Ethanol-Induced Water Diuresis: One of a Spectrum of Renal Defects Resulting from Ethanol Toxicity

Marchi, Sergio De; Cecchin, E

doi:10.1159/000183729

Cited by 5 publications

(3 citation statements)

References 4 publications

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“…Furthermore, subclinically impaired renal function may contribute to hypervolemia in our long-term abstinent alcoholics. In fact, tubular dysfunction has been demonstrated for 30 -40% of alcoholics during the first weeks of abstinence (Angeli et al, 1991;De Marchi and Cecchin, 1986a;De Marchi et al, 1993;Martines et al, 1989;Sadler et al, 1995;Tang, 1991;Vamvakas et al, 1998), together with morphological alterations of the kidneys (Sadler et al, 1995). That these renal alterations might partly persist is supported by the increased NT-pro-ANP, known to be high in renal dysfunction (Sundsfjord et al, 1988), and by the decreased creatinine clearance over the entire study period as compared with controls.…”

Section: Discussionmentioning

confidence: 96%

“…At 5 days and as late as 3 months of abstinence, an oral water load test resulted in an increased urinary volume of alcoholics as compared with controls (Ogata, 1963). In addition, renal dysfunction seems to be common during alcohol withdrawal (Angeli et al, 1991;De Marchi and Cecchin, 1986a;De Marchi et al, 1993;Labib et al, 1989;Martines et al, 1989;Tang, 1991). Renal weight and glomerular diameter were found to be greater in alcoholics than in controls (Sadler et al, 1995).…”

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confidence: 98%

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Persistent Alterations of Vasopressin and N‐Terminal Proatrial Natriuretic Peptide Plasma Levels in Long‐Term Abstinent Alcoholics

Döring

Herzenstiel

Krampe

et al. 2003

Alcoholism Clin & Exp Res

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Chronic alcohol abuse causes severe and persistent alterations in the hormonal regulatory systems of electrolyte and water balance. The suppressed basal secretion of AVP may reflect a dysregulation in the brain that influences the hypothalamic-pituitary-adrenal axis function, mood, memory, addiction behavior, and craving during alcohol abstinence. These findings may provide a ground for future therapeutic approaches to stable abstinence.

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Section: Discussionmentioning

confidence: 96%

mentioning

confidence: 98%

Persistent Alterations of Vasopressin and N‐Terminal Proatrial Natriuretic Peptide Plasma Levels in Long‐Term Abstinent Alcoholics

Döring

Herzenstiel

Krampe

et al. 2003

Alcoholism Clin & Exp Res

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“…51 Acute renal failure following binge drinking Binge drinking of ethanol is frequently associated with volume depletion due to water diuresis induced by inhibition of the release of antidiuretic hormone by alcohol, as well as from decreased sensitivity of the collecting tubules to antidiuretic hormone. 52,53 In consumers of large quantities of beer with low total solute intake, the reduced renal sensitivity to vasopressin may be due, at least in part, to a decrease in the medullary solute gradient secondary to the prolonged and severe ingestion of hypotonic fluids. The use of nonsteroidal anti-inflammatory drugs (NSAIDs) while in such a state may precipitate renal functional deterioration by interfering with renal autoregulatory mechanisms.…”

Section: Acute Renal Failure and Methanol/ethylene Glycol Poisoningmentioning

confidence: 99%

Alcohol misuse and renal damage

Cecchin¹,

Marchi²

1996

Addiction Biology

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Recent clinical and experimental studies have demonstrated that the habitual consumption of large amounts of ethanol has deleterious effects on the kidney. A variety of tubular defects have been described in patients with chronic alcoholism. Evidence is emerging that tubular dysfunction has an important pathophysiological role in a wide range of electrolyte and acid-base disturbances commonly observed in these patients, and possibly in alcohol-induced bone disease. These renal abnormalities are often reversible, disappearing with abstinence. However, since 1990 a few cases of a syndrome of acute tubular necrosis due to binge drinking of ethanol in the absence of other evident nephrotoxic mechanisms, or in association with the use of nonsteroidal anti-inflammatory drugs, have been reported. A link between glomerulonephritis and alcoholism has become evident. IgA nephropathy has been demonstrated at autopsy in 64% of chronic alcoholics and, more recently, the association between alcoholism and postinfectious glomerulonephritis has been described. Structural and functional abnormalities of the kidney are reported with increasing frequency in the fetal alcohol syndrome seen in children who have been prenatally exposed to ethanol. In addition, over the last few years experimental studies in vitro or in animal models have provided information about the biochemical and molecular basis of alcohol-induced injury to kidney. It is hoped that future experimental and clinical research will provide us with a more comprehensive knowledge of the mechanisms of renal damage in alcohol misuse.

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Somnolence, hypotension, and metabolic acidosis following high-dose teniposide treatment in children with leukemia

McLeod

Baker

Pui

et al. 1991

Cancer Chemother. Pharmacol.

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This report describes an unexpected adverse effect in three children receiving teniposide at 3-5 times the conventional dosage (i.e. 200 mg/m2) plus cytarabine as part of continuation therapy for acute lymphocytic leukemia. Pharmacokinetic studies in each patient had demonstrated high teniposide clearances, and thus the increased dosage requirements were necessary to attain plasma concentrations similar to those expected for patients with average drug clearance. At 3-4 h after the beginning of the 4-h simultaneous infusions of teniposide and cytarabine, these patients experienced somnolence, hypotension, and metabolic acidosis. The adverse events were associated with elevated teniposide plasma concentrations during the infusions compared with those in patients receiving similar doses without toxicity, and clinically significant ethanol concentrations, presumably from the teniposide formulation. Blood concentrations of cremophor and histamine, which are also constituents of the teniposide formulation, were not measured. In addition, concomitant therapy with antiemetic agents in patients who may have been mildly volume-depleted due to emesis may also play a contributory role. Prolonging the infusion time for patients receiving teniposide doses above 500 mg/m2 will avoid excessive teniposide and ethanol plasma concentrations and minimize the risk of this potentially serious side effect.

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Ethanol-Induced Water Diuresis: One of a Spectrum of Renal Defects Resulting from Ethanol Toxicity

Cited by 5 publications

References 4 publications

Persistent Alterations of Vasopressin and N‐Terminal Proatrial Natriuretic Peptide Plasma Levels in Long‐Term Abstinent Alcoholics

Persistent Alterations of Vasopressin and N‐Terminal Proatrial Natriuretic Peptide Plasma Levels in Long‐Term Abstinent Alcoholics

Alcohol misuse and renal damage

Somnolence, hypotension, and metabolic acidosis following high-dose teniposide treatment in children with leukemia

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