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Despite being recommended by most guidelines, the metabolic evaluation of patients with nephrolithiasis has limited diffusion due to difficulties relating both to the access to laboratory investigations and to urine collection modalities. Consequently, in addition to the classical 24-h collection, alternative and simplified collection modes have been proposed. We report here on the comparison between metabolic evaluation carried out on 24-h double collection (Lithotest) and overnight spot urines (RF test). Fifty-four patients with stone disease were enrolled, excluding patients with infection or cystine stones. For Lithotest, we measured all analytes necessary to calculate state of saturation (ß) with calcium oxalate, brushite and uric acid, by means of Lithorisk.com. For RF, we measured calcium, magnesium, oxalate, citrate, sulphate, phosphate, pH and creatinine. The comparison was made with creatinine ratios. An estimate of ßCaOx, ßbrushite and ßAU was obtained also on RF urines by using simplified algorithms. We found highly significant correlations between all parameters, despite quite different means. There was a nice correspondence between the two sets of measurements, assessed by the Bland-Altmann test, for calcium, oxalate, citrate, sulphate, urate and pH. Overnight urine had higher saturations compared to 24-h one owing to higher concentration of the former. In conclusion, RF test on overnight urine cannot completely replace Lithotest on 24-hr urine. However, it can represent a simplified tool for either preliminary evaluation or follow-up of patients with stone disease., (Copyright by Società Italiana di Nefrologia SIN, Rome, Italy.)

The natural history of urinary kidney stone disease includes the risk of relapses and can be associated with the risk of chronic kidney disease, bone and cardiovascular disease. For this reason, a wide clinical-metabolic assessment of the kidney stone patient is of great importance since the first presentation of the stone, to set an appropriate preventive treatment. The proposed diagnostic-therapeutic pathway includes a careful medical history, in order to highlight a secondary kidney stone disease and the main risk factors for kidney stones, chronic renal disease, or cardiovascular and bone disease; a metabolic evaluation on multiple levels, according to the severity of the disease, and the presence or absence of risk factors, and appropriate instrumental investigations. Thus, the information collected makes it possible to set a preventive treatment consisting of general rules and, if necessary, specific pharmacological or nutritional interventions. This paper has been prepared by the Italian Multidisciplinary Study Group for Kidney Stone Disease, and it is addressed to the several professional figures involved in the management of patients suffering from nephrolithiasis, from the emergency doctor to the general practitioner, urologist, nephrologist, radiologist, and dietician. A diagnostic-therapeutic pathway for patients with kidney stone disease was first published on this Journal in 2010. The present contribution aims at amending and updating the article published exactly ten years ago, to serve as an easy-to-use reference and to guide good clinical practice in this field., (Copyright by Società Italiana di Nefrologia SIN, Rome, Italy.)

Introduction: In this paper we investigated whether cholecalciferol supplementation, prescribed to treat vitamin D deficiency in patients with nephrolithiasis, increased the risk of stone recurrence., Methods: Calcium excretion and urine supersaturation with calcium oxalate (βCaOx) and brushite (βbsh) were evaluated in 33 kidney stone formers (aged 56±17; 12 males), both before and after therapy with cholecalciferol, prescribed as oral bolus of 100.000-200.000 UI, followed by maintenance doses, repeated every week (5.000-10.000 UI) or month (25.000-50.000 UI). During the study, patients followed a dietary regimen which included a daily calcium intake of about 800-1000 mg., Results: Urinary nitrogen, sodium and ash-acid excretion did not significantly change during the study. After cholecalciferol supplementation, the main results were as follows: both serum calcium and phosphate did not vary significantly; 25(OH)VitD₃ increased from 11,8±5,5 to 40,2±12,2 ng/mL (p<0,01); 1,25(OH) ₂ VitD₃ increased from 41,6±17,6 to 54,0±16,0 pg/mL (p<0,01); PTH decreased from 75,0±27,2 to 56,7±21,1 pg/mL (p<0,01); daily urinary calcium increased from 2,7±1,5 to 3,6±1,6 mg/Kg b.w. (p<0,01), whereas fasting urinary calcium did not change significantly. After therapy, βbsh increased from 0,9±0,7 to 1,3±1,3 (p=0,02) and βCaOx did not vary significantly. Before cholecalciferol supplementation, 6/33 patients (18.2%) were hypercalciuric, whereas 13/33 patients (39,4%) showed hypercalciuria after supplementation (pX²=0,03)., Conclusions: Cholecalciferol supplementation for vitamin D deficiency may increase both urinary calcium and urine supersaturation in stone formers. If vitamin D supplements are needed in these patients, a careful monitoring of urine metabolic profile is warranted, in order to customize the metaphylaxis accordingly (hydration, potassium citrate, thiazides)., (Copyright by Società Italiana di Nefrologia SIN, Rome, Italy.)

