 1.51.71.823.2Hosking16.Hosking D.H. Erickson S.B. Van den Berg C.J. et al.The stone clinic effect in patients with idiopathic calcium urolithiasis.J Urol. 1983; 130: 1115-1118Abstract Full Text PDF PubMed Scopus (160) Google ScholarRetrospective108Men: 49Women: 435.2V>2.5Recurrence: 1.6No recurrence: 1.61.72.142.2Daudon18.Daudon M. Hennequin C. Boujelben G. et al.Serial crystalluria determination and the risk of recurrence in calcium stone formers.Kidney Int. 2005; 67: 1934-1943Abstract Full Text Full Text PDF PubMed Scopus (103) Google ScholarRetrospective181Recurrence: 28No recurrence: 323.0V>2Recurrence: 1.4No recurrence: 1.61.72.139.8Embon17.Embon O.M. Rose G.A. Rosenbaum T. Chronic dehydration stone disease.Br J Urol. 1990; 66: 357-362Crossref PubMed Scopus (61) Google ScholarRetrospective98434.9V>3Recurrence: 1.4Overall: 1.72.02.47.1Borghi19.Borghi L. Meschi T. Amato F. et al.Urinary volume, water and recurrences in idiopathic calcium nephrolithiasis: a 5-year randomized prospective study.J Urol. 1996; 155: 839-843Abstract Full Text Full Text PDF PubMed Scopus (697) Google ScholarProspective199Water therapy: 40Control: 425.0V>2Fluid therapy: 1.1Control: 1.02.61.0Fluid therapy: 12.1Control: 27.0Sarica20.Sarica K. Inal Y. Erturhan S. et al.The effect of calcium channel blockers on stone regrowth and recurrence after shock wave lithotripsy.Urol Res. 2006; 34: 184-189Crossref PubMed Scopus (43) Google ScholarProspective70Water therapy: 31Control: 352.5V>2.5NANAFluid therapy: 8.3Control: 55.0Abbreviations: NA, not available; V, urine volume. Open table in a new tab Abbreviations: NA, not available; V, urine volume. In prospective studies, Borghi et al. randomized 199 patients with idiopathic calcium stones to either no intervention or to increased water intake sufficient to produce urine volumes of >2l/day. Significantly greater daily urine volumes were achieved in the treatment arm (2.6l vs. 1.0l in the controls, P<0.0001), accompanied by a significant lowering of the stone recurrence rate (12 vs. 27%, P=0.008).19.Borghi L. Meschi T. Amato F. et al.Urinary volume, water and recurrences in idiopathic calcium nephrolithiasis: a 5-year randomized prospective study.J Urol. 1996; 155: 839-843Abstract Full Text Full Text PDF PubMed Scopus (697) Google Scholar In 70 stone formers, Sarica et al.20.Sarica K. Inal Y. Erturhan S. et al.The effect of calcium channel blockers on stone regrowth and recurrence after shock wave lithotripsy.Urol Res. 2006; 34: 184-189Crossref PubMed Scopus (43) Google Scholar found that increasing fluid intake to a level sufficient to achieve daily urine volumes of >2.5l was associated with a lower recurrence rate compared with the group that did not increase water intake (increased water, 8.7%; placebo, 55.0%, P<0.05). Taken together four of the studies in which data are available show that the average follow-up urine volume in those with recurrent stones (1.8l/day) was consistently less than in those who passed no stones (2.1l/day). The real-world effectiveness of increased water intake outside of study environments remains uncertain. The retrospective studies16.Hosking D.H. Erickson S.B. Van den Berg C.J. et al.The stone clinic effect in patients with idiopathic calcium urolithiasis.J Urol. 1983; 130: 1115-1118Abstract Full Text PDF PubMed Scopus (160) Google Scholar, 17.Embon O.M. Rose G.A. Rosenbaum T. Chronic dehydration stone disease.Br J Urol. 1990; 66: 357-362Crossref PubMed Scopus (61) Google Scholar, 18.Daudon M. Hennequin C. Boujelben G. et al.Serial crystalluria determination and the risk of recurrence in calcium stone formers.Kidney Int. 2005; 67: 1934-1943Abstract Full Text Full Text PDF PubMed Scopus (103) Google Scholar showed that those who do not develop more stones drank ∼500ml more fluid than repeat stone formers. This suggests that at least some patients are able to maintain substantially increased water intake. However, only one study has specifically examined the issue of adherence utilizing pre- and post-study questionnaires.21.Fuss M. Simon J. Fontinoy