Impact of Solute Intake on Urine Flow and Water Excretion

Berl, Tomás

doi:10.1681/asn.2007091042

Cited by 144 publications

(101 citation statements)

References 12 publications

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“…Whereas increased plasma osmolality stimulates the release of arginine vasopressin, causing the kidney to retain water and decrease urine production, decreased plasma osmolality inhibits the excretion of vasopressin, causing the kidney to increase urine output (30,31). In addition to regulating fluid balance, the kidneys filter waste from the blood and require a minimum obligate urine volume to remove the solute load (31,32). Kidneys may function more efficiently in the presence of an abundant supply of water (33).…”

Section: Discussionmentioning

confidence: 99%

Urine Volume and Change in Estimated GFR in a Community-Based Cohort Study

Clark

Sontrop

Macnab

et al. 2011

Clinical Journal of the American Society of Nephrology

161

146

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SummaryBackground and objectives The effect of increased fluid intake on kidney function is unclear. This study evaluates the relationship between urine volume and renal decline over 6 years in a large community-based cohort.Design, setting, participants, & measurements This prospective cohort study was undertaken in Canada from 2002 to 2008. We obtained 24-hour urine samples from adult participants with an estimated GFR (eGFR) Ն60ml/min per 1.73 m 2 at study entry. Percentage annual change in eGFR from baseline was categorized as average decline Ͻ1% per year, between 1% and 4.9% (mild-to-moderate decline) or Ն5% (rapid decline).Results 2148 participants provided valid 24-hour urine samples, grouped as Ͻ1 L/d (14.5%); 1 to 1.9 L/d (51.5%); 2 to 2.9 L/d (26.3%); and Ն3 L/d (7.7%). Baseline eGFR for each category of urine volume was 90, 88, 84, and 87 ml/min per 1.73 m 2 , respectively. Overall, eGFR declined by 1% per year, with 10% demonstrating rapid decline and 40% demonstrating mild-to-moderate decline. An inverse, graded relationship was evident between urine volume and eGFR decline: For each increasing category of 24-hour urine volume, percentage annual eGFR decline was progressively slower, from 1.3%, 1.0%, 0.8%, to 0.5%, respectively; P ϭ 0.02. Compared with those with urine volume 1 to 1.9 L/d, those with urine volume Ն3 L/d were significantly less likely to demonstrate mild-to-moderate decline (adjusted odds ratio 0.66; 95% confidence interval 0.46 to 0.94) or rapid decline (adjusted odds ratio 0.46; 95% confidence interval 0.23 to 0.92); adjusted for age, gender, baseline eGFR, medication use for hypertension (including diuretics), proteinuria, diabetes, and cardiovascular disease. ConclusionsIn this community-based cohort, decline in kidney function was significantly slower in those with higher versus lower urine volume.

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Section: Discussionmentioning

confidence: 99%

Urine Volume and Change in Estimated GFR in a Community-Based Cohort Study

Clark

Sontrop

Macnab

et al. 2011

Clinical Journal of the American Society of Nephrology

161

146

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“…It does so by inducing a solute (urea) diuresis that, by increasing urine flow rate, decreases the concentration of sodium and potassium in the urine and hence increases excretion of electrolyte-free water (22). Although a recent study by Soupart and colleagues in 13 patients with SIADH found that urea was as effective in raising serum sodium levels and was as well tolerated as the vasopressin antagonist tolvaptan (23), in my experience and in informal surveys of practicing nephrologists in North America, urea is not widely used in North America, primarily because of limited availability.…”

Section: Ureamentioning

confidence: 99%

An Elderly Patient with Chronic Hyponatremia

Berl

2013

Clinical Journal of the American Society of Nephrology

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SummaryHyponatremia is the most common electrolyte disorder. With the aging of the population and the greater propensity of the elderly to develop hyponatremia, this electrolyte disorder is of increasing importance to the practicing nephrologist. In this Attending Rounds, an illustrative patient with hyponatremia is presented. The reasons for the increased incidence and prevalence of hyponatremia in the elderly are discussed, with emphasis on the effects of aging on urinary dilution, the frequently multifactorial nature of hyponatremia in this population, and the absence of a definite cause for inappropriate and persistent vasopressin release in many such patients. The rationale for treating the hyponatremia, even when apparently asymptomatic, is discussed, with attention to cognitive function, gait, and bone structure disturbances that increase the risk for fractures. The various available treatment approaches, including water restriction, demeclocycline, loop diuretics with NaCl supplementation, urea, and vasopressin antagonists are summarized, with emphasis on the efficacy and limitations of each of these therapies.Clin J Am Soc Nephrol 8: 469-475, 2013469-475, . doi: 10.2215 Case Description L.G. is a 73-year-old woman referred for management of chronic hyponatremia. She was known to have had hyponatremia for several years, with serum sodium levels in the range of 121-127 mEq/L. She has had four pulmonary bacterial infections during the last 7 years and was found to have radiologic evidence of bronchiectasis. She has also had several episodes of transient cerebral ischemia leading to numbness and weakness. In the last year she has had increased gait instability and sustained a fall that resulted in a pelvic fracture. She had no history of cardiac or liver disease. She has long-standing rheumatoid arthritis. Medications included omeprazole, 20 mg daily; conjugated estrogens (Premarin), 0.3 mg daily; folic acid, 0.4 mg three times daily; aspirin, 81 mg daily; and monthly vitamin B 12 injections. On physical examination she appeared to be a fragile elderly woman in no acute distress. BP was 148/78 mmHg, pulse rate was 98 beats/min, and she weighed 65 kg. She appeared to be euvolemic by examination. There were deformities of the proximal interphalangeal joints. Her neurologic examination revealed that she was fully oriented, with no focal findings, but she had an obvious gait disturbance that necessitated a walker for ambulation. Laboratory results were as follows: serum sodium, 124 mEq/L; chloride, 95 mEq/L; potassium, 4.1 mEq/L; bicarbonate, 22 mEq/L; creatinine, 0.7 mg/dl; glucose, 66 mg/dl; and uric acid, 3.8 mg/dl. Urinary sodium concentration was 75 mEq/L with a urine osmolality of 382 mOsm/kg. Result of a cosyntropin stimulation test was normal, with a baseline cortisol level of 9.2 mg/dl and a stimulated level of 18.7 mg/dl. Thyroid-stimulating hormone was normal at 3.29 mIU/L. Magnetic resonance imaging of the brain and pituitary revealed no significant abnormalities. DiscussionGiven the absence of liv...

