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Summary Parathyroid hormone (PTH) has important applications in the clinical practice both primary (PHP) and secondary (SHP) hyperprathyroidisms. However, assays of PTH are liable to interferences. This study is aimed at assessing diagnostic efficiency of different PTH assays associated with pertinent markers of mineral metabolism. We studied 84 patients prior to and three to six months after successful parathyroidectomy (PTX) for PTH and pertinent chemistries. Prospectively, 171 subjects on the whole were assessed for I-PTH by four methods (N-Tact, Advantage, Elecsys, Scantibodies), whole-(1–84) PTH, defined as Cyclase Activating PTH (CAP), total and ionised calcium, phosphate, vitamin D, osteocalcin and crosslaps. There were significant changes of PTH after PTX and these were paralleled by concurrent changes in pertinent chemistries. Despite relating to each other (r > 0.97), PTH values varied remarkably among methods. For all, reference intervals differed from those provided by the producer. Ten CaSF had over-range values not always associated with abnormalities of mineral metabolism. One of the PHP patients was normal for I-PTH with 2/4 methods. Among HD differences among methods were even greater, there were direct relationships with osteocalcin and crosslaps (p

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Western diets rich in animal protein result in long-term acid loading that, despite corresponding increases in net renal acid excretion, may induce a chronic state of acidemia. This may have deleterious effects on both the kidney and bone, by increasing the risk of calcium stone in the former and leading to chemical dissolution of mineral alkaline salts in the latter. Whereas supplementation with alkaline citrate has been shown to reduce stone recurrences, its effect on bone turnover has received less attention. The aim of the present study was to evaluate whether potassium citrate favorably affects bone turnover markers in postmenopausal females with low bone density. Thirty women, aged 58 +/- 8.1 years, were enrolled and studied on basal conditions and after a 3-month course of potassium citrate supplementation (0.08-0.1 g/kg b.w. daily). Twenty-two women concluded the study while 8 withdrew. Twenty-four age-matched healthy women were taken as control cases. All were evaluated for electrolyte and acid-base balance-related parameters, bone turnover, markers and renal function. A significant decrease in net acid excretion was observed upon citrate supplementation, and this was paralleled by a significant decrease of urinary deoxypyridinolines, hydroxyproline-to-creatinine ratios, and, to a lesser extent, serum osteocalcin. Percent variations of urine citrate were inversely related to those of deoxypyridinolines and hydroxyproline. No change in these chemistries occurred in the control group. Our results suggest that treatment with an alkaline salt, such as potassium citrate, can reduce bone resorption thereby contrasting the potential adverse effects caused by chronic acidemia of protein-rich diets.

QT interval prolongation increases the risk of ventricular arrhythmias and sudden death in diabetic autonomic neuropathy and ischemic heart disease. In end-stage renal disease (ESRD), the effects of hemodialysis on QT interval are diverse and the influence of autonomic neuropathy has yet to be clearly defined.Sixty-nine ERSD patients (age 64 +/- 14) were studied. Prior to the dialysis session, patients underwent four standard autonomic cardiovascular tests; before and after the dialysis session, a 12-lead ECG was recorded. Corrected QT intervals (QTc) were measured and QT dispersion (QTd) was calculated. Twelve subjects (age 59 +/- 6) with normal renal function served as control group.Compared to controls, ESRD patients showed a longer QTc (434 +/- 26 vs 414 +/- 28 ms; p = 0.016) and a similar QTd (35 +/- 13 vs 37 +/- 14 ms; p = 0.54).QTc was440 ms in 33.3% of the patients. No difference in the prevalence or score of autonomic neuropathy was observed between the subgroups with and without a prolonged QTc. After the hemodialysis session, QTc increased in 56% and decreased in 43% of the patients, and QTd increased in 45 % and decreased in 55% of the patients. QTc and QTd changes were not related to the presence of autonomic neuropathy.A large variability in QTc and QTd response was observed after hemodialysis. Autonomic neuropathy did not contribute to QTc and QTd length, nor to QTc and QTd change after dialysis.

The specificity of the assay of liver alanine: glyoxylate aminotransferase (AGT) activity is affected by the presence of glutamate: glyoxylate aminotransferase (EC 2. 6. 1. 4) (GGT), which cross-reacts with alanine and glyoxylate. As a consequence, the assay for GGT activity must be coupled to that of the “raw” AGT activity to obtain an indirect estimate of the “true” AGT activity.

The risk of calcium stone formation in the course of primary hyperparathyroidism (PHPT) is known to arise from increases in excretion of promoters such as calcium1, phosphate2 and perhaps oxalate. In contrast, the role of inhibitors has so far received less attention and very little is known about citrate, which is a main inhibitor of calcium salt crystallization in urine. Therefore, we have studied patterns of citrate excretion and renal handling in patients with PHPT and calcium nephrolithiasis and their changes after successful parathyroidectomy (PTX).

