The Thyroid and the Kidney: A Complex Interplay in Health and Disease

Abstract

Thyroid hormones may directly affect the kidney and altered kidney function may also contribute to thyroid disorders. The renal manifestations of thyroid disorders are based on hemodynamic alterations or/and to direct effects of thyroid hormones. The renin-angiotensin system plays a crucial role in the cross-talk between the thyroid and the kidney. Hypothyroidism may be accompanied by an increase of serum creatinine and reduction of glomerular filtration rate (GFR), whereas hyperthyroidism may increase GFR. Treatment of thyroid disorders may lead to normalization of GFR. Primary and subclinical hypothyroidism and low triiodothyronine (T3) syndrome are common features in patients with chronic kidney disease (CKD). In addition low levels of thyroid hormones may predict a higher risk of cardiovascular and overall mortality in patients with end-stage renal disease. The causal nature of this correlation remains uncertain. In this review, special emphasis is given to the thyroid pathophysiology, its impact on kidney function and CKD and the interpretation of laboratorial findings of thyroid dysfunction in CKD.

Evaluation of Serum Symmetric Dimethylarginine Concentration as a Marker for Masked Chronic Kidney Disease in Cats With Hyperthyroidism

“…When all 131 I‐treated cats were categorized as euthyroid or hypothyroid, the post‐treatment serum SDMA concentrations were higher in hypothyroid cats than euthyroid cats. This increase in serum SDMA concentration in the hypothyroid cats could be expected, as hypothyroidism in known to decrease GFR both in dogs and humans, which can sometimes be normalized with thyroid hormone replacement alone . Direct GFR measurements have not been reported in hypothyroid cats—neither before nor after levothyroxine replacement—but those studies are needed.…”

Alteration of thyroid hormone signaling triggers the diabetes-induced pathological growth, remodeling, and dedifferentiation of podocytes

“…Nevertheless, translating this strategy into clinical practice will not be easy. To achieve an efficient therapeutic effect on stressed cells (overexpressing both TRα1 and DIO3) under conditions of systemic hypothyroidism, very high doses of T 3 would be needed; but this can cause various adverse effects -such as tachycardia, arrhythmias (65), hyperfiltration (66), dysfunction of the thyroid gland (67), and even death in the case of long-term treatment (68). As a matter of fact, when we tried to test the therapeutic potential of T 3 treatment in diabetic rats (our unpublished data), we needed to use very high doses of T 3 in order to reach an initial beneficial effect in function; however, this caused significant complications and we needed to interrupt the study.…”

Unusual Presentation of Central Diabetes Insipidus in a Patient With Neurosarcoidosis

“…It decreases the renal plasma flow (RPF) and glomerular filtration rate (GFR) via prerenal or systemic and intrinsic renal dysfunction or by direct effects of thyroid hormones on the kidney respectively. 4 , 7 , 9 …”

“…The highlight of this case report is the reversible nature of renal dysfunction after replacing thyroid hormone deficiency. 4 This documentation is made to add clinical evidence to existing knowledge while interpreting similar observations.…”