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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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We report a case of hypercalcemia in a female patient who was restarted on hemodialysis 22 years after renal transplantation. Graft biopsy showed chronic post-transplant nephropathy. Treatment with immunosuppressants and steroids was maintained owing to residual graft function. She was then given oral paracalcitol 1 µg/d for secondary hyperparathyroidism (iPTH 850 pg/mL) and her transplant medication was reduced and then discontinued. After this, the patient referred widespread joint pain, especially in the hips and subsequently presented with erythema nodosum. She also developed hypercalcemia and hyperphosphatemia which persisted after stopping paracalcitol. The clinical picture of increased serum calcitriol, with depressed PTH, suggested sarcoidosis, despite normal ACE levels, a chest X-ray and skin biopsy confirmed the diagnosis, and the patient was started on prednisone 50 mg/day, resulting in prompt normalization of both symptoms and blood chemistry. This is a rare case of hypercalcemia secondary to sarcoidosis in an uremic patient. The sarcoidosis was most likely suppressed by the transplant therapy and rapidly developed after this was suspended. Prompt diagnosis resulted in a good therapeutic response.

The wide distribution of the vitamin D receptor (VDR) suggests that its activators (VDRAs) are involved in diverse organ functions including the cardiovascular, immune, and reproductive systems. These actions are likely to be independent of PTH and calcium/phosphorus levels. Earlier studies had shown that calcitriol was able to favorably influence experimental nephritis, remnant kidney glomerulosclerosis, and interstitial fibrosis, mediated through inhibition of inflammatory cytokines. Recently, VDRAs were shown to inhibit the reninangiotensin system (RAS), acting directly on the renin gene promoter. This action is independent of the systemic RAS blockade. VDRAs also inhibit other important gene promoters including NF-kB and p65, which are known to foster inflammation and fibrogenesis. These multiple actions result in a decrease in macrophage infiltration, fibroblast activation, and endothelial mesenchymal transition in the kidney. These findings represent the rationale for the use of VDRAs, in association with RAS blocking agents, to counteract the progression of renal injury characterized by inflammation and neofibrogenesis. However, despite promising preliminary results, the human studies available to date do not allow to draw definitive conclusions on this matter.

PTH measurements are widely used by nephrologists because parathyroid function is frequently altered in uremic patients, with clinical implications for bone and the cardiovascular system. This is why both national and international guidelines recommend target values for PTH. However, the reliability of PTH assays is hampered by the presence of many circulating molecular types of the hormone, which are known to have different biological effects. The so-called first-generation methods measuring all C-term fragments were replaced by second-generation ones based on the double-antibody technique; the latter were shown to be more reliable and easy to use. These methods have been widely adopted, proving helpful for diagnosis, prognosis and treatment in clinical settings. However, when different second-generation methods were compared, inconsistent values were obtained. Moreover, it was shown that they cross-reacted with N-truncated fragments, including C-term 7-84 PTH, which do not display PTH activity. The more recently introduced third-generation methods exhibit higher specificity for the 1-84 whole molecule and are not liable to interference by N-truncated fragments. When compared to intact PTH, the whole-PTH methods yield about 50% lower values, but the difference remains constant through the entire range of PTH values. Indeed, despite different absolute results either between whole and intact PTH or within identical-generation methods, there are very close correlations among them, with coefficients above 0.95. Thus, most assays can be considered reliable but the different results, if not correctly interpreted, may give rise to misinterpretation on clinical grounds. It is agreed that these differences depend on the use of both different calibration standards and antibody specificity. We conclude that, irrespective of the method used, one should clearly know what PTH is being measured, using specific reference ranges and applying specific targets.

