Endocrine Abstracts

A 60-year-old lady with known Rheumatoid arthritis, Ulcerative colitis and hypothyroidism was admitted with a 10-day history of diarrhoea and vomiting in June 2017. Sodium on admission was 107. Sodium rapidly improved with intravenous (IV) saline. She had 3 further admissions in quick succession in July and August. She always had a quick response to IV saline, but sodium dropped once IV Saline was withdrawn. She was started on oral sodium replacement but this had no effect on her sodium. It was felt that she had hyponatremia secondary to dehydration but also possible saltwasting nephropathy secondary to Golimumab. SF had been started on Golimumab in January of 2017 and this seems to have been the beginning of her sodium problems. The cause of diarrhoea was extensively investigated by Gastro services and felt it was not related to her ulcerative colitis. She had a normal pituitary profile. By this time she had been in the hospital for 30 days.

Hypothesis: Given the persistent Hyponatraemia, we hypothesized that she had proximal as well as distal renal tubular damage and her aldosterone was not able to compensate for this loss of function. To prove this hypothesis we did a series of tests and calculations.

Urine 24 Protein Excretion 0.23 (Normal<0.15)

Serum Uric Acid 0.09 mmol/l (Normal 0.14–0.34)

Urate Excretion - 1.3 mmol/24H (1.2–5.9) - Inappropriately normal.

TTKG - 5.8 (A TTKG of less than 8 implies inadequate potassium excretion, which is usually secondary to aldosterone deficiency or unresponsiveness)

TMP/GFR- 1.008 (Normal 0.8–1.35 mmol/l)-Low levels suggest renal tubular phosphate wasting.

Aldosterone-780 pmol/l (90–700) Renin-0.9 nmol/l per hr (0.5–3.5)

Aldo/Renin Ratio 867 (Ratio >850 Conn’s likely)

Beta 2 Microglobulin-Normal

Interpretation: These tests suggest this patient had damage to proximal as well as distal renal tubules. Furthermore, she had a high aldosterone level and a high Aldosterone/ Renin ratio of Conn’s range. This again suggests there was an element of distal tubular dysfunction.

Treatment: She was started on fludrocortisone at a dose of 100 mcg OD and it was gradually increased to 300 mcg and this stabilized her sodium. In the next 24 to 48 hours sodium continued to improve without any intravenous normal saline. She was discharged with a serum sodium of 130 about a week after starting her on fludrocortisone. Her sodium continued to remain normal on fludrocortisone post discharge.