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When a Gap Leads to an Answer Abstract. We report the case of a 22-year-old patient who was found somnolent after previously complaining of nausea, abdominal pain, and vomiting. The main findings were high anion gap metabolic acidosis and lactatemia. Causative was the ingestion of ethylene glycol using a car antifreeze agent with suicidal intent.

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Record-Breaking Acidosis Abstract. To maintain a stable cellular metabolism, tight regulation of blood pH within a normal range (pH 7,35-7,45) is essential. Even small aberrations can have detrimental effects, and pH values <6,8 or pH >7,8 are considered - based on current medical and physiological knowledge - incompatible with life [9-19].

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Lactic Acidosis and Other Misunderstandings Abstract. Lactic acidosis is a frequently encountered clinical problem in intensive care medicine. Nevertheless, many of the underlying biochemical processes are insufficiently understood, which leads to various misconceptions. Physiologically, lactate is an important, continuously produced carrier of energy and by no means a metabolic 'waste product'. Lactate is the corresponding base to lactic acid and is produced directly from pyruvate. In this reaction H+ is consumed and therefore lactate production itself cannot be directly responsible for the simultaneously arising acidosis. An elevated lactate level allows no conclusions about the underlying pathophysiological process, and, more importantly, it is not an appropriate marker for tissue oxygenation.

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A Sweet Drink with Consequences Abstract. Intoxications with ethylene glycol are rare, however, small quantities from the substance can be life-threatening. Regarding the treatment it is important to recognize the intoxication quickly and to immediately start the appropriate treatment. Intoxications with ethylene glycol or with methanol should always be considered as differential diagnosis in patients with severe metabolic acidosis. It is also very important to calculate the osmolal gap.

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The Sour Patient Abstract. We report the case of a 75-year-old woman presenting with an elevated anion gap metabolic acidosis. The evaluation proved a 5-oxoprolin acidosis due to acetaminophen in therapeutic dose and concomitant risk factors such as malnutrition, chronic alcohol abuse, renal insufficiency, hepatopathy, and female sex. After stopping paracetamol medication and admission of bicarbonate and N-acetylcysteine, there was a rapid improvement in clinical symptoms and blood analysis.

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CME: Ethylene Glycol Intoxication Abstract. Ethylene glycol is a sweet-tasting alcohol used in common antifreeze and other industrial solutions. Without appropriate therapy, intoxication with ethylene glycol can result in severe metabolic acidosis, acute renal failure, and in death. After gastrointestinal resorption, hepatic metabolism starts with oxidation by alcohol dehydrogenase and results in severe anion gap metabolic acidosis. Other metabolic products are calcium oxalate crystals, which can deposit in several tissues like the kidneys and lead to acute tubular necrosis with reversible renal failure. The crucial therapeutic step is rapid inhibition of alcohol dehydrogenase with fomepizole or ethanol to avoid the formation of toxic metabolites. Additionally, haemodialysis is the most effective way to eliminate ethylene glycol as well as its toxic metabolites. If therapy is initiated rapidly, prognosis is favorable.

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The optimal diet for chronic kidney disease (CKD) is an issue frequently brought up by patients and/or their relatives during outpatient visits. For patients without malnutrition who are motivated and supported by an experienced multidisciplinary team, the optimal protein intake of 0,6 g/kg of ideal body weight/day is recommended to halt the progression of CKD. A calorie intake of 30 to 35 kcal/kg of ideal body weight/day is necessary to reduce the risk of malnutrition from a low protein diet and to maintain a neutral nitrogen balance. A low-salt diet, namely 5 to 6 g/d, is useful to optimize the treatment of hypertension associated with CKD and to limit fluid overload. At the advanced stage of CKD, it is also necessary to restrict the intake of phosphorus and sometimes potassium. Given the complexity of optimal renal diet, coordination between general practitioners, nephrologists and dietitians is essential to foster optimal care.

La diète optimale pour la maladie rénale chronique (MRC) est un thème fréquemment discuté par les patients en consultation ambulatoire et/ou par leurs proches. Une diète optimale en protéines, réduite à 0,6 g/kg de poids idéal par jour est proposée pour ralentir la progression de la MRC chez des patients non dénutris, motivés et supportés par une équipe multidisciplinaire et expérimentée. Un apport calorique de 30 à 35 kcal/j est nécessaire pour limiter le risque de dénutrition par une diète pauvre en protéines et pour maintenir une balance azotée neutre. Une diète pauvre en sel, soit 5 à 6 g/jour, est utile pour optimaliser le traitement de l'hypertension artérielle associée à la MRC et pour limiter la surcharge hydrosodée. Lorsque la MRC est avancée, il est nécessaire de limiter également l'apport en phosphore et parfois celui en potassium. Compte tenu de la complexité de la diète rénale optimale, une coordination entre les praticiens, les néphrologues et les diététicien(ne)s est indispensable pour favoriser la prise en charge.

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