N. et al.High fluid-low calcium intake: not all renal stone formers adhere to this simple treatment.Eur Urol. 1979; 5: 97-99PubMed Google Scholar Episodes of ‘dehydration’ (e.g., exposure to high ambient temperature or barriers at work to water drinking or to urination) were reported by nearly 50% of first-time stone formers. After the patients were counseled to increase water intake, the investigators found that 11% of patients were still unable to increase water intake; 35% of patients had daily urine volumes not greater than 2l; and 30% could drink sufficient water only during non-working hours. Consequently, adherence to an increased fluid intake prescription remains a problem. More fundamentally, this suggests the possibility that individuals who can adhere to therapy might differ in important ways from those who cannot (such as in adherence to other health-promoting behaviors), and, consequently, that the ability to adhere to therapy in such studies might confound the effects attributed solely to increased water intake. In summary, increased fluid intake has been shown to be effective in primary and secondary prevention in stone formation, but adherence to prescribed regimens has been suboptimal as many barriers are present. Insights into specific therapeutic recommendations are probably best derived from prospective studies. The prospective observational work of Curhan et al.9.Taylor E.N. Stampfer M.J. Curhan G.C. Dietary factors and the risk of incident kidney stones in men: new insights after 14 years of follow-up.J Am Soc Nephrol. 2004; 15: 3225-3232Crossref PubMed Scopus (361) Google Scholar,11.Curhan G.C. Willett W.C. Rimm E.B. et al.Family history and risk of kidney stones.J Am Soc Nephrol. 1997; 8: 1568-1573PubMed Google Scholar demonstrated that intake of >2.5l/day was associated with an ∼29% risk reduction in first stone occurrence, while Borghi et al.19.Borghi L. Meschi T. Amato F. et al.Urinary volume, water and recurrences in idiopathic calcium nephrolithiasis: a 5-year randomized prospective study.J Urol. 1996; 155: 839-843Abstract Full Text Full Text PDF PubMed Scopus (697) Google Scholar showed that fluid intake exceeding 2l/day reduced stone recurrence by ∼15%, providing a rational basis for a water ‘prescription’ in these settings. While pollakiuria and nocturia are nontrivial complications of increased water intake, there is no evidence so far suggesting that doing so would risk serious urological or other complications. It is not an uncommon practice for physicians to recommend a high fluid intake (3–4.5l/day) to individuals with kidney diseases22.Kunau R.T. Nephrology and Hypertension. Medical Knowledge Self-Assessment Program. 2nd edn. American College of Physicians, Philadelphia, PA, USA1998Google Scholar,23.Stefanski A. Ritz E. Amann K. Factors affecting progression of renal failure—experimental data.in: Kopple J.D. Massry S.G. Nutritional Management of Renal Disease. Williams & Wilkins, Baltimore, MD, USA1997: 277-316Google Scholar based on the following lines of evidence. Older studies in humans noted that urea clearance was significantly increased as urine flow doubled from 1–2ml/min (ref.24.Pitts R.E. Physiology of the Kidney and Body Fluids. 3rd edn. Yearbook Medical Publisher, 1974Google Scholar) and that blood urea nitrogen levels were lower in patients who, on average, drank more fluid.25.Anastasio P. Cirillo M. Spitali L. et al.Level of hydration and renal function in healthy humans.Kidney Int. 2001; 60: 748-756Abstract Full Text Full Text PDF PubMed Scopus (81) Google Scholar Moreover, glomerular filtration rate (GFR) measured by inulin clearance declined in humans experiencing severe dehydration.26.McCance R.A. Young W.F. Black D.A. The secretion of urine during dehydration and rehydration.J Physiol. 