Osteocalcin is an Independent Predictor for Hungry Bone Syndrome After Parathyroidectomy.

BACKGROUND: Hungry bone syndrome is characterized by prolonged and severe hypocalcemia following parathyroidectomy. Previously, we reported that preoperative alkaline phosphatase is a major factor predicting prolonged hospital stay. Nonetheless, some patients with low alkaline phosphatase levels presented with hungry bone syndrome, suggesting that additional factors may play a role. METHODS: From September 2010 to December 2017, consecutive dialysis patients who underwent parathyroidectomy for secondary hyperparathyroidism were analyzed. Length of hospital stay was used as a surrogate marker for postoperative bone hunger. RESULTS: A total of 260 patients were included in the study. The median postoperative hospital stay was 3 days, and 69 (27%) patients had a stay longer than 3 days. Multivariate logistic regression analysis revealed that alkaline phosphatase (odds ratio [OR] = 1.005), osteocalcin (OR = 1.001), and subtotal parathyroidectomy (OR = 0.061) were associated with prolonged hospital stay. Multivariate linear regression analysis indicated that age (ß = - 0.170), alkaline phosphatase (ß = 0.430), and osteocalcin (ß = 0.166) were correlated with the length of stay. After surgery, the median osteocalcin level increased from 264 to 478 ng/mL (P < 0.001). CONCLUSIONS: Alkaline phosphatase is the main predictor of hungry bone syndrome after parathyroidectomy, and preoperative osteocalcin is an additional independent predictor. Patients with a high osteocalcin level may prone to have a higher demand for calcium supplementation.

Aristolochic acid downregulates monocytic matrix metalloproteinase-9 by inhibiting nuclear factor-κB activation.

Aristolochic acid (AA)-associated nephropathy was described as being characterized by a rapid progressive enhancement of interstitial renal fibrosis. Renal tissue fibrosis occurs because of an imbalance of extracellular matrix (ECM) accumulation and matrix metalloproteinase (MMP) activation. Much evidence indicates that inflammatory renal disease including monocyte and mesangial interactions is linked to the development and progression of renal remodeling. In this study, we found that AA showed concentration-dependent inhibition of tumor necrosis factor (TNF)-α-induced MMP-9 activation with an IC(50) value of 6.4±0.5µM in human monocytic THP-1 cells. A similar effect was also noted with different ratios of AAs (types I and II). However, AA had no inhibitory effect on the intact enzymatic activity of MMP-9 at a concentration of 20µM. On the other hand, the level of tissue inhibitor of metalloproteinase (TIMP)-1 was not induced by AA, but it suppressed TNF-α-induced MMP-9 protein and messenger RNA expressions. AA also significantly inhibited TNF-α-induced IκBα degradation. Furthermore, an electrophoretic mobility shift assay and a reported gene study, respectively, revealed that AA inhibited TNF-α-induced NF-κB translocation and activation. In addition, compared to other NF-κB inhibitors, AA exerted significant inhibition of MMP-9 activation and monocyte chemotactic protein-1-directed invasion. From these results, we concluded that AA, a natural compound, inhibits TNF-α-induced MMP-9 in human monocytic cells possibly through the NF-κB signal pathway. These results also imply that AA may be involved in alteration of matrix homeostasis during renal fibrosis in vivo.

Neuroprotection by the Traditional Chinese Medicine, Tao-Hong-Si-Wu-Tang, against Middle Cerebral Artery Occlusion-Induced Cerebral Ischemia in Rats.

Tao-Hong-Si-Wu-Tang (THSWT) is a famous traditional Chinese medicine (TMC). In the present study, oral administration of THSWT (0.7 and 1.4 g kg(-1)day(-1)) for 14 days before MCAO dose-dependently attenuated focal cerebral ischemia in rats. MCAO-induced focal cerebral ischemia was associated with increases in hypoxia-inducible factor (HIF)-1α, inducible nitric oxide synthase (iNOS), tumor necrosis factor (TNF)-α, and active caspase-3 expressions in ischemic regions. These expressions were obviously inhibited by 0.7 g kg(-1)day(-1) THSWT treatment. In addition, THSWT inhibited platelet aggregation stimulated by collagen in washed platelets. In an in vivo study, THSWT (16 g kg(-1)) significantly prolonged platelet plug formation in mice. However, THSWT (20 and 40 µg mL(-1)) did not significantly reduce the electron spin resonance (ESR) signal intensity of hydroxyl radical (OH(•)) formation. In conclusion, the most important findings of this study demonstrate for the first time that THSWT possesses potent neuroprotective activity against MCAO-induced focal cerebral ischemia in vivo. This effect may be mediated, at least in part, by the inhibition of both HIF-1α and TNF-α activation, followed by the inhibition of inflammatory responses (i.e., iNOS expression), apoptosis formation (active caspase-3), and platelet activation, resulting in a reduction in the infarct volume in ischemia-reperfusion brain injury.

