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Low-turnover bone disease is a complication of chronic kidney disease and a long-term steroid therapy. Currently, the only bone anabolic treatment available is teriparatide (TPTD). So far, no data exist in heart transplant patients, and only one single case with histomorphometric analysis of a dialysis patient with a low-turnover bone disease has been published. The current report shows the effect of a 1-year TPTD therapy in a cardiac transplant patient with 10 vertebral and 3 peripheral fractures who had developed a chronic kidney failure while receiving triple immunosuppressive therapy. A transiliac bone biopsy following tetracycline labeling was performed prior and after 1 year of treatment, showing an increase in the bone formation and improvement of the structural indices (20-fold increase of osteoid volume/bone volume, fourfold increase of osteoid surface/bone surface and increases of wall thickness (+15%), trabecular thickness (+9%), and trabecular number (+38%)). Bone mineral density was stable, no new vertebral fractures had occurred, the therapy was well-tolerated, and the patient improved clinically.

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Methemoglobinemia usually results from exposure to oxidizing substances such as nitrates or nitrites. Iron within hemoglobin is oxidized from the ferrous (Fe2+) state to the ferric (Fe3+) state, resulting in the inability to transport oxygen and carbon dioxide. Clinically, this condition causes functional cyanosis. As methemoglobin levels increase, patients show evidence of cellular hypoxia in all tissues. Death usually occurs when methemoglobin fractions approach 70% of total hemoglobin. We describe the case of a 35-year-old female patient with severe life-threatening isobutyl nitrite-induced methemoglobinemia of 75% of total hemoglobin. Toluidine-blue was administered as first-line antidotal therapy immediately, followed by hyperbaric oxygenation. The patient recovered uneventfully and could be discharged 3 days later.

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INTRODUCTION: Loss of renal function is accompanied by progressive increase in serum levels of intact parathyroid hormone (iPTH) in patients with end-stage renal disease (ESRD). There is a paucity of data regarding levels of PTH-(1-84) and its large carboxyl-terminal fragments (large C-PTH fragments) and progressive loss of kidney function in patients with chronic kidney disease (CKD). The current study was undertaken to describe the glomerular filtration rate (GFR)-dependent plasma concentrations of PTH-(1-84) and related large C-PTH fragments in adult patients with CKD by using different commercially available PTH assays. METHODS: We studied 80 Caucasian patients with CKD stages 1-5 without renal replacement therapy. Creatinine clearance was calculated by the Modification of Diet in Renal Disease (MDRD) formula. Levels of iPTH were determined by second-generation assays (iPTH Elecsys system, Roche Diagnostics; DUO total iPTH, Scantibodies Laboratory, Inc.; iPTH, Nichols Institute Diagnostics). Third-generation assays were used to measure PTH-(1-84) (CAP (cyclase activating PTH), Scantibodies; Bio-Intact PTH, Nichols). Levels of large C-PTH fragments and ratios of PTH-(1-84)/large C-PTH fragments were calculated and statistical analyses performed. RESULTS: Levels of iPTH and PTH-(1-84) showed CKD stage-dependent increases. Variations among the assays increased with progressive loss of kidney function. The assay from Scantibodies showed a GFR-dependent decrease of the ratio 1-84 PTH / large C-PTH fragment that was not observed with the Nichols assay. CONCLUSION: Increasing variations among the assays with progression of CKD emphasize the fact that the interpretation of measurements must take into consideration the specific assay. We found evidence for a possible preferential increase of the level of large C-PTH fragments over 1-84 PTH in a CKD stage-dependent manner (Scantibodies). The clinical implications of this finding have to be further evaluated by bone biopsy studies.

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True access recirculation (AR) measured by ultrasound dilution technique is usually absent in well-working shunts. It occurs with low access flows (Qa). High access flow rates are assumed to prevent AR. Two major exceptions to these rules are known: presence of intra-access strictures and inadvertently reversed blood lines. We present an additional exception in which true access recirculation occurred in a native arteriovenous (AV) fistula with correct placement of bloodlines. Surprisingly, access blood flow exceeded pump blood flow (Qb) almost threefold. The situation was clarified by a magnetic resonance angiogram showing a collateral forming a functional loop. This loop led to true access recirculation in one branch, although overall blood flow through both branches appeared to be adequate. The different findings in this shunt over time give insight into the often complex pathophysiology of native fistulae. This case proves that seemingly adequate access flow does not necessarily prevent access recirculation in native AV fistulae. We suggest monitoring both access flow and recirculation in hemodialysis accesses on a regular basis.

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Enoyl-CoA hydratase:3-hydroxyacyl-CoA dehydrogenase bifunctional enzyme is one of the four enzymes of the peroxisomal beta-oxidation pathway. Here, we report the full-length human cDNA sequence and the localization of the corresponding gene on chromosome 3q26.3-3q28. The cDNA sequence spans 3779 nucleotides with an open reading frame of 2169 nucleotides. The tripeptide SKL at the carboxy terminus, known to serve as a peroxisomal targeting signal, is present. DNA sequence comparison of the coding region showed an 80% homology between human and rat bifunctional enzyme cDNA. The 3' noncoding sequence contains 117 nucleotides homologous to an Alu repeat. Based on sequence comparison, we propose that these nucleotides are a free left Alu arm with 86% homology to the Alu-J family. RNA analysis shows one band with highest intensity in liver and kidney. This cDNA will allow in-depth studies of molecular defects in patients with defective peroxisomal bifunctional enzyme. Moreover, it will also provide a means for studying the regulation of peroxisomal beta-oxidation in humans.

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After mimosa and quebracho extracts, chestnut extract is the third most important vegetable tannin used for leather production. It is produced only in Europe on the northern side of the Mediterranean sea. The extract is prepared by hot water extraction of the bark and timber, followed by spray-drying of the solution. Analysis shows that there are insignificant variations in extract quality between batches, so the extract can be used with modern automated leather production systems. The extract contains approximately 75 percent active tanning substances. The primary component is castalagin, along with smaller amounts of vescalagin, castalin, and vescalin. A castalagin-based pharmaceutical product is currently in use for prevention and treatment of diarrhea in pigs and cattle that is caused by changes in diet. The beneficial effect is due to prevention of water losses through mucous membranes. The castalagin may also form chelates with iron, which influences the reabsorption of the metal in the animal digestive tract.

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