Citrate is a tricarboxylic acid and an intermediate metabolite of Krebs cycle. It contributes to oxidative metabolism of both kidney and liver. Alkaline sodium or potassium salts have the potential to increase alkaline reserve. In the kidney citrate is completely filtered at the glomerulus, undergoing to 10-40% tubular resorption. Renal insufficiency, even early, metabolic acidosis, potassium depletion induce hypocitraturia. Its importance in nephrolithiasis stems from its ability to form soluble complexes with calcium and to interfere with crystal formation, thus exerting a dual inhibition, thermodynamic and kinetic. Moreover, its alkalizing property has shown benefits of bone mineralization. The alkalizing effect is also useful in uric acid and cystine stone disease. Hypocitraturia has a significant incidence in the course of calcium nephrolithiasis, either secondary to aforementioned causes, or in idiopathic and/or familial forms. Citrate is used in the prevention of stone recurrences and given as tripotassic or potassium-magnesium salt, 0.1 mmol/kg/day in 2-3 dosages. In uric acid disease, in addition to prevention, it can induce dissolution of renal stones, provided urine pH is maintained at higher than 6.5 values. As concerns its effects on bone, it was shown to induce both decreases in marker of bone resorption and increases in bone mineral density., (Copyright by Società Italiana di Nefrologia SIN, Rome, Italy.)

Primary hyperparathyroidism (PHPT) may favor nephrolithiasis mainly through an increase in calcium and phosphate urinary excretion. Cinacalcet exhibits good efficacy to control hypercalcemia in PHPT, but it is not so far known whether it might be a useful tool to prevent stone recurrences. Of 67 patients with PHPT and recurrent nephrolithiasis, 55 underwent parathyroidectomy (PTX) and 12, not eligible to PTX, were prescribed Cinacalcet. All the patients were evaluated for mineral metabolism, including estimation of state of saturation for calcium oxalate (CaOx) and brushite (bsh), both at baseline and after either PTX or Cinacalcet. PTX compared to baseline reduced PTH (4617 vs 15786 pg/mL, p<0.01), calcemia (9.40.5 vs 11.30.9 mg/dL, p<0.01), calciuria (3.62.3 vs 9.24.5 mmol/24h, p<0.01), phosphaturia (18.47.1 vs 21.99.9 mmol/24h, p<0.05), CaOx (4.73.9 vs 9.86.8, p<0.01) and bsh (1.10.9 vs 3.22.2, p<0.01). Cinacalcet decreased both PTH (13379 vs 17187 pg/mL, p<0.05) and calcemia (9.70.6 vs 11.20.8 mg/dL, p<0.001), whereas no change was seen in calciuria (7.42.2 vs 7.42.4 mmol/24h, p=ns), phosphaturia (21.97.3 vs 23.06.5 mmol/24h, p=ns), CaOx (6.92.7 vs 5.42.5, p=ns) and bsh (1.71.1 vs 1.31.3, p=ns). We conclude that in patients with PHPT, PTX is able to decrease the risk for crystallization of calcium salts, whereas calcimimetic Cinacalcet did not. Therefore, in patients with PHPT complicated with nephrolithiasis only PTX can improve urine biochemistries thereby reducing the risk for recurrent calcium stone disease.

