We present a 34-year-old Emirati gentleman who presented with multiple episodes of hypokalemic periodic paralysis. Blood test revealed thyrotoxic state, with highly positive serology for thyroid peroxidase, anti-thyroglobulin and thyrotropin receptor antibodies. Thyroid uptake scan confirmed homogenous diffuse uptake consistent with toxic diffuse goitre [Graves’ disease]. In view of recent fracture, bone profile and DXA scan were done. Investigations revealed vitamin D deficiency and below expected for age bone mass density.
The patient was started on symptomatic treatment with propranolol, IV and oral potassium along with IVF hydration. Routine blood work during admission showed a persistent normal anion Gap metabolic acidosis, serum bicarb 15 mmol/l. 24 hours urine electrolytes revealed normal potassium, sodium, high magnesium, low calcium and PH levels. Biochemical lab results suggested type 1 renal tubular acidosis. As the patient had hypokalaemia, high urine magnesium and low urine calcium and limbs weakness, Gitleman Syndrome was considered in the differential diagnosis. Whole Exome Sequencing (CentoXome GOLD®) was sent which came back negative. The following gene panels were studied: Renal tubular acidosis panel: ATP6V0A4, ATP6V1B1, CA2, EHHADH, HNF4A, SLC34A1, SLC4A1, SLC4A4. Bartter Syndrome panel: ATP6V1B1, BSND, CA2, CASR, CLCNKA, CLCNKB, CLDN16, CLDN19, FXYD2, HSD11B2,KCNJ1, KCNJ10, KLHL3, NR3C2, SCNN1A, SCNN1B, SCNN1G, SLC12A1, SLC12A2, SLC12A3, SLC4A1, SLC4A4, WNK1. Gene related to Gitelman syndrome: SLC12A3
Renal tubular acidosis was treated with KCL 600mg PO TID, Na bicarb 1200mg PO BID and spironolactone 25 mg PO OD. The patient received radioactive iodine (RAI) as the ultimate treatment for Graves’ disease. He developed hypothyroidism post RAI ablation and commenced on levothyroxine. Improvement of the metabolic acidosis was noticed in line with improvement of thyroid function. Na bicarb and spironolactone tablets were stopped eventually as the patient was euthyroid clinically and biochemically.
Overt hyperthyroidism is associated with accelerated bone remodelling, leading to hypercalciuria, which can predispose to nephrocalcinosis and renal tubular damage, and therefore causes type 1 renal tubular acidosis. Once the patient becomes euthyroid, bone remodelling and urine calcium return to normal levels and that would correct the renal acidosis.
This case report serves to highlight the effect of Graves’ disease on renal tubules which may result in type 1 renal tubular acidosis. This effect could be reversible with normalization of thyroid function.