Effect of furosemide on free water excretion in edematous patients with hyponatremia

Schrier, Robert W.; Lehman, David H.; Zacherle, Barry J.; Earley, Laurence E.

doi:10.1038/ki.1973.5

Cited by 55 publications

(12 citation statements)

References 18 publications

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“…In agreement with our results and results from others [3,16], furosemide clearly did not abolish the free-water clearance in the absence of ADH. In contrast, free-water reabsorption during antidiuresis was abolished by fu- Table III.…”

Section: Resultssupporting

confidence: 83%

“…Since the addition of chlo rothiazide rendered the urine isotonic at this early distal sampling site, it is very likely that reabsorption by the cortical DT was responsible for the lack of isotonicity during furosemide alone. Furthermore, the sudden fall in urine osmolality towards plasma values in man [38] and animals [22,23] indicates that the osmotic gradient be tween interstitium and tubular fluid has been abolished even when the experiments are performed under condi tions of maximal ADH output [16].…”

Section: Discussionmentioning

confidence: 99%

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Sodium Reabsorption by the Henle Loop in Humans

Bartoli¹,

Branca²,

Satta³

et al. 1987

Nephron

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In a previous study, we described a new method [3] to measure Na reabsorption by each segment of the human nephron independently. Reabsorption was expressed as equivalent volumes of solute-free water (CH₂O) generated by the loop of Henle (CH₂O-HL) and by the distal tubule (CH₂O-DT), and dissipated by back diffusion (BD) across collecting ducts (CH₂O-BD). These data were obtained during maximal water diuresis (MWD). The present study was undertaken to calculate CH₂O-HL by experiments performed during maximal antidiuresis (MA). For this purpose, a new theoretical approach was devised, described by algebraic equations which allowed calculations of segmental transport during MA alone, where only CH₂O-HL could be calculated independently. The study was performed on 14 normal volunteers who were studied twice by clearance measurements, firstly during MWD and again during MA. In each experiment, clearance periods were performed during baseline conditions and during the administration of furosemide (0.7 mg/kg bolus injection followed by 0.06 mg/kg/min maintenance infusion). From the values measured during either condition, segmental reabsorption was calculated. During MWD, CH₂O-HL averaged 19.4 +10.4, during MA 20.4 + 8.0 ml/min/GFR × 100; p > 0.05. The paired measurements were significantly correlated (r = 0.80; p < 0.01). These data demonstrate that CH₂O-HL obtained with the original theory is a reproducible result that can be confirmed with independent measurements obtained during different experimental conditions. Thus, measurements of segmental Na transport in the human nephron are feasible and can contribute important informations on disease states.

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Section: Resultssupporting

confidence: 83%

Section: Discussionmentioning

confidence: 99%

Sodium Reabsorption by the Henle Loop in Humans

Bartoli¹,

Branca²,

Satta³

et al. 1987

Nephron

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“…Therefore, in contrast to thiazides, they inhibit concentrating as well as diluting ability [5,7,38]. In fact, loop diuretics have been used successfully to increase water excretion and correct hyponatremia in edematous states and SIADH [8,44,45]. Second, in contrast to thiazides, these powerful diuretics have a short duration of action; therefore, they induce brief bursts of electrolyte excretion.…”

Section: Hyponatremia Caused By Loop Diureticsmentioning

confidence: 99%

“…However, it is important to resist the temptation to stop loop diuretics when hyponatremia develops in patients with heart failure (or other major edema-forming states). In these patients, induction of a negative salt and water balance is essential, and loop diuretics may actually increase water excretion [8,45]. Appropriate therapy includes water restriction and sometimes angiotensin-converting enzyme inhibitors [38,48].…”

Section: Hyponatremia Caused By Loop Diureticsmentioning

confidence: 99%

Diuretic-Induced Hyponatremia

Spital

1999

Am J Nephrol

119

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Diuretics are one of the most common causes of severe hyponatremia. Yet, despite several relevant studies and years of clinical experience, the mechanism and optimal treatment of diuretic-induced hyponatremia remain unclear. What is clear is that most cases are caused by thiazide rather than loop diuretics and that severe hyponatremia can develop very rapidly in susceptible patients. In this review, I will discuss the pathogenesis, clinical features, prevention, and treatment of diuretic-induced hyponatremia in the hope that increased awareness and understanding will reduce the incidence and complications of this potentially life-threatening syndrome.

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“…The condition of ECF volume expansion in the patients of group 2b, in fact, would have prevented the occurrence of hypovolemia and the resulting proximal tubular over reabsorption. Under such circumstances the proximal effect of the diuretic, by increasing the distal delivery of filtrate, would greatly blunt the inhibiting effect of the drug on free-water generation, as also hypothesized by other authors [10,15].…”

Section: Discussionmentioning

confidence: 60%

Effects of Furosemide Therapy on Free-Water Excretion in Uremic Patients

Conte

Fuiano

Sabbatini

et al. 1988

Nephron

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To assess the intrinsic effects of treatment with furosemide on free-water excretion in patients with chronic renal failure, two groups of patients with and without replacement of diuretic-induced salt losses have been studied. Furosemide therapy was administered for 1 week during constant sodium intake (100 mEq/day). In neither of the groups did furosemide cause hyponatremia, while it did decrease the urine to plasma osmolality ratio, an effect lasting even when the diuretic effect was exhausted. During water diuresis, furosemide decreased the fractional sodium reabsorption in diluting segments but not the absolute rate of the free-water generation (CH₂O). Presumably the expected decrease of CH₂O was masked by the increased distal delivery of tubular fluid mainly due to an additional effect of the diuretic on the proximal tubule. The hypotonicity of urine after furosemide treatment may be secondary to the dissipation of medullary hypertonicity, caused by furosemide, in the condition of decreased water permeability of the collecting duct due to uremic disease.

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Effect of furosemide on free water excretion in edematous patients with hyponatremia

Cited by 55 publications

References 18 publications

Sodium Reabsorption by the Henle Loop in Humans

Sodium Reabsorption by the Henle Loop in Humans

Diuretic-Induced Hyponatremia

Effects of Furosemide Therapy on Free-Water Excretion in Uremic Patients

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