Role of alcohol in clinical nephrology

Heidland, A.; Hörl, Walter H.; Schaefer, R. M.; Teschner, Matthias; Weipert, J.; E, Heidbreder

doi:10.1007/bf01738150

Cited by 11 publications

(10 citation statements)

References 107 publications

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“…After ethanol administration, ethanol and its metabolites go through kidneys and are excreted into urine, and its content in the urine is higher than that of the blood and the liver. The kidney is often involved in the development, maintenance and counter regulation of complex electrolyte disturbances (1). Some studies suggest that chronic ethanol ingestion per se is not nephrotoxic (2).…”

Section: Introductionmentioning

confidence: 99%

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Effects of chronic ethanol exposure on renal function tests and oxidative stress in kidney

Das

Varadhan

Dhanya

et al. 2008

Indian J Clin Biochem

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After administration, ethanol and its metabolites go through the kidneys and are excreted into urine. The kidney seems to be the only vital organ generally spared in chronic alcoholics. Therefore, we investigated the multiple effects of chronic ethanol exposure on renal function tests and on oxidative stress related parameters in the kidney. Chronic ethanol (1.6 g ethanol/ kg body weight/ day) exposure did not show any significant change in relative weight (g/ 100g body weight) of kidneys, serum calcium level or glutathione s-transferase activity. However, urea and creatinine concentration in serum, and TBARS level in kidney elevated significantly, while reduced glutathione content and activities of glutathione peroxidase, glutathione reductase and superoxide dismutase diminished significantly after 12 weeks of ethanol exposure. Catalase activity showed increased activity after 4 weeks of ethanol exposure and decreased activity after 12 weeks of ethanol exposure. Genesis of renal ultrastructural abnormalities after 12 weeks of ethanol exposure may be important for the development of functional disturbances. This study revealed that chronic ethanol exposure for longer duration is associated with deleterious effects in the kidney.

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Section: Introductionmentioning

confidence: 99%

“…The kidney seems to be the only vital organ generally spared in chronic alcoholics without advanced alcoholic liver disease or hepato-renal syndrome. But, regular alcohol consumption raises the blood pressure, which per se is a risk factor for renal damage (1). Large amounts of ethanol have deleterious effects on the kidney (3).…”

Section: Introductionmentioning

confidence: 99%

Effects of chronic ethanol exposure on renal function tests and oxidative stress in kidney

Das

Varadhan

Dhanya

et al. 2008

Indian J Clin Biochem

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“…Fibre size and muscle mass is reversible upon abstinence. 9. Strength is improved upon abstinence but in some subjects full muscle strength is not attained despite 5 years abstinence.…”

Section: Respiratory Complications Of Alcohol Misusementioning

confidence: 95%

“…Some have argued that alcohol misuse may increase the risk of at least 120-200 disease entities of varying severity. These diseases can be categorised into the following: hepatobiliary and pancreatic [3,4]; gastrointestinal [5]; nervous system [6,7]; cardiovascular [8]; nephrological [9]; musculoskeletal [10]; respiratory [11]; genitourinary and reproductive [12,13]; haematological [14]; endocrine and metabolic [15]; and dermatological systems. This is a broad analysis and sub-classifications reveal specific disease entities or conditions that are highlighted below in Tables I and II.…”

Section: Systems Affected By Alcohol Misusementioning

confidence: 99%

Alcohol as a toxic and disease‐forming agent: Not just the liver and brain and not every drinker