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“…The maximal capacity to excrete a water load depends on appropriate osmolar excretion, complete suppression of AVP release, and intact renal diluting mechanisms to produce urine osmolalities as low as 60 mosm/kg H 2 O. To illustrate the important role of osmolar excretion, (38) Figure 3 shows that the excretion of 300 or 900 mosm in 60 mosm/kg H 2 O urine generates 4 L of solute-free water (in 5 L of urine) or 12 L of solute-free water (in 15 L of urine), respectively. Osmolar excretion, U osm , and urine volume are affected by gender and race.…”

Section: Relationship Between Osmolar Excretion Urine Osmolality Anmentioning

confidence: 99%

A Case for Water in the Treatment of Polycystic Kidney Disease

Torres¹,

Bankir²,

Grantham³

2009

Clinical Journal of the American Society of Nephrology

131

101

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Autosomal dominant polycystic disease (ADPKD) is an inherited disorder characterized by the development within renal tubules of innumerable cysts that progressively expand to cause renal insufficiency. Tubule cell proliferation and transepithelial fluid secretion combine to enlarge renal cysts, and 3-5-cyclic adenosine monophosphate (cAMP) stimulates that growth. The antidiuretic hormone, arginine vasopressin (AVP), operates continuously in ADPKD patients to stimulate the formation of cAMP, thereby contributing to cyst and kidney enlargement and renal dysfunction. Studies in animal models of ADPKD provide convincing evidence that blocking the action of AVP dramatically ameliorates the disease process. In the current analysis, the authors reason that increasing the amount of solute-free water drunk evenly throughout the day in patients with ADPKD and normal renal function will decrease plasma AVP concentrations and mitigate the action of cAMP on the renal cysts. Potential pitfalls of increasing fluid intake in ADPKD patients are considered, and suggestions for how physicians may prudently implement this therapy are offered.Clin J Am Soc Nephrol 4: 1140 -1150, 2009. doi: 10.2215/CJN.00790209 C onvergent findings in the last decade have established that 3Ј-5Ј-cyclic adenosine monophosphate (cAMP) stimulates mural epithelial cell proliferation and secretion of fluid into cysts of patients with autosomal dominant polycystic kidney disease (ADPKD), contributing to massive renal enlargement and dysfunction (1). AVP promotes cAMP production in the distal nephron and collecting ducts (CDs) by acting on AVP-V2 receptors (V2R). Preclinical evidence has shown in four different genetic models of polycystic kidney disease (PKD) that blocking the effect of AVP, thereby decreasing cAMP levels, slows cyst and renal enlargement and improves renal function (2-4).A novel treatment for ADPKD that targets AVP/cAMP is currently being evaluated in an international clinical trial (TEMPO NCT00428948). An inhibitor of V2R (tolvaptan) is administered to patients with the intent to diminish intracellular cAMP levels in cyst epithelial cells. V2R inhibition also diminishes the reabsorption of solute-free water in CDs, thereby causing partial nephrogenic diabetes insipidus and thirst. Daily urine volumes 5 d after starting different split doses of tolvaptan (15/15, 30/0, 30/15, 30/30 mg) in a preliminary phase 2 study were 4 to 6 L (5). This polyuria requires ingestion of enough water to maintain normal fluid balance, and TEMPO trial participants are instructed to drink enough to prevent or minimize thirst.Another way to decrease the effect of AVP on the kidney is to suppress its secretion by increasing fluid ingestion above what normal thirst would command. This strategy is hardly new, as a high fluid intake to dilute the urine likely is the oldest existing treatment in nephrology. Up to 3000 cc of water per day, drunk relatively evenly throughout waking hours and before going to bed, is frequently recommended to prevent urine supersaturatio...

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Impact of Solute Intake on Urine Flow and Water Excretion

Cited by 144 publications

References 12 publications

Urine Volume and Change in Estimated GFR in a Community-Based Cohort Study

Urine Volume and Change in Estimated GFR in a Community-Based Cohort Study

An Elderly Patient with Chronic Hyponatremia

A Case for Water in the Treatment of Polycystic Kidney Disease

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