The current 3rd edition of the Italian Society of Nephrology guidelines has been drawn up to summarize evidence of key intervention issues on the basis of systematic reviews (SR) of randomized trials (RCT) or RCT data only. In the present guideline, evidence of the use of calcimimetics, phosphate binders, vitamin D and vitamin D analogues for treating secondary hyperparathyroidism in chronic kidney disease (CKD) is presented.SR of RCT and RCT on interventions for secondary hyperparathyroidism in CKD were identified referring to a Cochrane Library and Renal Health Library search (2005 update).Three SR and 8 RCT were found addressing this intervention issue. Methodological quality of available RCT was suboptimal according to current methodological standards. Calcimimetics used in patients receiving haemodialysis or peritoneal dialysis are more effective than placebo in controlling secondary hyperparathyroidism (reduced parathyroid hormone levels, calcium levels and phosphorus levels). All phosphate binders are effective in controlling hyperphosphatemia but different doses are to be used with different agents to achieve similar targets. Dosing needs to be adjusted according to phosphorus levels. Vitamin D and its analogues are recommended in CKD patients, although there is no significant evidence of superiority of individual agents in head-to-head comparisons. Dosing should be based on baseline parathyroid hormone levels, but the risk of hypercalcemia should also be considered.Available evidence suggests that calcimimetics, phosphate binders and vitamin D or its analogues are effective in the treatment of secondary hyperparathyroidism. Superiority of individual agents or doses is still deeply debated. Further studies are necessary to test these issues.

The epidemiological impact of nephrolithiasis stems from a significant and increasing prevalence in western countries. While the kidney is the end-organ of the disease, the causes are often more general, including metabolic derangements, pri-mary diseases of other organs and systems, hereditary renal or non-renal defects. In this context, nephrological expertise is highly recommended and could considerably improve disease outcomes. The nephrologist's involvement should start while the patient is acutely affected by renal colic. In this setting medical intervention is aimed at counteracting pain, favoring progression in the urinary tract, and preventing renal injury. The choice for urological procedures should take into account the potential for harmful effects of obstruction, infection, and prolonged pain. After the patient has undergone non-invasive procedures medical intervention improves the management of residual fragments, reduces the risk of stone recurrence, and increases compliance to the stone center, as a premise for considering patients for metabolic evaluation and subsequent medical treatment. Current study protocols, including chemistries, physicochemistry and possibly genetics, are the basis for a rational treatment of recurrent stone disease. Secondary nephrolithiasis caused by systemic disorders is screened out and treated specifically. Hereditary forms can be identified by genetic analysis and strictly followed and treated. While medical therapy can cure some types of renal stones, prolonged remission is seldom obtained in calcium nephrolithiasis. However, recurrence rates are greatly reduced, and this lessens the need for urological procedures, risk of infection/obstruction and, ultimately, progression to renal insufficiency. In the face of a multidisciplinary approach to renal stone disease, the nephrologist has a key role in the successful management of these patients.

A four-year-old male child was admitted with severe renal failure, apparently recent in onset and he was treated with peritoneal dialysis (PD). A renal biopsy showed interstitial cellular infiltration with crystals within the tubules and sclerotic glomeruli. Type I hyperoxaluria was diagnosed and the child received a liver and kidney transplant after 10 months of dialysis. Two years later, he has normal renal function, and blood and urine oxalate levels are within normal ranges.

The pathogenesis of nephrolithiasis, based on the anomalies of the urinary environment, demands metabolic and physicochemical assessment for the medical management of patients. Standard metabolic protocols include the measurement of pertinent urine chemistry values and the calculation of the extent of saturation in stone-forming salts. However, patients are often given fragmentary and hard-to-consult reports and so this weakens the strength of the therapeutic recommendations. This paper introduces LithoRisk, a dedicated software which graphically represents risk profiles of stone formation, including the extent of saturation.LithoRisk uses the results of 24-h urine chemistry values widely available in hospital laboratories, i.e., sodium, potassium, calcium, magnesium, ammonia, phosphate, sulphate, citrate, oxalate, chloride, pH and urine volume. Uric acid and cystine are optional. The relative supersaturation (beta), estimated according to our own ab initio calculation, is given in a scale whereby beta=1 is saturation, beta1 under - and beta1 oversaturation. LithoRisk is available as a CD-ROM and can be loaded on Windows 95/98/Millenium/XP. Colour or laser printers are suitable for printed records.LithoRisk is easily loaded on any PC by following video instructions. Once the loading of the program is completed a grey icon LithoRisk appears on the Desktop. The program can be opened by clicking twice on the icon. The patients data page first appears on the screen and is followed by the evaluation page for the input of variables. This generates the graph representing the diagnostic lithorisk profile, which is drawn as a line connecting different values, according to a specific scale and related to an arbitrary normal point. Normal values are shown as green lines, whereas abnormal ones are red. The beta values for calcium oxalate and phosphate, uric acid and cystine are instantaneously calculated and reported on the graph.LithoRisk produces a complete, unique and easy to understand report that includes all relevant parameters, it therefore expresses the overall risk of stone formation. It requires the results of chemistry tests done on the same 24-h urine collection, and carried out using suitable preservatives. If the tests for unusual parameters, i.e. sulphate and ammonia, are unavailable, one can use default values with minimal alterations on beta calculation. In spite of being arbitrary, the normal thresholds values are based on widely accepted literature data. The risk profile recognises the most relevant abnormalities and enables the establishment of individual targets aimed at reducing the propensity towards stone formation.