The importance of oxalate (Ox) in human pathology stems from the very low solubility of its calcium salts in biological fluids. Renal excretion is the exclusive way of Ox removal from the body and the efficiency of renal clearance fixes plasma Ox in the order of μmol/l and plasma saturation with calcium oxalate (βc a O x ) safely low. However urine turns out to be near always supersaturated and this accounts for the outermost prevalence of CaOx nephrolithiasis (NL) in man. This crucial role of the kidney accounts for the risk of Ox deposition within renal tissues whenever Ox generation increases, featuring Oxalate Nephropathy. Moreover when renal function is lost, progressive Ox retention induces systemic oxalosis. Severe hyperoxaluria (HOx) is produced by two variants of a rare inborn defect of Ox metabolism. Biochemical features of 5 patients with type I primary HOx (PHOx) are described and the mechanisms of renal and systemic oxalosis discussed. Crohn’s and other ileal diseases are well known causes of enteric HOx. Intestinal absorption of Ox raises to twofold normal and increases urine Ox in such a way as to yield very high values of βc a ox. Recurrent CaOx stones represent a threat for renal function, namely if renal amyloidosis superimposes. Mild Hox may occur in some 20% of idiopathic CaOx stone-formers (ICaSF). This novel entity is currently under study and is held to represent a heterogeneous syndrome. Renal failure which occurs in less than 20% of ICaSF appears to be poorly related to changes in Ox metabolism.

Muzolimine (M) is a potent diuretic drug recently introduced into clinical use, which shows both high cieling and long acting properties (1,2). It has been held effective in hypertension and in oedematous syndromes from cardiac, hepatic and renal aetiology (3,4,5). This study was designed to evaluate the diuretic or any other effect on tubular transport in patients (pts) with oedema from nephrotic syndrome in course of diverse renal diseases.

We have previously reported our experience with the long-term management of idiopathic calcium stone disease (ICaSD) and observed that the administration of drugs such as thiazides (HCT) and/or allopurinol (ALP) in addition to careful dietary management failed to give further benefit to the patient. The aim of this paper was to relate the clinical response to the biochemical and physico-chemical changes induced by three therapies in order to try to explain why different kinds of treatment provided similar results.

The Authors present their results on the intestinal absorption and renal handling of oxalate in normal subjects.

From 1963 through 1979 we saw 106 patients with cystinuria: 62 had recurrent stone disease and 44 were stone free. Three of the stone-forming patients had the “pure” form of cystinuria1,2, and 59 had the classic form. They came from 35 families and we were able to study 18 families. In all cases the diagnosis was made by chemical analysis and/or I.R. spectrography, and/or x-ray diffraction of the stone, and by urinary aminoacid patterns (ion exchange column, lithium buffer3).

Objective: Gout is the most common arthritis in adults. Despite the availability of valid therapeutic options, the management of patients with gout is still suboptimal. The Italian Society of Rheumatology (SIR) aimed to update, adapt to national contest and disseminate the 2006 EULAR recommendations for the management of gout. Methods: The multidisciplinary group of experts included rheumatologists, general practitioners, internists, geriatricians, nephrologists, cardiologists and evidence-based medicine experts. To maintain consistency with EULAR recommendations, a similar methodology was utilized by the Italian group. The original propositions were translated in Italian and priority research queries were identified through a Delphi consensus approach. A systematic search was conducted for selected queries. Efficacy and safety data on drugs reported in RCTs were combined in a meta-analysis where feasible. The strength of recommendation was measured by utilising the EULAR ordinal and visual analogue scales. Results: The original 12 propositions were translated and adapted to Italian context. Further evidences were collected about the role of diet in the non-pharmacological treatment of gout and the efficacy of oral corticosteroids and low-dose colchicine in the management of acute attacks. Statements concerning uricosuric treatments were withdrawn and replaced with a proposition focused on a new urate lowering agent, febuxostat. A research agenda was developed to identify topics still not adequately investigated concerning the management of gout. Conclusions: The SIR has developed updated recommendations for the management of gout adapted to the Italian healthcare system. Their implementation in clinical practice is expected to improve the management of patients with gout.

Primary hyperoxaluria type 1 is an autosomal recessive disorder of glyoxylate metabolism, caused by a deficiency of alanine:glyoxylate aminotransferase, which is encoded by a single copy gene (AGXT). The aim of this research was to standardize denaturing high-performance liquid chromatography, a new, sensitive, relatively inexpensive, and automated technique, for the detection of AGXT mutation. Denaturing high-performance liquid chromatography was used to analyze in blind the AGXT gene in 20 unrelated Italian patients with primary hyperoxaluria type 1 previously studied by other standard methods (single-strand conformation polymorphism analysis and direct sequencing) and 50 controls. Denaturing high-performance liquid chromatography allowed us to identify 13 mutations and the polymorphism at position 154 in exon I of the AGXT gene. Hence the method is more sensitive and less time consuming than single-strand conformation polymorphism analysis for the detection of AGXT mutations, thus representing a useful and reliable tool for detecting the mutations responsible for primary hyperoxaluria type 1. The new technology could also be helpful in the search for healthy carriers of AGXT mutations amongst family members and their partners, and for screening of AGXT polymorphisms in patients with nephrolithiasis and healthy populations.