Parathyroidectomy in Persistent Post-transplantation Hyperparathyroidism - Single-center Experience.

BACKGROUND: Hyperparathyroidism is a common complication in chronic kidney disease and might persist in up to 25% of patients after transplantation. In this setting, vitamin D analogues further aggravate persistent hypercalcemia and cinacalcet has not been approved for these patients, some of whom will require parathyroidectomy to correct post-transplantation hyperparathyroidism. OBJECTIVES: In this single-center, retrospective study we aimed to analyze the long-term effect of parathyroidectomy on calcium, phosphorus, and parathyroid hormone (PTH) levels and its effect on allograft function in kidney transplantation patients submitted to parathyroidectomy. PATIENTS AND METHODS: Fifteen patients underwent parathyroidectomy between January 2005 and January 2015; median age 54 years old; 8 (53.3%) were receiving cinacalcet at the time of surgery. Pre-parathyroidectomy median values of intact PTH, calcium, and phosphorus were, respectively, 262 pg/mL, 10.8 mg/dL, and 2.4 mg/dL. Surgery consisted of uniglandular parathyroidectomy in 5 (33.3%) patients, biglandular in 4 (26.7%), and subtotal in 6 (40%). There was no surgery-related mortality. RESULTS: Compared with baseline, there was a decrease of PTH (262 pg/mL vs. 106 pg/mL, P = .001), calcium, and phosphorus levels (10.8 mg/dL vs. 10.4 mg/dL, P = .3; 2.4 vs. 2.9 mg/dL, P = .05) 1 year after surgery; with normalization of serum calcium at the end of follow-up (10.8 mg/dL vs. 9.4 mg/dL, P = .04). A decrease in estimated glomerular filtration rate occurred 1 month post-surgery (62.7 mL/m vs. 49.7 mL/m, P = .006) but returned to baseline 1 year after surgery (62.7 mL/m vs. 60.8 mL/m, P = .73). CONCLUSION: Parathyroidectomy appears to be a safe procedure and should be considered in kidney transplantation patients with persistent post-transplantation hyperparathyroidism. Although there was an acute estimated glomerular filtration rate decrease, we observed no long-term deterioration in allograft function.

Jejunal dopamine and Na,K+-ATPase activity in nephrotic syndrome.

BACKGROUND: The occurrence of complementary functions in sodium transport between the intestine and the kidney was suggested to occur when the renal function is immature or compromised and jejunal dopamine has been implicated in this renal-intestinal cross-talk. The jejunal sodium transport was not previously evaluated in the nephrotic syndrome. METHODS: We examined the jejunal Na(+),K(+)-ATPase activity and the role of dopamine in puromycin aminonucleoside (PAN) and HgCl(2)-induced nephrotic syndrome rat models. RESULTS: In both nephrotic syndrome rat models, the jejunal Na(+),K(+)-ATPase activity was reduced during greatest sodium retention and ascites accumulation (PAN nephrosis, day 7; HgCl(2) nephrosis, day 14), whereas during enhanced sodium excretion and ascites mobilization the jejunal Na(+),K(+)-ATPase activity was increased in HgCl(2) nephrosis (day 21) and was similar to controls in PAN nephrosis (day 14). In both PAN- and HgCl(2)-induced nephrosis, the jejunal aromatic L-amino acid decarboxylase (AADC) activity, the enzyme responsible for the synthesis of jejunal dopamine, did not differ from controls. In addition, the jejunal Na(+),K(+)-ATPase activity was not sensitive to inhibition by dopamine (1 microM) in both experimental groups throughout the study. CONCLUSIONS: In the nephrotic syndrome the jejunal Na(+),K(+)-ATPase activity may respond in a compensatory way to changes in extracellular volume, through dopamine-independent mechanisms.

Mercury contamination in Lavras do Sul, south Brazil: a legacy from past and recent gold mining.