Parathyroid hormone (PTH) has important applications in the nephrological clinical practice. Because assays of Intact PTH (I-PTH) are liable to interferences by N-truncated fragments, a novel method for whole-(1-84) PTH has been proposed. This study is aimed at comparing the latter with some of the previous I-PTH assays. For each method the results are referred to pertinent markers of mineral metabolism.We enrolled 171 subjects, including 56 healthy controls (C), 65 calcium stone- formers (CaSF), 40 haemodialysis patients (HD), 10 with primary hyperparathyroidism (PHP). On blood samples we measured: I-PTH by four methods (N-Tact, Advantage, Elecsys, Scantibodies), whole-(1-84) PTH, defined as CAP (Cyclase Activating PTH), total and ionised calcium, phosphate, vitamin D, osteocalcin and Crosslaps. The difference between I-PTH and CAP Scantibodies is defined as CIP (Cyclase Inhibiting PTH).Despite relating to each other (r0.97) PTH values varied remarkably among methods. For all methods, the reference intervals differed from those provided by the producer. Assuming these new ranges, 10 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. In HD the differences among methods were even greater, there were inverse (p0.05) and direct (p0.001) relationships with ionised calcium and osteocalcin-crosslaps, respectively. The CAP/CIP ratio was lower in low bone turnover patients, but the two subgroups widely overlapped.This study indicates that the reliability of I-PTH assays is still unsatisfactory, and none of the four methods emerged as the best. Assay for CAP only improves diagnostic efficiency, whereas the CAP/CIP ratio does not exhibit powerful discriminating capacity. Our suggestion is that each Centre should establish its own reference ranges. PTH assay should always be coupled with measurements of other markers of mineral metabolism as well as renal function.

Despite intensive studies in the last decades many aspects of nephrolithiasis still remain to be elucidated. Supersaturation with respect to lithogenic substances explains stones composed of cystine, uric acid, struvite, and calcium stones secondary to systemic diseases. In this subset there is a clear separation between patients and controls, and stone activity is well related to alterations in the physicochemistry of the urine environment. The understanding of the mechanisms of idiopathic calcium nephrolithiasis, on the other hand, is controversial, because we are still unable to establish clear-cut cause-effect relations between metabolic and physicochemical abnormalities and stone formation. Recent studies have been centered on the kidney, not only as the end organ of biochemical derangements due to systemic or environmental factors, but also as a complex laboratory where some events conduct to and others defend from lithogenesis. Many of these phenomena occur in the proximal tubule. Molecular biology has explained some types of hypercalciuria, which are due to genetic mutations altering tubular function, and similar results are expected for hypocitraturia and hyperoxaluria. The latter is conducive to stone formation through several mechanisms including supersaturation, oxidative stress on tubular cells, and interference with some natural inhibitors. The long list of inhibitors includes ionic and macromolecular moieties, some being produced within the nephron in response to lithogenic insults, and some affecting not only crystallization but also crystal cell adherence. Crystal trapping is believed to anticipate a renal stone. However, much has still to be clarified on their actual role in calcium nephrolithiasis, by what mechanisms they act, if patients and controls differ in the excretion and structure of some inhibitors, and whether differences are genetically determined.

