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.

A patient with monoclonal gammopathy and renal failure due to K light chain deposition in the glomerular basement membrane is reported. After 8 months, he developed a progressive and severe renal failure requiring haemodialysis. 30 months later, the monoclonal gammopathy was unchanged. Clinical features, as well as kinetic and immunological studies, were consistent with a diagnosis of benign monoclonal gammopathy (BMG). This case suggests that the renal failure complicating a monoclonal gammopathy is not related to its malignancy.

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Introduction: Increased urinary albumin excretion in uncomplicated hypertension has been recently associated with impaired vascular reactivity (NO dependent and independent vasodilation) and increased levels of adhesion molecules (2), thereby suggesting that endothelial dysfunction is responsible for the increased cardiovascular (CV) risk associated with albuminuria (1,2). Methods: In light of this reports, we have used our human model of vascular tone control, Bartter's/ Gitelman's syndromes (BS/GS) patients, which have biochemical and hormonal characteristics typical of hypertension, yet normo/hypotension hyporesponsiveness to pressors and reduced vascular resistance (3-5), to assess the urinary albumin/creatinine ratio (UACR) as a potential marker of endothelial dysfunction. Results: We found that UACR in BS/GS did not differ from healthy subjects (12.07±8.3 mg/g Cr vs 11.5±9.2). Conclusions: These results are perfectly in keeping with the evidence in these patients of a markedly higher insulin sensitivity compared with healthy normotensive subjects and an Ang II signalling/ insulin-glucose metabolism relationships which points toward reduced insulin resistance, which are opposite of those typical of diabetes and hypertension, including the absence of microalbuminuria and endothelial dysfunction. This evidence in BS/GS is sustained by reduced oxidative stress and inflammatory status, up-regulation of NO system down-regulation of RhoA-Rho kinase pathway, activation of Akt pathway and blunted Ang II signalling which joined with the absence of albuminuria depict a biochemical and molecular picture of reduced CV risk and therefore indirectly support the association of endothelial dysfunction and albuminuria with increased CV risk.

Introduction: Patients with mild renal failure are characterised by a marked increase in muscle sympathetic neural outflow. No data are available on whether this adrenergic activation 1) is generalised to the whole circulation and 2) is related to the metabolic (insulin resistance) and cardiac (left ventricular hypertrophy) abnormalities frequently detected in this condition. Methods: In 16 patients (8 females, 8 males, age 60.4+2.4 yrs, mean ± SEM) with mild renal failure (creatinine clearance ranging from 36 to 66 ml/min), we measured beat-to-beat arterial blood pressure (Finapres), heart rate (EKG, HR) and efferent postganglionic muscle sympathetic nerve traffic (microneurography, MSNA) during a 20 min resting period. Measurements also included 1) glucose and insulin assay (radioenzymatic method) and HOMA index calculation, 2) echocardiographic assessment of left ventricular mass index (LVMI) and 3) microneurographic recording of skin sympathetic nerve traffic (SSNA). Results: For similar blood pressure values, patients with mild renal failure displayed MSNA values significantly greater than those found in age-matched controls, both when expressed as bursts incidence over time (51.3±2.8 vs 38.4±3.5 bs/min, p±3.2 vs 54.8±5.6 bs/100 hb, p controls (HR: 72.2±3.1 vs 70.5±1.4 b/min, p=NS; SSNA: 12.3±1.3 vs 14.4±1.8 bs/min, p=NS). Furthermore, in renal failure patients with (n=6) and without (n=10) insulin resistance (HOMA index: 5.5±1.8 vs 1.4±0.2 a.u., p±3.3 vs 70.5±4.2 bs/100 hb). Similarly, renal failure patients with (n=8) and without (n=8) left ventricular hypertrophy (LVMI: 130.5±5.3 vs 93.1±2.8 g/m 2 , p±4.0 vs 73.9±4.1 bs/100 hb).Conclusions: Thus in mild renal failure sympathetic activation does not appear to be generalised to the whole circulation, the cardiac and the skin district not displaying the adrenergic overdrive seen in the muscle circulation. They also show that, in contrast to what found in other pathologic states, sympathetic activation is not related to insulin resistance or potentiated by left ventricular hypertrophy.