1944; 102: 415-428Crossref PubMed Scopus (13) Google Scholar Recent studies on vasopressin have rekindled interest in the possibility that increased water intake may ameliorate the progressive decline in GFR that occurs regularly with aging and at a more rapid pace in those with chronic, progressive renal diseases. Arginine vasopressin (AVP), a crucial peptide hormone that regulates water homeostasis, is recently suggested to contribute to CKD progression. In the rat model of 5/6 nephrectomy, increasing water intake, which decreases AVP, slowed the decline in GFR and reduced histological damage and protein excretion.27.Bouby N. Bachmann S. Bichet D. et al.Effect of water intake on the progression of chronic renal failure in the 5/6 nephrectomized rat.Am J Physiol. 1990; 258: F973-F979PubMed Google Scholar,28.Sugiura T. Yamauchi A. Kitamura H. et al.High water intake ameliorates tubulointerstitial injury in rats with subtotal nephrectomy: possible role of TGF-beta.Kidney Int. 1999; 55: 1800-1810Abstract Full Text Full Text PDF PubMed Scopus (56) Google Scholar Conversely, fluid restriction (which results in sustained high levels of AVP) accelerated CKD progression in the same animal model, an effect duplicated by AVP infusion.29.Bardoux P. Bichet D.G. Martin H. et al.Vasopressin increases urinary albumin excretion in rats and humans: involvement of V2 receptors and the renin-angiotensin system.Nephrol Dial Transplant. 2003; 18: 497-506Crossref PubMed Scopus (111) Google Scholar Several mechanisms of the deleterious effect of AVP on kidney were suggested (Figure 2). First, AVP induces glomerular hyperfiltration and hypertension via V2 receptor–mediated, enhanced urea recycling30.Bouby N. Ahloulay M. Nsegbe E. et al.Vasopressin increases glomerular filtration rate in conscious rats through its antidiuretic action.J Am Soc Nephrol. 1996; 7: 842-851PubMed Google Scholar, 31.Bardoux P. Martin H. Ahloulay M. et al.Vasopressin contributes to hyperfiltration, albuminuria, and renal hypertrophy in diabetes mellitus: study in vasopressin-deficient Brattleboro rats.Proc Natl Acad Sci USA. 1999; 96: 10397-10402Crossref PubMed Scopus (111) Google Scholar, 32.Zong H.Y. Wang K.R. Xie X.L. Effects of long-term fertilization on soil organic nitrogen components in paddy soil derived from red earth.[Ying yong sheng tai xue bao=The journal of applied ecology/Zhongguo sheng tai xue xue hui, Zhongguo ke xue yuan Shenyang ying yong sheng tai yan jiu suo zhu ban]. 2008; 19: 1721-1726PubMed Google Scholar and/or tubular sodium reabsorption,33.Perucca J. Bichet D.G. Bardoux P. et al.Sodium excretion in response to vasopressin and selective vasopressin receptor antagonists.J Am Soc Nephrol. 2008; 19: 1721-1731Crossref PubMed Scopus (82) Google Scholar,34.Bankir L. Bichet D.G. Bouby N. Vasopressin V2 receptors, ENaC, and sodium reabsorption: a risk factor for hypertension?.Am J Physiol Renal Physiol. 2010; 299: F917-F928Crossref PubMed Scopus (88) Google Scholar as well as partial V1a receptor-mediated vasoconstriction.33.Perucca J. Bichet D.G. Bardoux P. et al.Sodium excretion in response to vasopressin and selective vasopressin receptor antagonists.J Am Soc Nephrol. 2008; 19: 1721-1731Crossref PubMed Scopus (82) Google Scholar Second, AVP stimulates renin synthesis by the activation of V2 receptor,35.Schweda F. Klar J. Narumiya S. et al.Stimulation of renin release by prostaglandin E2 is mediated by EP2 and EP4 receptors in mouse kidneys.Am J Physiol Renal Physiol. 2004; 287: F427-F433Crossref PubMed Scopus (88) Google Scholar which is the first step in a well-characterized cascade of events leading to scar formation in the kidney.36.Ruster C. Wolf G. Renin-angiotensin-aldosterone system and progression of renal disease.J Am Soc Nephrol. 2006; 17: 2985-2991Crossref PubMed Scopus (340) Google Scholar Third, AVP exerts a direct effect on mesangial cell contraction and proliferation.37.Ganz M.B. Pekar S.K. Perfetto M.C. et al.Arginine vasopressin promotes growth of rat glomerular mesangial cells in culture.Am J Physiol. 1988; 255: F898-F906PubMed Google Scholar,38.Higashiyama M. Ishikawa S. 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• W2019019895 title "The medicinal use of water in renal disease" @default.
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