The relationship between thyroid dysfunction and nephrotic syndrome: a clinicopathological study.

Abnormalities of thyroid function are common in patients with nephrotic syndrome (NS). However, a limited number of studies have reported on the association between clinicopathologic features and thyroid dysfunction in patients with NS. We retrospectively studied 317 patients who had been definitively diagnosed with NS. The NS patients with thyroid dysfunction showed higher urine protein, creatinine and lipid levels and lower albumin and hemoglobin than those with normal thyroid function, with no significant differences of pathological types. After dividing thyroid dysfunction groups into five subgroups, interestingly, membranous nephropathy was the most common pathologic type, both in normal thyroid group and in subclinical hypothyroidism group (40.4% and 46.7%, respectively), followed by minimal change disease (28.1% and 21.7%, respectively); while in the hypothyroid, low T3, and low T3T4 groups minimal change disease is now the leading type (48.8%, 33.3% and 38.6%, respectively). High levels of urinary protein, creatinine, cholesterol, and platelets were independent risk factors predicting thyroid dysfunction, while higher albumin and hemoglobin were protective factors. We demonstrated that the type of renal pathology was different among NS patients in different thyroid dysfunction subgroups. Interpretation of the interactions between thyroid and renal function is a challenge for clinicians involved in the treatment of patients with NS.

Transiently decreased sialylation of thyrotropin (TSH) in a patient with the euthyroid sick syndrome.

A 60-year old woman was admitted to the medical intensive care unit with respiratory distress and worsening renal function, and was found to have bilateral renal artery occlusion. Aggressive nutrition per nasogastric tube was begun on day 8 of her illness, and she eventually recovered after bilateral renal artery bypass surgery, which was performed on day 15. She developed the euthyroid sick syndrome. Levels of serum TSH, T3, and T4 fell during the first few days of her illness, then all trended to normal levels by day 28. The TSH level declined from 1.6 microU/mL on day 2 to 0.2 microU/mL on day 5, then rose to 4.5 microU/mL on day 10, and was 3.8 microU/mL on day 14. The ratios of free T4/TSH, a crude measure of the bioactivity of TSH, were 1.4, 8.0, 0.16, 0.32, and 1.14 on days 2, 5, 10, 14 and 28, respectively. TSH was immunoaffinity concentrated from serum collected on four dates. The TSH oligosaccharides were enzymatically released, treated with or without neuraminidase, labeled with a fluorescent probe, and analyzed by gel electrophoresis. The TSH oligosaccharides were found to be transiently less sialylated on day 13 as compared to days 2, 4, and 24. Three gel bands representing poorly sialylated oligosaccharides represented a mean of 20.6% of TSH oligosaccharides on days 2, 4, and 24, but represented 33.7% of TSH oligosaccharides on day 13. This is the first report of altered TSH oligosaccharide sialylation in the euthyroid sick syndrome. If confirmed by studies of additional patients, altered TSH sialylation may, in part, explain the altered TSH bioactivity that has been described in the euthyroid sick syndrome.