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.

Age Distribution↗

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Renal stones: from metabolic to physicochemical abnormalities. How useful are inhibitors?

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.

Chemical Phenomena↗

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[Intact whole bioactive parathormone: problems arising from comparing different methods].

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.

Adult↗

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[Utilization of EPO in CAPD].

From January 1988 to September 1990 14 uremic patients in CAPD underwent EPO therapy in the Nephrology and Dialysis Unit of the "E. Agnelli" Hospital in Pinerolo. Intravenous routes were used in 5 patients and subcutaneous routes in the remaining 9 patients, with a unified dose of 4000 IU/three times a week. Both methods were equally efficacious in achieving the set target: partial correction of anemia together with an improvement in the patients' well-being. The most frequent side-effect was increased blood pressure, above all in those patients with pre-existing hypertension. Satisfactory control was achieved by adjusting anti-hypertensive therapy. Low EPO doses, administered via a subcutaneous route once and twice a week (mean dose: 61.6 +/- 35.8 IU/kg/week), allowed hemoglobin values to be maintained at previous levels. On these grounds the method could also be used for patients in hemodialysis.

Adult↗

PubMedDate not supplied