Prevalence and outcomes of hypothyroidism-induced acute kidney injury.

Introduction: Hypothyroidism is an important reversible cause of acute kidney injury (AKI), acting through various mechanisms, including rhabdomyolysis, metabolic, and systemic effects.

Materials and methods: We screened all patients presenting with AKI for hypothyroidism, and suspected hypothyroid-induced AKI patients were followed up.

Results: The prevalence of hypothyroidism-induced AKI was 1.9%, with the commonest presenting symptom being pedal edema. The mean thyroid-stimulating hormone levels (mIU/L) and estimated glomerular filtration rate (eGFR) (mL/min/1.73m²) were 123.5 ± 22.32 and 29.4 ± 20.54, respectively, at presentation, and 3.28 ± 4.91 and 71.39 ± 40.28, respectively, at the end of 8 weeks. Creatine Phosphokinase (CPK) was significantly elevated in only 1 patient. One patient became dialysis-dependent (11.1%), 2 had partial renal recovery (22.2%), and 6 patients had complete renal recovery (66.7%). There was a significant positive correlation between renal recovery and CPK at admission, eGFR at admission, and hemoglobin, and a significant negative correlation with the presence of chronic kidney disease, urea at admission, and creatinine at admission.

Discussion: Thyroid hormones exert various effects on the kidney, and their imbalance can significantly alter renal function. Elevated creatinine with normal GFR can occur due to increased release of creatinine. Our study is the first published series of hypothyroid-associated AKI with follow-up data.
.