The overall probability of forming stones differs in various parts of the world: 1-5% in Asia, 5-9% in Europe, 13% in North America, 20% in Saudi Arabia. The composition of stones and their location in the urinary tract, bladder or kidneys may also significantly differ in different countries. Moreover, in the same region, the clinical and metabolic patterns of stone disease can change over time. We examined some epidemiological evidence about the main risk factors for stone formation, both individual and environmental. A slightly higher rate of renal stone disease emerged in males than in females, and in white Caucasians than in Blacks. Stones in the upper urinary tract appear to be related to the life-style, being more frequent among affluent people, living in developed countries, with high animal protein consumption. Bladder stones are nowadays mainly seen in the Third World, on account of very poor socio-economic conditions. A high frequency of stone formation among hypertensive patients has been reported, and among those with high body mass as well. There is no evidence of any rise in the risk of stone formation in relation to dietary calcium intake or tap water hardness.

In this paper, the clinical and metabolic patterns of nephrolithiasis in different ages of adulthood are studied.Eight-hundred patients observed at the Mauriziano Hospital between 1990 and 1995, were classified into 3 groups, on the basis of age at the onset of disease: A: 20 through 39 years; B: 40 through 59; C: 60 years and over.Calcium-oxalate stones had a lower recurrence in C (19.1%) and B (31.5%) than in A (41.7%). Pure uric acid stones recurred in 18.9% of C, 16.7% of B and 4.3% of A. The prevalence of hypercalciuria was higher in A (50.3%) than in B (35.9%) and C (36%); so did hypocitraturia. Hyperuricuria was lower in A (5%, p0.05) than in B (9.4%) and C (10%). Low urine pH (5.5) was 13% in A, 21.3% in B, 38% in C. Prevalence of hyperoxaluria was about 14% in all groups. The whole prevalence of secondary forms of stone disease was 13% in A, 12% in B and 30% in C. Differences among groups were mainly due to prevalence of urological abnormalities and urinary tract infection. In patients without metabolic disturbances. urological abnormalities or urinary tract infections altogether, were 4.6% in A; 5.2% in B; 33% in C. Urological approach removed 8% of stones in A, 5.6% in B and 10.2% in C.Higher morbidity in younger patients could be due to a lower prevalence of easier-passing uric acid stones. The higher occurrence of urological disturbances and struvite stones in the elderly could explain the higher morbidity in this group.

Specimens were collected from 22 Italian patients with primary hyperoxaluria type 1 (PH1). Ten of them had already been analyzed by molecular biology. To clarify the molecular characteristics of the AGXT gene disease responsible for PH1, DNA samples were examined for known mutations by hybridisation of PCR products with Sequence Specific Oligonucleotides (PCR-SSO). We planned to identify new mutations of the AGXT gene by heteroduplex analysis followed by direct sequencing. We had already standardized a) the conditions for the amplification of the 11 exons of AGXT, b) the PCR-SSO technique and c) the heteroduplex analysis of amplified products. Preliminary results demonstrated that the AGXT mutations described in previous studies were found only in 40% of the examined Italian patients with PH1. The remaining 60% of mutations should be characterised in future studies.

The hyperoxaluria syndromes can be differentiated by the assessment of associated abnormalities in generation and urine excretion of metabolically related molecules. Based on the experience gained in our laboratory during the last decade, we have developed a comprehensive diagnostic work-up, which includes measurements of oxalate, glycolate and L-glycerate in plasma, urine and dialysis fluids, and an assay for AGT activity on liver biopsy. The availability of reliable assays for each of these parameters is indispensable for the recognition and differentiation of hyperoxalurias. Patients suspected to have abnormalities in oxalate metabolism are first screened by analysing spot urines and serum, and subsequently are subjected to more extensive studies using properly pre-treated blood samples and 24-hour urine collection. AGT activity, in the case of PH1, is assayed on few milligrams liver specimen by using a sensitive chromatographic procedure. Pertinent biochemistries will also assist in the long-term medical follow-up of these patients and in view of the choice of renal replacement or transplantation strategies.

