Abstract: SA-PO047
Hypothyroidism: A Known but Neglected Cause of AKI
Session Information
- AKI Clinical: Epidemiology and Outcomes
November 04, 2017 | Location: Hall H, Morial Convention Center
Abstract Time: 10:00 AM - 10:00 AM
Category: Acute Kidney Injury
- 003 AKI: Clinical and Translational
Authors
- Jha, Chandra Mauli, Gulf Diagnostic Center Hospital, Abu Dhabi, United Arab Emirates
- Dastoor, Hormaz Dara, Rahba Hospital, ABU DHABI, United Arab Emirates
- El shahat, Yassin, Burjeel Hospital, Abu Dhabi, United Arab Emirates, United Arab Emirates
- Khan, Sarah Hussain, Mafraq Hospital, Abu Dhabi, United Arab Emirates, United Arab Emirates
- Jabar, Ammar M, Burjeel Hospital, Abu Dhabi, United Arab Emirates, United Arab Emirates
Group or Team Name
- ADHARR
Background
Acute Kidney injury (AKI) of variable severity is common. Its recovery rests upon early diagnosis & specific intervention. We report a case of severe AKI due to hypothyroidism which recovered completely with the treatment of hypothyroidism. Literature review revealed that association of AKI with hypothyroidism has been recognized but standard textbooks on medicine, Endocrinology & Nephrology have failed to mention either AKI caused by hypothyroidism or hypothyroidism due to AKI.
Methods
A 26 year old Bangladeshi male electrician, smoker and occasional alcohol user, had symptoms of “not being well” & low back pain of one week duration. He had nonoligouric severe AKI (urea 6.3 mmol/L, creatinine 860 μmol/L, Creatinine clearance 5.02 ml/minute) without significant proteinuria (244 mg/day), normal electrolytes & normal ultrasonological study of Kidney, ureter and bladder. Moderately high CPK (1078 IU/L) without myoglobuniuria normalized within 72 hours but creatinine continued to rise. A history of weight gain & constipation of two months duration prompted us to check for thyroid function test. TSH was 590 miU/L, more than 140 times upper limit of normal. T3 & T4 were low. Thyroglobulin antibody & TSH receptor antibody were normal while microsomal antibody was elevated (326.8 KIU/L).
Results
Institution of levothyroxine therapy resulted in rapid decline of creatinine and symptomatic improvement of patient. His Creatinine clearance increased from 5.02 ml/minute to 49 ml/minute over two weeks and his creatinine level normalized over 4 weeks period. It saved the patient from kidney biopsy and dialysis.
Conclusion
We suggest that thyroid function test should always be part of investigation of AKI and renal function test should be part of investigation of hypothyroidism. Hypothyroidism should be included in the table of causes of AKI in standard textbooks.
High Creatinine and its response to Thyroxine treatment