Oxalate (Ox) is an end-product of metabolism, important for poor solubility of its calcium salt in biological fluids. Ox can therefore be found in about 70% of urinary calculi. Hyperoxaluria (HOx) defined as Ox exceeding 0.5 mmol)/day, may cause nephrolithiasis/nephrocalcinosis and may be classified as dietary (DH), enteric (EH) or primary (PH). Fractional intestinal absorption of Ox is less than 10%, but increases to over 20% at calcium intakes below 200 mg/day. DH is often related to low-calcium diets. EH is caused by non-absorbed fatty acids which bind to calcium and lower its concentration in the intestinal lumen. Ox forms more soluble complexes with other cations and results in HOx. Similar mechanisms may cause HOx following bariatric surgery. PHs are the most severe causes of HOx. Three types have so far been described, all being autosomic recessive. PH1 is due to mutations of AGXT gene encoding liver alanine-glyoxylate aminotransferase, PH2 is caused by mutations of GR-HPR gene encoding glyoxylate reductase and PH3 by mutations of HOGA1 encoding for hydroxyl-oxoglutarate aldolase. HOx results from deficient detoxification from glyoxylate, which is oxidized to Ox. The three PHs have different severity, though not always clinically distinguishable. They are identified through genetics and, in PH1, good genotype/phenotype correlations have been established. Thanks to early biochemical and genetic diagnosis, which are crucial to either prevent progression to ESRF or choose adequate transplantation strategies, the outlook of PH patients has dramatically improved in the last decades and will furtherly do in view of new therapeutic strategies.

Nephrolithiasis (NL) has high and increasing prevalence in western countries. Most renal stones contain calcium and/or uric acid and often occur as idiopathic stones, while seldom are caused by genetic disorders. Conversely, cystinuria, xantinuria, 2-8 dihydroxyadeninuria only occur in patients with mutations of corresponding genes. Inherited NL must be suspected in case of early onset, positive family history, severe recurrence rate, associated biochemical disorders, abnormal urinary sediment, renal insufficiency, involvement of other organs or apparatus. Pathophysiology is based on different mechanisms: electrolytic abnormalities, altered tubular transport, acid-base imbalances, cystic renal diseases. Sometimes NL is iatrogenic. Here we review some genetic NL, not only characterized by clinical relevance but also by the scientific interest in view of our better understanding of mechanisms of stone formation. Namely, Dents syndrome, calcium sensing receptor mutations, familial hypopomagnesiemic hypercalciuria (FHHNC), hypophosphatemic rickets (HHRH), renal tubular acidosis (dRTA), primary hyperoxaluria (PH), cystinuria, 2-8 dihydroxyadeninuria (2-8 DHA). We will briefly report on prevalence, genetics, pathophysiology, clinical aspects and treatment. The need for early diagnosis stems from the fact that, for most of these, selective treatment may be highly effective and can prevent progression to ESRD. Lastly, a better knowledge and understanding of genetic NL is a premise to study polymorphisms of candidate genes also in the setting of so-called idiopathic disease.

A 85-year-old man, with CKD (e-GFR 35 mL/min), had been given Dabigatran (a direct thrombin inhibitor) at 110 mg daily dose because of atrial fibrillation. Due to intercurrent diarrhea and dehydration, renal function worsened (e-GFR 11 mL/min) and Dabigatran excretion decreased, thereby inducing drug overload. In this case, Dabigatran must be removed by dialysis, but the most appropriate schedule is still undefined. The effects of both continuous haemodiafiltration (CVVHDF) and intermittent haemodialysis (IHD) on plasma Dabigatran (Echarin Chromogenic Assay) were reported. Dialysis clearance of Dabigatran was reported as ratio to urea clearance (Dab/Urea(Cl)). Coagulation was assessed by both DOA-aPTTratio and Thrombin Time-ratio (TTratio). Dabigatran was elevated at 597 ng/mL predialysis (bleeding threshold being 30 ng/mL), and decreased to 96 ng/mL (-84%) after 20 hours of CVVHDF (Urea(Cl) = 67 mL/min). Dab/Urea(Cl) was 0.49. Three hours after dialysis, Dabigatran rebounded to 208 ng/mL. On IHD (Urea(Cl)=238 mL/min), predialysis Dabigatran was 52 ng/mL and decreased to 8 ng/mL (-85%) after 3.5 hours of treatment. Dab/Urea(Cl) was 0.47. Fourteen hours later, Dabigatran rebounded at 19 ng/mL. There was a positive correlation between Dabigatran and TTratio (r = 0.92; p<0.0001), whereas DOA-aPTT did not increase above 2.5 times the reference values, even in face of the highest values of Dabigatran. Therefore, TTratio is more reliable than DOA-aPTT in detecting Dabigatran overdose. Post-dialysis rebound of Dabigatran occurred also with CVVHDF, thereby suggesting that accurate monitoring of both Dabigatran levels and bleeding risk are mandatory, also after long-lasting dialysis sessions.