To investigate patterns of monolateral and bilateral nephrolithiasis, we enrolled 196 patients with idiopathic calcium stone disease (ICaSD) and 36 with proven primary hyperparathyroidism (PHP). Monolateral disease occurred in 45 subjects with ICaSD and 3 with PHP. All had had three or more stone events. They were studied for a number of clinical and biochemical parameters. The expected prevalence of monolateral stone disease was calculated according to the binomial distribution of random events. Whereas the observed and expected prevalence of monolateral nephrolithiasis did not differ in PHP, the distribution did not follow a chance pattern in ICaSD, since monolateral disease was still frequent among patient with more than 6 episodes. To find out whether monolateral and bilateral ICaSD had distinct pathogenic mechanisms the two groups were compared for clinical and biochemical patterns: no differences emerged concerning metabolic derangements, urine saturation and diet-related biochemistries. Bilateral stone-formers had a higher recurrence rate, but a similar number of stone-operations or ESWL. In 81 of 151 bilateral idiopathic stone-formers in which we were able to assess the exact number of stone events in left and right kidney, the distribution of stones between kidneys did not differ from the binomial distribution. In conclusion, while PHP-associated nephrolithiasis presents predictable patterns, ICaSD comprises a subset in which the disease occurs monolaterally. These forms cannot be distinguished from bilateral forms with common clinical features or routine biochemistries.

An enzyme-spectrophotometric method to determine citrate in biological fluids is proposed, based on citrate lyase-catalyzed and phenylhydrazine reactions. The enzyme converts citrate into oxaloacetate, which, in the presence of phenylhydrazine, is transformed into the corresponding phenylhydrazone. The ultraviolet-absorbing product is determined by absorbance measurement at 330 nm. The method is more precise and twice as sensitive as the traditional citrate lyase method and, because it does not require the use of additional enzymes and coenzymes, is cheaper and simpler. Mean analytical recovery of citrate averaged 100.7% +/- 2.2%, imprecision (CV) of the assay for citrate at 0.96 mmol/L (urine) was 2.0%, and the lower limit of quantification was 0.08 mmol/L. Results correlated well with those by both ion-chromatographic and traditional citrate lyase methods.

Primary hyperoxaluria (PH) type 1 and type 2 are autosomal recessive defects of oxalate metabolism resulting from glyoxylate accumulation which occurs by two distinct pathways. PH1 is associated to glycolic aciduria; PH2 to L-glyceric aciduria. Because hyperoxaluria leads to nephrolithiasis or nephrocalcinosis in both, they can be differentiated only through detection of the associated acidurias. However, glycolate and L-glycerate assays are not widely available and, in the setting of ESRF, diagnosis is hampered by a number of misleading events. At any stage of the disease diagnosis is crucial because there are differences between the two forms in clinical behaviour, long-term prognosis, and treatment. In this paper we outline diagnostic criteria for identification of PH2 in two patients, one with maintained renal function and one with ESRF on CPD, based on the use of a novel HPLC assay of L-glycerate in different body fluids. With the routine application of this procedure PH2 has been identified in two of 23 patients fulfilling criteria for diagnosis of PH. This suggests that the type 2 variant of PH may occur more frequently than so far suspected, and should be tested for even in the setting of ESRF.

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).

Urinary L-glycerate was formerly determined by an isotope-dilution colorimetric method coupled with both the chiralselective enzyme reaction and evaluation of the optical rotatory dispersion curve. More recently, gas-liquid chromatography has been used for the screening of glyceric aciduria, but this technique requires a further enantio-selective gas-chromatographic separation for characterizing the L-(S)-configuration. These methods require liquid-liquid extraction, evaporation to dryness of the extract, chromatographic purification of the reconstituted extract, lyophilization of the eluate and derivatization of the residue. The resulting procedure is therefore complex and time consuming.