Srirajaskanthan

Preedy

2007

Journal of Nutritional & Environmental Medicine

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Purpose: Excessive alcohol, defined as beyond the limits suggested by various government and statutory bodies, is damaging. This article aims to show that there may be as many as 120-200 adverse medical conditions and pathologies associated with alcohol misuse. Design and method: This review examines the different organ systems within the body and the effect of alcohol on nutrition, bone, skin, the gastrointestinal tract and skeletal muscle. Results: We identified that nearly all organ systems have the potential to be affected by alcohol or its ensuing metabolite acetaldehyde; as a result, the presence of two or more pathologies or conditions in alcohol misusers is not unusual. However, there are genetic factors that make individuals more susceptible to developing alcoholism and alcohol-related disease. These include genes for acetaldehyde formation and oxidation and possibly some neurotransmitters such as GABA, dopamine and 5-HT. For example, in simple terms, subjects with the dysfunctional ALDH2*2 allele which oxidises acetaldehyde less effectively than those with the ALDH2*1 allele generate high concentrations of acetaldehyde. This acts as a deterrent to alcoholism as acetaldehyde produces nausea and adverse cardiovascular symptoms. At the same time those with the ALDH2*2 allele who do consume alcohol have poorer outcome measures than those with the ALDH2*1 allele, due to the cytotoxic effects of acetaldehyde. Conclusions: Excessive ethanol consumption can lead to development of disease in many different organs, through its direct effect and also its toxic metabolites. However, not all individuals are susceptible and there are likely to be genetic as well as environmental factors that increase individuals' predisposition to develop alcohol related co-morbidity.Abbreviations: ADH: alcohol dehydrogenase, ALDH: aldehyde dehydrogenase, GABA: caminobutyric acid, 5-HT: serotonin

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“…However, apart from reports about the importance of alcoholism as a cause of IgA nephropathy [2] or reversible proximal tubular dys function [3], alcoholism seems to be a predisposing factor for acute renal failure since there is a coincidence of chronic alcoholism and acute myoglobinuric renal fail ure from rhabdomyolysis [4], Furthermore, in animal experiments, alcohol pretreatment worsened the course of glycerol-induced ARF [5] and it has been demonstra ted that the kidney exposed to chronic ethanol-intake is more susceptible to an ischemic insult [6], Since it is well established, that chronic ethanol-intake is a catabolic event, as shown in animal experiments by enhanced urea production in ethanol-fed rats [7,8] and in the clinical setting by the characteristic skeletal muscle wasting of the alcoholic patient [9,10], chronic ethanol intake may represent a risk factor for enhanced catabo lism in ARF, a metabolic complication which predomi nantly influences the outcome of the illness [II]. In fact, patients with acute renal failure (ARF) can sustain mas sive net protein degradation; especially those suffering from underlying illnesses like septicemia [12].…”

Section: Introductionmentioning

confidence: 99%

Chronic Ethanol Ingestion Enhances Catabolism and Muscle Protease Activity in Acutely Uremic Rats

Teschner¹,

Schaefer²,

Weißinger³

et al. 1988

Nephron

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Skeletal muscle wasting in men as well as enhanced urea production in animals due to ethanol consumption has been demonstrated by numerous authors. Furthermore, the outcome of acute renal failure is closely related to the extent of catabolism. The present study was performed to investigate whether chronic ethanol exposition prior to binephrectomy (BN) may represent a predisposing factor for enhanced protein breakdown. Rats underwent BN after exposure to ethanol or isocaloric substrate for 4 weeks. Blood chemistries and muscle samples were obtained 48 h after BN. Animals fed with ethanol revealed significantly higher levels of serum urea nitrogen (SUN) and urea nitrogen appearance (UNA) in comparison to controls. Preconditioning on ethanol-derived calories induced an accelerated fractional degradation rate of myofibrillar protein as demonstrated by a significantly enhanced serum N^t-methylhistidine/creatinine ratio. The increase in serum indicators of enhanced myofibrillar breakdown correlated with the stimulated activities of alkaline myofibrillar protease and cathepsin B. Finally, serum corticosterone levels were enhanced in the experimental group in comparison to controls, indicating an ethanol-related adrenocortical stimulation to be a possible mediating factor of enhanced catabolism in ARF. Thus, chronic ethanol intake prior to the onset of ARF seems to be a risk factor for enhanced catabolism in the course of acute uremia.

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Role of alcohol in clinical nephrology

Cited by 11 publications

References 107 publications

Effects of chronic ethanol exposure on renal function tests and oxidative stress in kidney

Effects of chronic ethanol exposure on renal function tests and oxidative stress in kidney

Alcohol as a toxic and disease‐forming agent: Not just the liver and brain and not every drinker

Chronic Ethanol Ingestion Enhances Catabolism and Muscle Protease Activity in Acutely Uremic Rats

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