AZEVEDO, A.

CRUZ, S.

CUNHA, L.

CUNHA, T.

FERREIRA, J.

OLIVEIRA, A.

RODRIGUES, B.

SILVA, B.

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S. CRUZ, B. SILVA, A. OLIVEIRA, T. CUNHA, L. CUNHA, J. FERREIRA, B. RODRIGUES, A. AZEVEDO Hospital de Vila Franca de Xira, PortugalSevere hyperchloremic metabolic acidosis with SGLT2 inhibitors in patients with urinary diversionRESULTSINTRODUCTION AIM Gold standard in urinary tract diseases. Correlation between the use of SGTL2 inhibitors and severe hyperchloremic metabolic acidosis in patients with bowel conduit.METHOD Consultation of medical records.URINARY DIVERSION WITH AUTOLOGOUS INTESTINAL SEGMENTS SGLT2 INHIBITORS Most frequent metabolic abnormality is hyperchloremic metabolic acidosis, due to ammonium absorption alongside chloride gain and bicarbonate excretion in the bowel conduit, as well as volume depletion due to reduced sodium absorption in the gout.  Antihyperglycemic agents;  Recently revolutionized the paradigm of chronic kidney disease. Block the SGLT2 proteins in the renal proximal convoluted tubules and the reabsorption of filtered glucose, promoting a greater urinary glucose excretion. Figure adapted from (2).Routine arterial blood gas (ABG)2018 February 2022pH 7.45 7.25pCO2 (mmHg) 28 27.5pO2 (mmHg) 81 75HCO3- (mmol/L) 19.3 12Na+ (mmol/L) 134 143K+ (mmol/L) 3.25 3.74Cl- (mmol/L) 107 122Lactate (mmol/L) 0.75 0.69Anion gap (AG) (mmol/L) 7.7 9Glucose (mg/dL) 135 26162-year-old Medical history: orthotopic neobladder since 2005 (malignancy), type 2 diabetes, nonspecific interstitial pneumonia Pulmonology appointmentAggravated hyperchloremic metabolic acidosisAsymptomatic Normal vital signs No major signs Blood workup: urea 81 mg/dL, creatinine 1.6 mg/dL Ketone bodies: negative OBSERVATION OTHER RESULTSSGLT2 inhibitor withdrawn Supportive treatment (bicarbonate, hydration, …)Metabolic normalization and dischargeCyclophosphamide (5 cycles) 10 months prior Empagliflozin 10mg id (add on to metformin 1000mg id 7 months prior … … Emergency department63-year-old Medical history: ileal conduit since 2018 (malignancy), type 2 diabetes, chronic kidney disease (serum creatinine 1.5-2 mg/dL) 10 months prior Empagliflozin 10mg id (add on to vildagliptin/metformin 50/1000mg bid) 3-day history of lethargy and anorexiaEmergency departmentABG September 2022pH 6.98pCO2 (mmHg) 20.5pO2 (mmHg) 124.4HCO3- (mmol/L) 4.7Na+ (mmol/L) 129K+ (mmol/L) 3.54Cl- (mmol/L) 120Lactate (mmol/L) 0.5AG (mmol/L) 4.3Glucose (mg/dL) 200EXAMSSevere hyperchloremic metabolic acidosisLethargy, glasgow coma scale 15 Normal vital signs No other major signs OBSERVATIONBlood workup: urea 209 mg/dL, creatinine 2.8 mg/dL Ketone bodies: negative Head and abdominopelvic computed tomography without acute complications Intensive care unitCONCLUSIONS Chronic hyperchloremic metabolic acidosis is a frequent and known complication of urinary diversion, due to the reabsorption of urinary solutes by the intestinal mucosa.Euglycemic ketoacidosis and metformin-associated lactic acidosis were ruled out.The acute kidney injury presented was mild compared to the grade of metabolic exacerbation.Regarding the cases reported:SGLT2 inhibitors may exacerbate the chronic hyperchloremic metabolic acidosis by increasing urinary sodium and glucose excretion (volume depletion) and posterior re-uptake through the intestinal conduit, leading to hyperglycemia.First two cases reported of severe hyperchloremic metabolic acidosis in this setting.Further studies are needed to establish the exact underlying physiopathology.Hypotesis:REFERENCES 1. Sperling C, Lee D, Aggarwal S, Urinary Diversion: Core Curriculum 2021. Am J Kidney Dis. 78(2):293-304; 2. Thomson SC, Vallon V. Renal Effects of Sodium-Glucose Co-Transporter Inhibitors. Am J Cardiol. 2019 Dec 15;124 Suppl 1(Suppl 1):S28-S35.! CONTACT INFORMATION ana.c.azevedo@hvfx.min-saude.ptCASE 1 CASE 2 

Severe hyperchloremic metabolic acidosis with SGLT2 inhibitors in patients with urinary diversion

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Severe hyperchloremic metabolic acidosis with SGLT2 inhibitors in patients with urinary diversion

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