This new procedure for determining oxalic acid in plasma is based on sample deproteinization with hydrochloric acid and acetonitrile and subsequent ion-chromatographic assay of the neutralized supernate. Sample pretreatment produces very clean samples, which ensures long column life. Mean analytical recovery of oxalate (5.0-10.0 mumol/L) added to plasma samples averaged 98.6 +/- 6.2%; imprecision (CV) was 5.2% (at 2.2 mumol/L) and the detection limit was 0.5 mumol/L at a signal-to-noise ratio of 5:1. Ascorbate to oxalate conversion was0.2%, indicating that the procedure is free from ascorbate interference. Plasma oxalate concentrations, measured in samples from 31 healthy persons, ranged from 0.8 to 3.4 mumol/L (mean 1.89, SD 0.75 mumol/L), which agrees with results from indirect radioisotopic dilution methods.

Regular dialysis treatment (RDT) does not obviate hyperoxalemia of chronic renal failure (CRF). However, there is emerging evidence suggesting that current dialysis prescription is not always associated with progressive oxalate accumulation. In view of the controversy still concerning this issue we have investigated on plasma profiles and dialysis kinetics of oxalate in patients on RDT. Oxalate was determined by ion chromatography on serum ultrafiltrates and on the whole dialysate in 23 stable patients on RDT for end-stage renal failure unrelated to primary hyperoxaluria. Nine patients were on traditional hemodialysis (HD) and 14 on soft hemodiafiltration (HDF). Plasma profiles showed that dialysis patients were virtually always hyperoxalemic. Dialysis reduced plasma oxalate by more than 60%. There was a post-dialysis oxalate rebound averaging 9.6% at 30 minutes from the end of dialysis. Oxalate dialyzer clearances were mildly higher on HDF than on HD, and were lower than both urea and creatinine clearances, irrespective of the dialysis technique. Distribution space of oxalate was 21.5 1, that is 37.3% of dry body weight, and was quite similar to estimates obtained in normal subjects and in patients with CRF by alternative isotope dilution methods. Oxalate appearance rate averaged 337 +/- 69 mumol/24 h and was not different from the daily oxalate excretion assessed in 40 healthy subjects. Oxalate appearance was significantly related to urea generation and protein catabolic rates. From our results we conclude that, unless metabolic generation of oxalate is increased, current dialysis programs should prevent progressive oxalate accumulation in the majority of the patients.

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.

In an attempt to decrease ascorbate interference on the ion-chromatographic determination of urinary oxalate, we compared the effectiveness of four different methods for ascorbate elimination by analyzing a representative urine pool supplemented with successive ascorbate additions. Two of the methods--treatment with ferric ions or boric acid--have been described elsewhere; treatments with nitrites or ascorbate oxidase (EC 1.10.3.3) are investigated here as possible alternatives. Consideration of the main features, advantages, and drawbacks of the four procedures leads us to conclude that boric acid dilution is a good routine method and that pre-incubation with ascorbate oxidase reliably prevents ascorbate interference in assays of urinary oxalate.

Keeping calcium (Ca) balance in equilibrium is one of the main goals in dialysis patients, and the dialysis schedule by itself can affect mineral metabolism. The aim of this paper is to evaluate Ca and magnesium (Mg) balances on different Quf in patients on RDT. Twenty-one patients [7 on hemodialysis (HD), 14 on hemodiafiltration (HDF)] were studied. Ca and Mg balances were assessed by measuring Ca and Mg in whole dialysis fluid. One patients on HDF was observed for three dialysis sessions, on different Quf, and negative values were observed for Quf above 70 ml/min. Mg balance was always negative. We conclude that an accurate survey of Ca balance is mandatory in high-efficiency dialysis, when high fluxes may produce adverse effects on mineral 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.

Oxalosis is a rare disorder, in which there are widely and evenly spread deposits of oxalate crystals in the kidneys with progressive renal failure. An inborn error of metabolism is the cause of oxalosis. The incidence of this disease in boys and girls is practically equal. Most patients do not survive their 20th year. In our case there were changes in the skeleton and extensive deposits of oxalates in the kidneys.

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.