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Mécanismes et prise en charge de la tubulopathie liée à la rhabdomyolyse

Kidney injury after rhabdomyolysis: What is new?

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Médecine Intensive Réanimation

Résumé

La tubulopathie liée à la rhabdomyolyse est une variété peu fréquente (≈ 10 %) d’insuffisance rénale aiguë (IRA), mais elle est identifiée chez 13 à 50 % des patients présentant une rhabdomyolyse. Toutes les causes de rhabdomyolyse peuvent s’accompagner d’une IRA. Plusieurs mécanismes lésionnels concourent à la toxicité rénale de la myoglobine relarguée par le muscle lésé : une hypovolémie, une vasoconstriction locale, une agression tubulaire proximale, une obstruction tubulaire distale, le recrutement des macrophages notamment, exerçant des effets pro-inflammatoire à court terme et profibrosant à long terme. En pratique, une élévation des enzymes musculaires (créatine-kinase > 5 000 UI/l) permet le diagnostic. La présentation clinique est celle d’une IRA de profil tubulaire, avec un risque élevé d’hyperkaliémie menaçante. La prise en charge consiste en une réhydratation essentielle par sérum salé et une épuration extrarénale (EER) rapide, dont les indications reposent sur la kaliémie et le degré d’acidose métabolique. Les caractéristiques de l’hémodialyse intermittente en font la technique de choix. Ni l’alcalinisation des urines ni le recours à une EER prophylactique, en particulier avec une membrane à haute perméabilité, n’ont démontré de supériorité sur le pronostic rénal à long terme. Le pronostic global est étroitement lié à la cause de la rhabdomyolyse, la mortalité passant de 22 à 59%en présence d’IRA. Le pronostic rénal tardif est inconnu chez l’homme, mais se révèle péjoratif chez l’animal qui développe une fibrose rénale infraclinique après rhabdomyolyse. Une évaluation néphrologique systématique doit donc être proposée aux patients à distance d’une rhabdomyolyse, afin de dépister une maladie rénale chronique débutante.

Abstract

Severe damage of skeletal muscle, referred to as rhabdomyolysis, is the cause of 10% of acute kidney injury (AKI) cases and AKI complicates 13–50% of traumatic or nontraumatic rhabdomyolysis. Hypovolemia and the direct nephrotoxic effect of myoglobin are thought to be the main factors involved in rhabdomyolysis-induced AKI. Myoglobin promotes kidney injuries through vasoconstrictive properties, proximal tubular injuries, and distal obstruction. Recently, we demonstrated that macrophages influence the long-term prognosis of this disease by exerting proinflammatory as well as profibrotic properties. Clinical management relies on early diagnosis (creatine kinase > 5,000 UI/l) and fluid resuscitation using isotonic sodium chloride. Despite optimal rehydration, patients can develop AKI and require renal replacement therapy (RRT). Severe hyperkalemia or metabolic acidosis is the main cause of RRT. Thus, intermittent hemodialysis rather than continuous RRT should be used as frontline RRT, if available. To date, alkalinization, as well as prophylactic intermittent hemodialysis with high cut-off membrane, did not demonstrate superiority on long-term renal function compared to conventional approach. While global prognosis is depending upon the cause of rhabdomyolysis, mortality increases from 22% to 59% as soon as patients develop AKI. Long-term prognosis is unknown. Animal models demonstrated that rhabdomyolysis can lead to renal fibrosis after several months of followup. This suggests that patients with rhabdomyolysis should be considered as at high risk to develop chronic kidney disease and therefore referred to nephrologists to minimize long-term consequences of chronic kidney disease.

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Belliere, J., Chauveau, D., Bascands, JL. et al. Mécanismes et prise en charge de la tubulopathie liée à la rhabdomyolyse. Méd. Intensive Réa 25, 557–569 (2016). https://doi.org/10.1007/s13546-016-1229-9

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