Recurrent calcium nephrolithiasis associated with primary aldosteronism

Shey, Jason; Cameron, Mary Ann; Sakhaee, Khashayar; Moe, Orson W.

doi:10.1053/j.ajkd.2004.03.037

Cited by 21 publications

(12 citation statements)

References 25 publications

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“…[24] We think that aldosteronism may cause a contemporary loss of urinary potassium, calcium and phosphorus and stimulate the secretion of the parathyroid hormone both in humans [26,31,32] and rats. [17,33,34] Aldosterone antagonists reduce the urinary loss of these ions, inducing sodium excretion that equilibrates tubular electronegativity.…”

Section: Discussionmentioning

confidence: 99%

“…[19] Calcitriol and dietary calcium and magnesium supplementation prevent oxidative stress in rats with aldosteronism. [20] A rare case of primary parathyroid adenoma associated with primary aldosteronism and breast cancer, possibly related to MEN1 gene mutations, [21] some cases of hyperparathyroidism associated with primary aldosteronism, [22,23] and a case of recurrent calcium nephrolithiasis associated with primary aldosteronism [24] have been reported in humans. Even liquorice can increase serum PTH and urinary calcium levels from baseline value in healthy women after only 2 months of treatment.…”

Section: Introductionmentioning

confidence: 97%

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Hyperparathyroidism Secondary to Hyperaldosteronism

Fortina¹,

Bellosta

2010

High Blood Pressure & Cardiovascular Prevention

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Introduction: Hyperparathyroidism has been associated with essential hypertension. In rats, volume expansion, the deoxycorticosterone (DOC)-salt hypertension model and primary aldosteronism cause a reduction in plasma calcium levels and secondary hyperparathyroidism. In these rats, urinary calcium decreases with thiazides and or aldosterone antagonists, while furosemide gives the opposite effect. Also, licorice causes an increase in parathyroid hormone and urinary calcium excretion. Aim: To report clinical observations on different clinical cases of aldosteronism, with and without nephrolithiasis, and to elucidate the mechanism causing lithogenesis in patients affected by this pathology. Methods: In our hypertension unit, we studied 11 patients with primary aldosteronism: 4 with adenomas and 7 with bilateral adrenal cortex hyperplasia. Only 6 of 11 showed calcium oxalate stones. In all patients we measured parathormone (PTH), calcium, potassium and phosphorus levels in serum and urine before and after treatment with aldosterone antagonists. None of the patients showed either chronic renal insufficiency or any pathologies at the parathyroid glands. No patients received diuretics in the month before the study. Results: All patients affected by primary aldosteronism showed an increased PTH level, which was reduced following therapy with aldosterone antagonists. Calcium and phosphorus serum levels remained unchanged, while the treatment reduced urinary calcium and phosphorus levels and increased serum potassium levels in a statistically significant manner (t-test = p < 0.01). Conclusions: Our data support the hypothesis of a hyperparathyroidism secondary to aldosteronism. In fact, the aldosterone antagonist normalizes all the values we measured. Therefore, we conclude that (i) aldosterone seems to play a new and important role in the pathogenesis of calcium nephrolithiasis; (ii) aldosterone antagonists may efficiently reduce calcium loss and PTH activation, thus preventing nephrolithiasis in aldosteronism, and most probably also in osteopenia; and (iii) nephrolithiasis is not automatically caused by these conditions, but it requires the contemporary presence of lithogenic factors or the absence of protective factors or it needs a prolonged stimulus.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 97%

Hyperparathyroidism Secondary to Hyperaldosteronism

Fortina¹,

Bellosta

2010

High Blood Pressure & Cardiovascular Prevention

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“…Renal calculi or nephrocalcinosis associated with primary aldosteronism has been rarely reported (2)(3)(4)(5). Primary aldosteronism is reported to elevate urinary calcium excretion (10).…”

Section: Discussionmentioning

confidence: 99%

A Case of Nephrocalcinosis Associated with Primary Aldosteronism

Yasuda¹,

Sasaki²,

Yamato³

et al. 2012

Intern. Med.

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Herein, we report a 37-year-old man presenting with nephrocalcinosis associated with primary aldosteronism. Primary hyperaldosteronism is reported to facilitate urinary calcium excretion; however, renal calculi or calcinosis in this disorder has been rarely reported. The patient had renal dysfunction and calcification in the renal medulla on both kidneys. A kidney biopsy was performed. His renal dysfunction seemed to be mainly caused by hypertension and tubulointerstitial damage. Furthermore, von Kossa-positive stones were seen in some tubules. X-ray element analysis revealed that the stones were composed of calcium phosphate.

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“…Furthermore, electrolyte disorders, 80 drugs, 81,82 changes in diet 83 or other disorders can be associated with low urine citrate. [84][85][86] Table 6). 87…”

Section: Hypocitraturiamentioning

confidence: 99%

Pathophysiology of Nephrolithiasis

Paliouras

Tsampikaki

Alivanis

et al. 2012

Nephrology Research & Reviews

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The incidence of nephrolithiasis has risen over the last twenty years and continues to rise. Although it is often referred to as a disease, recent advances in the understanding of the pathophysiology suggest that it is a systemic disorder. We conducted a PubMed based literature review on the recent advances in the pathophysiology of kidney stone formation. There is a link between diabetes, metabolic syndrome, obesity, insulin resistance and nephrolithiasis. Along with the aging population and a Western diet, these are the main reasons for the rising incidence and prevalence of nephrolithiasis. Different theories as to the pathophysiological mechanisms of lithogenesis have been proposed, including the free and fixed particle theories, and Randal’s plaque hypothesis. Among the different types of kidney stones, those containing calcium are the most common, followed by those containing uric acid, struvite and cystine. Supersaturated urine, acidic urine pH and reductions in kidney stone inhibitors in the urine are the main recognized causes that contribute to the formation of all these stonetypes. Nephrolithiasis is considered a systemic pathology that may lead to end-stage renal disease. Although much progress has been made, the underlying pathophysiological mechanisms of kidney stone formation are still not fully understood

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Recurrent calcium nephrolithiasis associated with primary aldosteronism

Cited by 21 publications

References 25 publications

Hyperparathyroidism Secondary to Hyperaldosteronism

Hyperparathyroidism Secondary to Hyperaldosteronism

A Case of Nephrocalcinosis Associated with Primary Aldosteronism

Pathophysiology of Nephrolithiasis

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