Endocrine Abstracts

AKI is a potentially a life threatening condition and it is extremely crucial to investigate the root cause it order to manage the patient appropriately.

Case report

A 30 years old female presented with complaints of generalized muscle weakness, lethargy and mood changes. She was found to have raised creatinine with significant drop in her GFR to 41. Rest of her electrolytes and full blood count were within normal range. She was commenced on Intravenous fluids with strict input/output monitoring. No obvious trigger for her decline in renal function could be found. In order to find the cause for renal deterioration and in view of her clinical presentation, thyroid function tests and creatinine Kinase was done subsequently. Her blood tests revealed TSH >100 mU/l with T4 <1.0 pmol/l. Creatnine Kinase was minimally raised around 322 u/l. Provisional impression of hypothyroidism induced myopathy and AKI was made. She was treated with levothyroxine 100 µg. Her Thyroid peroxidase AB -TPO (303 IU/ml) was positive. Rest of the renal investigations were normal. Renal team were in agreement of concluding that acute kidney injury was perhaps due to severe undiagnosed Autoimmune hypothyroidism. Following adequate rehydration and after commencing thyroxine, she improved significantly both clinically and biochemically. Her creatinine gradually decreased over time with reciprocal improvement in her GFR.

Discussion

Hypothyroidism causing acute kidney injury is a very rare presentation. The exact mechanism for kidney failure still remains unknown. It has been postulated that absence of thyroid hormone alters mitochondrial oxidation and reduces glycogenolysis resulting in muscular atrophy leading to decreased number of fast-twitching (Type 2 fibers) Subsequently, increased deposition of glycosaminoglycan and hypertrophy of slow muscle fiber occurs causing myopathy and increased fatigue. It has also been proposed that T4 deficiency alters muscle permeability resulting in release of muscle enzymes, known as creatnine kinase. Its accumulation, known as rhabomyolysis is a well-known attribute of AKI. Some studies have shown effect of Thyroid hormone on renal perfusion (Renal plasma flow) which can subsequently alter GFR and affect kidney function. It is also noteworthy that majority of the rare cases reported demonstrates rhabdomyolysis as major cause of AKI in Hypothyroidism. However, in our case, patient had minimally raised levels of CK and was found to be in AKI. This is the first case to be reported that doesn’t meet the criteria for rhabomyolysis in presence of AKI.