Joel Michels Topf

Resumo Tradicionalmente, o manejo da doença renal crônica (DRC) tem enfatizado a restrição dietética de proteínas para retardar a progressão da doença e atrasar a doença renal em estágio terminal (DRET). No entanto, evidências de estudos clínicos questionam a suposta eficácia dessa abordagem e também destacam potenciais riscos, como desnutrição e redução da qualidade de vida. Esta revisão discute os fundamentos para a restrição proteica na DRC, apresenta críticas às evidências existentes e defende um cuidado personalizado que priorize a adequação nutricional e uma farmacoterapia eficaz. Avanços importantes no tratamento da DRC, incluindo inibidores da ECA, inibidores de SGLT2 e agonistas do receptor de GLP-1, são discutidos com o objetivo de propor uma estratégia abrangente que otimize os desfechos dos pacientes.

Chronic kidney disease (CKD) management has traditionally emphasized dietary protein restriction to slow disease progression and delay end-stage renal disease (ESRD). However, evidence from trials questions the supposed efficacy of this approach and also highlights potential risks such as malnutrition and reduced quality of life. This review discusses the rational for protein restriction in CKD, critiques the existing evidence, and advocates for personalized care that focuses on nutritional adequacy and effective pharmacotherapy. Important advances in CKD treatment, including ACE inhibitors, SGLT2 inhibitors, and GLP-1 receptor agonists, are discussed to propose a comprehensive strategy that optimizes patient outcomes.

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Sodium-glucose cotransporter-2 inhibitors (SGLT2i) reduce cardiovascular, kidney, and overall mortality. SGLT2i are also associated with a rare adverse event, euglycemic diabetic ketoacidosis (EDKA). This report describes a case of EDKA one day after bariatric surgery in a 51-year-old female with type 2 diabetes mellitus managed with the SGLT2i, canagliflozin. She was following a ketogenic diet for three weeks prior to surgery. The patient made a steady recovery with rapid anion gap closure followed by prolonged non-anion gap metabolic acidosis. Her medical record was tagged with a life-threatening reaction to SGLT2i. The risk of EDKA from SGLT2i may be increased by a low carbohydrate diet or postoperative status. Our case was complicated by hypokalemia, exemplifying the need for aggressive electrolyte management. Further guidance is needed to manage risk factors provoking EDKA and the use of SGLT2i therapy after an episode of EDKA.