Abstract: PO0112
Hypothyroidism-Induced AKI: A Case Series
Session Information
- AKI Clinical, Outcomes, and Trials - 2
October 22, 2020 | Location: On-Demand
Abstract Time: 10:00 AM - 12:00 PM
Category: Acute Kidney Injury
- 102 AKI: Clinical, Outcomes, and Trials
Authors
- Ramineni, Spoorthi, Dr. Pinnamaneni Siddhartha Institute of Medical Sciences & RF, Gannavaram, Andhra Pradesh, India
- Bandi, Varun kumar, Dr. Pinnamaneni Siddhartha Institute of Medical Sciences & RF, Gannavaram, Andhra Pradesh, India
Introduction
Thyroid hormones affect the development and various functions of the kidney. Such effects are partly mediated by direct renal action and partly by cardiovascular and systemic effects
Case Description
We present a series of 3 patients who presented with unexplained acute kidney injury (AKI). All patients were male, and one was hypertensive on amlodipine. Investigations showed blood urea levels ranging from 20 to 88 mg/dl, serum creatinine between 1.3 to 3.65 mg/dL with estimated glomerular filtration rate (eGFR) of 17.88 to 63.18 ml/min/1.73m2. Urine routine and ultrasound abdomen did not reveal any abnormalities. The patients had features suggestive of hypothyroidism and thyroid evaluation was done. Thyroid stimulating hormone (TSH) was elevated in all patients and T3 and T4 were decreased. The TSH levels ranged between 88.4 to 100 mIU/l. Creatine phosphokinase (CPK) level was modestly elevated in only one case, with absent urine myoglobin in all cases. A possibility of hypothyroidism induced AKI was considered and renal biopsy was deferred. After starting levothyroxine, complete renal recovery was seen in 2 patients and partial recovery in one within 8 weeks (Table 1).
Discussion
AKI has been reported in patients with severe hypothyroidism, and most cases were suspected to be due to rhabdomyolysis and had rapid normalization. Few cases of slower and incomplete recovery have been noted in cases with prolonged periods of severe hypothyroidism. In our series, normal urinalysis, absence of myoglobin, and normal or modest elevation of CPK makes rhabdomyolysis unlikely. The AKI could be due to hypothyroidism induced changes in renal hemodynamics. Our study relies on eGFR for renal function, and extent to which this reflects true changes in GFR is unclear. Hypothyroidism is a reversible cause of AKI and should be evaluated in cases with unexplained AKI. These patients can attain normal renal function with prompt initiation of levothyroxine therapy.
Characteristics of patients
| Case No | Age (years) | Urea-0 weeks (mg/dl) | Urea-8 weeks (mg/dl) | Creatinine-0 weeks (mg/dl) | Creatinine-8 weeks (mg/dl) | eGFR (ml/min/1.73m2)-0 weeks | eGFR (ml/min/1.73m2)-8 weeks | TSH (mIU/l)-0 weeks | TSH (mIU/l)-8 weeks |
| 1 | 53 | 88 | 40 | 3.65 | 1.5 | 17.88 | 49 | 100 | 0.92 |
| 2 | 51 | 20 | 17 | 1.3 | 1.0 | 69.62 | 86.76 | 94.83 | 1.28 |
| 3 | 37 | 45 | 30 | 1.7 | 1.0 | 50.40 | 95.72 | 88.4 | 16.10 |