Minimal Change Nephropathy and Graves’ Disease: Report of a Case and Review of the Literature

Tanwani, Lal K.; Lohano, Vasdev; Broadstone, Vasti L.; Mokshagundam, Sri Prakash L.

doi:10.4158/ep.8.1.40

Cited by 64 publications

(22 citation statements)

References 15 publications

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“…Moreover, because proteinuria was also unrelated to BP or losartan administration, we suggest that proteinuria in the hyperthyroid state might be produced by a direct action of thyroid hormones, increasing the permeability of the glomerular barrier. In this context, Tanwani et al 37 reported a possible association between thyrotoxic patients and a nephrotic syndrome attributable to minimal change nephropathy, a clinical entity defined by selective proteinuria that occurs in the absence of lesions in the glomerular capillary wall. The only detectable abnormalities involve the epithelial visceral cells with effacement of foot processes.…”

Section: Discussionmentioning

confidence: 99%

Increased Pressor Sensitivity to Chronic Nitric Oxide Deficiency in Hyperthyroid Rats

et al. 2003

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Abstract-We studied the effects of a possible interaction between partial nitric oxide deficiency and thyroid hormone excess on the long-term control of blood pressure (BP) and morphological and renal variables and examined the role of the renin-angiotensin system in the increased BP of this interaction. Eight groups (nϭ8 each) of male Wistar rats were used: a control group; 3 groups that were treated with thyroxine (50 g/d), N w -nitro-L-arginine methyl ester (L-NAME; subpressor dose, 1.5 mg · kg, or thyroxine plus L-NAME; and another 4 similarly treated groups that received losartan (20 mg · kg Ϫ1 · d Ϫ1) in their drinking fluid. All treatments were maintained for 3 weeks. The time course of tail systolic BP was recorded once a week. At the end of the experimental period, we measured mean arterial pressure in conscious rats and assessed the morphological, metabolic, plasma, and renal variables. Thyroxine produced a mild BP increase from the second week of treatment and an increase in plasma angiotensin II and plasma nitrates/nitrites by the end of the study. Simultaneous administration of thyroxine and a subpressor dose of L-NAME produced a marked BP increase that reached significance from the first week of treatment. Losartan produced normotension in thyroxine-treated rats and attenuated the BP elevation in thyroxineϩL-NAME-treated rats. Hyperthyroid rats showed relative renal and ventricular hypertrophy, absence of absolute left ventricular hypertrophy, and proteinuria. These alterations were not changed by losartan. We conclude that an impaired nitric oxide system might have a counterregulatory homeostatic role against the prohypertensive effects of thyroid hormone and that the renin-angiotensin system plays an important role in thyroxineϩL-NAME hypertension. Key Words: blood pressure Ⅲ hypertrophy, cardiac Ⅲ losartan Ⅲ nitric oxide Ⅲ hyperthyroidism T he hyperthyroid state is an endocrine disorder associated with important changes in hemodynamic, renal, and cardiac function. 1-3 Hyperthyroidism manifests a hyperdynamic circulation, with increased cardiac output, increased heart rate, and decreased peripheral resistance. 2-4 These characteristic cardiovascular manifestations of hyperthyroidism have been reproduced in rats by thyroid hormone treatment. [1][2][3] Animal studies have reported a dose-and time-related increase in arterial pressure 5,6 and have shown that the hyperthyroid state affects cardiac and renal weight and reduces renal sodium excretion. 2,5,6 It is well known that nitric oxide (NO) plays a major role in the regulation of vascular tone, 7 renal sodium excretion, 8,9 and therefore, of arterial blood pressure (BP). 10 Both acute and chronic administration of NO synthase (NOS) inhibitors increase systemic arterial BP. 11,12 Hyperthyroidism in rats increases the responsiveness of resistance vessels to the endothelium-dependent vasodilator acetylcholine. 13 Fernández et al 14 demonstrated that hyperthyroidism leads to a significant and reversible enhancement in rat liver NOS activity. More rec...

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Section: Discussionmentioning

confidence: 99%

Increased Pressor Sensitivity to Chronic Nitric Oxide Deficiency in Hyperthyroid Rats

et al. 2003

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“…These observations suggest that proteinuria in the hyperthyroid state may be produced by a direct action of thyroid hormones, increasing the permeability of the glomerular barrier. In this context, Tanwani et al (114) reported a possible association between thyrotoxic patients and a nephrotic syndrome attributable to a minimal changes nephropathy, a clinical entity defined by selective proteinuria that occurs in the absence of lesions in the glomerular capillary wall. The only detectable abnormalities involve the epithelial visceral cells with effacement of foot processes.…”

Section: Proteinuriamentioning

confidence: 99%

Vascular and renal function in experimental thyroid disorders

Moreno²,

et al. 2006

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This review focuses on the effects of thyroid hormones in vascular and renal systems. Special emphasis is given to the mechanisms by which thyroid hormones affect the regulation of body fluids, vascular resistance and, ultimately, blood pressure. Vascular function is markedly affected by thyroid hormones that produce changes in vascular reactivity and endothelial function in hyper-and hypothyroidism. The hypothyroid state is accompanied by a marked decrease in sensitivity to vasoconstrictors, especially to sympathetic agonists, alteration that may play a role in the reduced blood pressure of hypothyroid rats, as well as in the preventive effects of hypothyroidism on experimental hypertension. Moreover, in hypothyroid rats, the endothelium-dependent and nitric oxide donors vasodilation is reduced. Conversely, the vessels from hyperthyroid rats showed an increased endothelium-dependent responsiveness that may be secondary to the shear-stress induced by the hyperdynamic circulation, and that may contribute to the reduced vascular resistance characteristic of this disease. Thyroid hormones also have important effects in the kidney, affecting renal growth, renal haemodynamics, and salt and water metabolism. In hyperthyroidism, there is a resetting of the pressure-natriuresis relationship related to hyperactivity of the renin-angiotensin system, which contributes to the arterial hypertension associated with this endocrine disease. Moreover, thyroid hormones affect the development and/or maintenance of various forms of arterial hypertension. This review also describes recent advances in our understanding of thyroid hormone action on nitric oxide and oxidative stress in the regulation of cardiovascular and renal function and in the long-term control of blood pressure.

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“…Thyroid disorders (both hyper and hypothyroidism) (87)(88)(89) and most commonly auto-immune thyroiditis are associated with glomerulonephritis (GN), including membranous nephropathy (88,90,91), focal segmental glomerulosclerosis (92), minimal change (89, 92), membranoproliferative GN (93) IgA nephropathy (94), and amyloidosis (92). Interestingly, anti-neutrophil cytoplasmic antibody (ANCA) positive crescentic GN has been reported after treatment with propylthiouracil for hyperthyroidism and membranous nephropathy after 131 I administration (95,96).…”

Section: Glomerular Diseases and Thyroid Disordersmentioning

confidence: 99%

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

et al. 2014

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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.

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Minimal Change Nephropathy and Graves’ Disease: Report of a Case and Review of the Literature

Cited by 64 publications

References 15 publications

Increased Pressor Sensitivity to Chronic Nitric Oxide Deficiency in Hyperthyroid Rats

Increased Pressor Sensitivity to Chronic Nitric Oxide Deficiency in Hyperthyroid Rats

Vascular and renal function in experimental thyroid disorders

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

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