An attempt is made, in this work, to establish approximate gold production and, consequently, mercury emission rates in Lavras do Sul during the 20th century, after a description of the historical background of the study area. The identification of two heavily polluted sites ('hot spots') shows the persistence of Hg contamination originated in the early 1900s until the 1950s, as well as more recent soil pollution, from the 1980s. The evaluation of natural and anthropogenic residual contamination is approached by the study of Hg concentrations in mineralized rock samples, in soil samples neighboring mining wastes and milling facilities and in stream sediments. Anthropogenic contamination in soil samples reached 110,000 ng/g Hg in bulk samples and 506,000 ng/g Hg in the silt-clay fraction, of which 82-83% as Hg(0), and 16-18% associated to the sulfide/residual fraction, according to complementary speciation analyses. The association of Hg with base metal sulfides may be contributing to local background concentrations varying from 140 to 207 ng/g in stream sediments.

Acute hypotensive, natriuretic, and hormonal effects of nifedipine in salt-sensitive and salt-resistant black normotensive and hypertensive subjects.

In a randomized double-blind study, we compared the short-term effects of nifedipine (10 mg 3x daily for 1 day) versus placebo on 24-h blood pressure, diuresis, natriuresis, urinary excretion of dopamine and metabolites, and on plasma renin activity (PRA) and plasma aldosterone levels in 18 black hypertensive (HT) patients [eight salt-resistant (HT-SR) and 10 salt-sensitive (HT-SS)], and in 20 black normotensive (NT) subjects (12 NT-SR and eight NT-SS) who were studied randomly with both a high- (HS) and a low-salt (LS) diet. In comparison to placebo, nifedipine significantly decreased 24-h mean BP in all groups either with HS or LS diets (all p<0.05). With HS, greater hypotensive effects were achieved in NT-SS (-10+/-2 mm Hg) versus NT-SR (-3+/-1 mm Hg; p<0.05) and in HT-SS (-18+/-2 mm Hg) versus HT-SR (-12+/-2 mm Hg; p<0.05). In NT-SS and HT-SS, nifedipine induced greater (p<0.05) BP decrease with HS (-10+/-2 and -18+/-2 mm Hg) than with LS (-4+/-1 and -9+/-1 mm Hg, respectively), whereas in NT-SR and HT-SR, the hypotensive effect did not differ between HS and LS. Nifedipine versus placebo significantly increased natriuresis and fractional excretion of sodium in all groups only with HS (p<0.05) but not with LS diets. Only in HT-SS were the hypotensive and natriuretic effects of nifedipine significantly correlated (r = -0.77; p<0.01). Nifedipine produced a similar increase of the urinary excretion of dopamine, L-DOPA, and of DOPAC in all subjects, which did not correlate with hypotensive and natriuretic effects. Nifedipine did not modify plasma levels of renin and of aldosterone except in NT-SS with HS, in whom nifedipine increased PRA levels (p <0.05). We conclude that although nifedipine reduces BP in all groups of NT and HT with LS and HS diets, the effect is greater in salt-sensitive subjects with HS. Although in HT-SS with HS, the short-term natriuretic response to nifedipine may contribute to its hypotensive effects, the diuretic-natriuretic effect of nifedipine is not necessary for the expression of its hypotensive effect. Moreover, it is unlikely that any short-term effects of nifedipine either on the renal dopaminergic system or on the secretion of aldosterone explain nifedipine short-term hypotensive and diuretic-natriuretic effects.

Bone changes in alcoholic liver cirrhosis. A histomorphometrical analysis of 52 cases.

Bone biopsies of 52 histologically confirmed alcoholic cirrhotic patients and 15 age- and sex-matched controls have been histomorphometrically analyzed determining trabecular bone volume (TBV), mineralized bone volume (MBV), and osteoid volume (OV). We also determined serum PTH, 25-OH-D3, calcitonin, FSH, LH, estradiol, testosterone, T3 and T4, urine cortisol, routine liver function tests, serum and urinary calcium, phosphorus, and magnesium. We found a high prevalence of osteoporosis: TBV was significantly lower in cirrhotic patients (T = 7.23, P less than 0.001), 41 of them being in the range of osteoporosis; none of them had osteomalacia. Levels of all the above-mentioned hormones and electrolytes were almost normal, and no correlation was found between them and liver function tests, as occurred with the bone parameters.