Renal Tubular Maximum Reabsorptive Capacity for Phosphate in Patients with Primary Hyperparathyroidism before and after Operation

Primary hyperparathyroidism (PHPT) is the most common endocrinopathy in multiple endocrine neoplasia type 1 (MEN1). Persistent levels of increased parathyroid hormone (PTH) result in a higher incidence of osteopenia and osteoporosis compared to the general population. Surgical removal of hyper-functioning parathyroid tissue is the therapy of choice. This retrospective study evaluated the effect of parathyroidectomy (PTX) on bone metabolism and bone mass in two series of patients with MEN1 PHPT and sporadic PHPT (sPHPT) by comparing bone metabolism-related biochemical markers and bone mineral density (BMD) before and after surgery. Our data confirmed, in a higher number of cases than in previously published studies, the efficacy of PTX, not only to rapidly restore normal levels of PTH and calcium, but also to normalize biochemical parameters of bone resorption and bone formation, and to improve spine and femur bone mass, in both MEN1 PHPT and sPHPT. Evaluation of single-patient BMD changes after surgery indicates an individual variable bone mass improvement in a great majority of MEN1 PHPT patients. In MEN1 patients, PTX is strongly suggested in the presence of increased PTH and hypercalcemia to prevent/reduce the early-onset bone mass loss and grant, in young patients, the achievement of the bone mass peak; routine monitoring of bone metabolism and bone mass should start from adolescence. Therapy with anti-fracture drugs is indicated in MEN1 patients with BMD lower than the age-matched normal values.

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Microperfusion study of proximal tubule bicarbonate transport in maleic acid-induced renal tubular acidosis

AJP Renal Physiology ◽

10.1152/ajprenal.1986.250.3.f476 ◽

1986 ◽

Vol 250 (3) ◽

pp. F476-F482

Author(s):

N. Bank ◽

H. S. Aynedjian ◽

B. F. Mutz

Keyword(s):

Proximal Tubule ◽

Renal Tubular Acidosis ◽

Maleic Acid ◽

Basolateral Membrane ◽

Bicarbonate Transport ◽

Mitochondrial Energy Metabolism ◽

Before And After ◽

Renal Tubular ◽

Blood Transport ◽

Acid Administration

Microperfusion studies were carried out in rats to examine the abnormality in proximal tubule HCO3- transport caused by maleic acid administration. Permeability of the proximal tubule to HCO-3 was measured by perfusing proximal tubules with a HCO3- -free low-buffer isotonic equilibrium solution containing acetazolamide after plasma [HCO3-] had been raised by intravenous NaHCO3 infusion. Insulin recovery in the collected perfusate was approximately 100% in control and maleic acid-treated rats. CO2 influx measured by microcalorimetry was not significantly different in control vs. maleic acid-treated rats. Thus maleic acid did not cause increased permeability of the proximal tubule to either inulin or HCO3-. In a second group of experiments, proximal tubule fluid and HCO3- efflux were measured in paired-reperfusion experiments before and after maleic acid administration. The perfusion fluid contained 25 mM HCO3- and 120 mM Cl-. HCO3- absorption was inhibited 25% (79 pmol/min), Na+ was inhibited 22% (164 pmol/min), and Cl- absorption (calculated as the anion gap) by 85 pmol/min. [HCO3-] in the collected perfusate rose significantly after maleic acid, presumably accompanied by a fall in [Cl-]. The observations indicate that proximal renal tubular acidosis (RTA) induced by maleic acid is characterized by impaired lumen-to-blood transport of sodium bicarbonate and chloride but not by increased backflux. Based on previously demonstrated effects of maleic acid on mitochondrial energy metabolism and cellular ATP levels, we postulate that the principal transport abnormality is impaired basolateral membrane active sodium transport, leading to a secondary reduction in brush border Na+-H+ exchange.(ABSTRACT TRUNCATED AT 250 WORDS)

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Distal renal tubular acidosis in primary hyperparathyroidism

BMJ Case Reports ◽

10.1136/bcr-2014-208120 ◽

2015 ◽

Vol 2015 (jan29 1) ◽

pp. bcr2014208120-bcr2014208120 ◽

Cited By ~ 2

Author(s):

T. E. N. Lo ◽

I. T. I. Tan

Keyword(s):

Primary Hyperparathyroidism ◽

Renal Tubular Acidosis ◽

Distal Renal Tubular Acidosis ◽

Renal Tubular

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Abstract 893: Contrast Medium-Induced Renal Damage is Tightly Associated with Endothelial Injury in Patients

Circulation ◽

10.1161/circ.118.suppl_18.s_626-c ◽

2008 ◽

Vol 118 (suppl_18) ◽

Author(s):

Kazuko Tajiri ◽

Hidekazu Maruyama ◽

Satoshi Sakai ◽

Noritake Shimojo ◽

Hideaki Aihara ◽

...

Keyword(s):

Oxidative Stress ◽

Renal Function ◽

Contrast Medium ◽

Renal Damage ◽

Cell Activation ◽

Endothelial Damage ◽

Endothelial Injury ◽

Specific Marker ◽

Before And After ◽

Renal Tubular

Background: Contrast-induced nephropathy (CIN) remains a common complication of radiographic procedures. We hypothesized that endothelial dysfunction is the main cause of CIN. To clarify whether contrast medium-induced renal damage is associated with endothelial injury, we measured microparticles derived from endothelial cells as markers of endothelial injury. Circulating microparticles are shed from cell surface respond to cell activation and apoptotic stimuli, reflecting the condition of damaged cells. Methods: Renal function of 35 adult patients was analyzed before and after the use of contrast medium for coronary angiography. Parameters for renal function and urinary 15-isoprostane F2t, a specific marker of oxidative stress were measured before and after radiocontrast administration. Flow cytometry was used to count circulating CD34 + microparticles, which is regarded as one of markers for endothelial damage. Results: The decrease of estimated glomerular filtration rate positively correlated with the amount of contrast medium (r=0.427; P=0.013). Urinary N-acetyl-beta-D-glucosaminidase, a marker of renal tubular injury, was increased after angiography (from 7.6+/− 6.8 to 9.1 +/− 6.0 U/g-CRE, P=0.011). Furthermore, urinary 15-isoprostane F2t positively correlated with the volume of contrast medium (r=0.421; P=0.012). CD34+ microparticle was significantly increased after angiography (1.3-fold increased from basal level, P=0.0017). The increase of CD34+ microparticle was associated with the insult of contrast medium, but not of the amount. Conclusion: Radiocontrast impaired renal function in accordant with the increase of oxidative stress. The release of CD34+ microparticle was also increased by use of radiocontrast. These data suggest that CIN is tightly associated with endothelial injury mediated by radiocontrast-induced oxidative stress.

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