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 percentage of patients on dialysis who do not adhere to their dietary and therapeutic regimens ranges from 25% to 86%. These data are relevant because nonadherence to the prescribed diet affects the mortality and morbidity of these patients. The aim of this study was to evaluate some indicators of nonadherence to drug therapy and diet. Patients showing serum potassium levels >6 mEq/L, serum phosphate levels >5.5 mg/dL, or interdialysis weight gain >5.7% of their body weight were considered as nonadherent. Behaviors, habits and adherence to prescribed therapies were investigated by administering a drug and diet questionnaire to the patients. The percentages of values exceeding the nonadherence threshold were 16.4% for potassium, 30.2% for phosphate, and 7.5% for weight gain. The weight gain index was significantly related to both potassium (p<0.01) and phosphate (p<0.05) indexes. Age was inversely correlated with non -adherence indexes of both phosphate (p<0.05) and weight gain (p<0.05). Residual diuresis was associated with better adherence to potassium (p<0.01). Factor analysis of the questionnaire suggested a 4-factor solution. None of these subscales were correlated with nonadherence indexes. ''Continuity in the intake of drugs'' showed a correlation with the ''trust in the drugs'' factor (p<0.01). Measurements of nonadherence remain a crucial step for understanding the impact on patients' quality of life.

The natural history of urolithiasis includes the risk of recurrence and of the development of chronic kidney and/or bone disease, which is why a thorough clinical and metabolic evaluation of these patients is of the utmost importance at disease onset. This paper is aimed at identifying the type of urolithiasis, the related risk factors, and the corresponding treatment options. The diagnostic and therapeutic approach described here includes 1) accurate history taking to detect secondary nephrolithiasis and screen for the main risk factors for kidney and bone disease; 2) metabolic evaluation graded according to different complexity levels based on the severity of the disease and the presence of risk factors; 3) carrying out appropriate imaging procedures. The resulting information allows to plan treatment based either on general rules of lifestyle and diet, or on selected medical intervention, if necessary. This report, which is based on current guidelines, was produced by the Gruppo Italiano di Studio Multidisciplinare per la Calcolosi Renale. It is addressed to all professionals involved in the management of patients suffering from nephrolithiasis, first of all general practitioners, who often become involved immediately at the onset of the disease.

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.

Background: 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., Methods: 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)., Results: 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., Conclusion: 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.

Background: 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., Methods: 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, beta < 1 under - and beta > 1 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., Results: 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., Conclusions: 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.

Background: 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., Methods: 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)., Results: Despite relating to each other (r>0.97) 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 (p<0.05) and direct (p<0.001) 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., Conclusions: 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.

Background: In this paper, the clinical and metabolic patterns of nephrolithiasis in different ages of adulthood are studied., Methods: 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., Results: 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%, p < 0.05) 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., Conclusions: 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.

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.

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.

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.

A case of acute hyperparathyroidism complicated by oliguric renal failure successfully resolved only after surgical removal of a parathyroid adenoma is reported. The need for early diagnosis of this rare condition is stressed and the commonest and most recent techniques for investigating primary hyperparathyroidism are discussed. In agreement with other reports, the importance of the earliest possible surgery, without which prognosis is almost always poor, is reiterated.