October 22, 2020 | 10:00 AM - 12:00 PM
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- AKI Mechanisms - 3
October 22, 2020 | Location: On-Demand
Abstract Time: 10:00 AM - 12:00 PM
Category: Trainee Case Report
- 103 AKI: Mechanisms
- Salcedo Betancourt, Juan David, University of Miami School of Medicine, Miami, Florida, United States
- Carias martinez, Karla G., University of Miami School of Medicine, Miami, Florida, United States
- Venkat, Vasuki N., Miami VA Healthcare System, Miami, Florida, United States
- Soberon, Daniel J., Miami VA Healthcare System, Miami, Florida, United States
- LadinoAvellaneda, Marco A., Miami VA Healthcare System, Miami, Florida, United States
Juan David Salcedo Betancourt,
Karla G. Carias martinez,
Vasuki N. Venkat,
Daniel J. Soberon,
Marco A. LadinoAvellaneda,
In severe hypothyroidism, acute kidney injury (AKI) may occur from hypothyroidism-induced myopathy. We report the first case of AKI in the setting of severe bradycardia without rhabdomyolysis.
An 85-year-old man with heart failure and a dual-chamber implantable cardio defibrillator was admitted with bilateral lower extremity edema. Vital signs included asymptomatic bradycardia 40 bpm (Figure 1), blood pressure 107/74 mmHg, without fever or respiratory distress. Laboratories showed serum creatinine (SCr) of 2.3 mg/gL (baseline 1.5 mg/dL), serum sodium 127 mg/dL, serum creatine kinase (CPK) levels of 170 U/L (38-174 U/L), thyroid secreting hormone levels (TSH) of 97.77 uIU/L (0.45 – 4.70 uIU/mL) and free thyroxine levels (Free T4) of 1.4 ng/dL (0.71 – 1.85 ng/mL). Renal ultrasound was unremarkable. The pacemaker was programmed to VVI mode 60 bpm (ventricular pacing and sensing) with prompt improvement in the heart rate and renal function. He was discharged on oral levothyroxine.
Hypothyroidism increases systemic vascular resistance and decreases blood volume, cardiac contractility, and heart rate, with an overall decrease in cardiac output. AKI may occur from hypothyroidism-induced rhabdomyolysis; however, SCr is rarely elevated or may increase over several weeks. Our case contrasts given the acute rise in SCr and prompt recovery after the bradycardia resolved. We believe that the AKI was predominantly due to hypothyroidism-induced bradycardia, with a subsequent reduced cardiac output and effective renal flow. AKI workup should include hypothyroidism screening, particularly in the context of persistent bradycardia, even with normal blood pressure and CPK levels. We propose the term Thyroid-Cardio-Renal syndrome for this unusual association.