Comparison of parenteral iron sucrose and ferric chloride during erythropoietin therapy of haemodialysis patients.

AIM: To compare the effects of i.v. iron sucrose and Fe chloride on the iron indices of haemodialysis patients with anaemia. METHODS: One hundred and eight haemodialysis patients receiving recombinant human erythropoiesis-stimulating agent (ESA) (mean age 59.37 years) were enrolled and randomly assigned to an iron sucrose or an Fe chloride group. Iron supplements were administered at 100 mg/week during the first 4 weeks (loading dose). Ferritin and transferrin saturation (TSAT) were then measured and dose adjusted. Ninety-eight subjects completed treatment; 51 in the iron sucrose group and 47 in the Fe chloride group. Ferritin, TSAT, haematocrit (Hct), reticulocyte count, serum albumin, fractional clearance of urea (Kt/V) and intact parathyroid hormone (iPTH) were measured. RESULTS: There was no significant difference in baseline characteristics between the groups. Significant differences between the groups were observed in both iron indices and ESA dosage. Hct at week 24 (31.1% vs 29.7%, P = 0.006) and ferritin at week 20 (731.3 vs 631.7 ng/mL, P = 0.006) in the iron sucrose group were significantly higher than in the Fe chloride group. ESA dosage used in the iron sucrose group at week 8 was significantly lower than in the Fe chloride group (244.9 vs 322.6 U/kg per month, P = 0.003), and iron sucrose group received significantly lower iron dose than the Fe chloride group at week 8 (P = 0.005). CONCLUSION: Although the differences in ESA dosage, ferritin and iron dosage between two groups were found during the study period while similar results were shown at the end of 24 week study. Thus, iron sucrose and Fe chloride are safe and work equally well for haemodialysis patients.

Plasma free amino acids and their metabolites in Taiwanese patients on hemodialysis and continuous ambulatory peritoneal dialysis.

BACKGROUND: The high prevalence of protein-energy malnutrition is a critical issue for patients with end stage renal disease (ESRD) on hemodialysis (HD) or continuous ambulatory peritoneal dialysis (CAPD). Levels of plasma and intracellular amino acids are significant indicators of protein metabolism and nutritional status assessment. We measured plasma FAAs in patients on maintenance dialysis and to provide information in monitoring the therapeutic strategy, particularly in AA supplementary therapy or protein restriction. METHODS: Fifty-five patients with ESRD were investigated, 25 on HD (male : female=14 : 11; 48-67 y) and 30 on CAPD (male : female=17 : 13; 45-64 y). The subjects had been on dialysis for an average of 13 months (range, 9 to 22 months). Their plasma FAAs (including their intermediate metabolites) were measured by ion exchange chromatography before and after HD or during CAPD and were compared with data obtained from 20 age- and sex-matched healthy controls. RESULTS: The total plasma FAA levels (urea and free ammonia, NH3 were excluded) in pre-HD samples (3911 +/- 709 micromol/l) was significantly higher than in the other groups (2570 +/- 378 in control, 3210 +/- 640 in post-HD, and 3468 +/- 271 in CAPD samples). The mean plasma FAA concentrations differed significantly between pre-HD and controls and between pre-HD and CAPD samples (p<0.05). No significant differences were found among the other group comparisons. Comparing individual FAA concentrations, only citrulline differed significantly among all groups (p<0.05), whereas serine, glutamine, beta-alanine, beta-aminoisobutyric acid, and gamma-aminobutyric acid were not different. Concentrations of some FAAs involved in the urea cycle, e.g., arginine, aspartic acid, citrulline, and ornithines, and solutes urea and NH3, were significantly increased. Ratios of tyrosine/phenylalanine and valine/glycine ratios were markedly reduced in all patients on dialysis compared with controls. CONCLUSION: FAAs either from dietary uptake or protein catabolism are substantially retained in the plasma of patients with ESRD, possibly producing higher levels of the waste products (urea and NH3) through the urea cycle and ammonia metabolism in liver. Maintenance dialysis can effectively eliminate excess FAAs in plasma, as there was a 17.9% reduction post-HD. The abnormalities in FAA metabolism found in patients with ESRD necessitate careful consideration of dialysis and dietary measures.

Acute renal failure directly caused by hemolysis associated with transurethral resection of the prostate.

Transurethral resection of the prostate (TURP) for the treatment of benign prostatic hyperplasia may lead to TURP syndrome, and in some cases, acute renal failure can develop. Hemolysis does happen during TURP. Whether hemolysis itself leads to acute renal failure merits discussion. We report a patient with chronic renal insufficiency who developed oliguric acute renal failure immediately as a major complication after TURP. The renal function of this patient recovered after six hemodialysis sessions, and the patient continued to do well in the subsequent follow-up period.