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The qualitative and quantitative analysis of crystalluria have clinical significance in the diagnosis and prognosis of urolithiasis. Optical methods used on a routine basis can fail the correct identification of crystal materials for several reasons, such as the small grains size of crystals or the morphological convergence of different crystal species. The aim of this research is to provide an new accurate methodology to better analyze the crystalluria in patients with renal stone disease. Subjects for study were selected on the basis of pre-determined criteria: 8 patients with lithiasis disease hospitalized at the San Carlo Hospital (Potenza); 3 healthy subjects with no history of renal calculi. The procedure involves an urine collection, the separation of the solid residual by centrifugation, and its analysis by X-ray diffraction. Since very low amount of solid residual is obtained from each patiet, a microdiffractometer was used instead of a more conventional instrument. The X-ray spectrum obtained from the sample and from a known standard was processed by Rietveld method in order to quantify crystalline species and the amorphous component. The proposed methodology has two main advantages: i) to properly identify the crystalline phases in the urine, according the crystallographic criteria, that are not biased by grain size, morphology or any other optical interferences due to dust, organic coatings or others; ii) accurately quantify both crystalline and amorphous components of the urine. The temperature of urine collection and the solid residual conservation represent critical phases of this methodology.

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The Italian Society of Nephrology recently proposed and published guidelines for the management of nephrolithiasis. This review reconsiders some aspects, and presents the scientific background and clinical-scientific evidence that suggested the guidelines for some of the more controversial and debated issues in the clinical-diagnostic approach to the disease, i. e., medical management of renal colic and the first episode of nephrolithiasis.

Nephrolithiasis is a complex, multifactorial disease resulting from an interaction between environmental and genetic factors, even if the actual contributions of these factors to stone disease are not yet quantifiable. The lack of convincing findings on genetic factors and genes responsible for nephrolithiasis is due to our still inadequate understanding of the pathogenesis. The hypothesis of an anomaly in cell membrane lipid composition might conceivably be the defect which links genetic and dietary factors and renal stone disease.

Greater arachidonic acid (AA) contents, which were correlated with erythrocyte transmembrane oxalate (Ox) transport, were observed in plasma and erythrocyte membrane phospholipids of patients with idiopathic calcium renal stones, suggesting a link between membrane phospholipid fatty acid composition and cellular Ox transport. To confirm this hypothesis, the effects of exogenous red blood cell incorporation of three different fatty acids (i.e., oleic acid, AA, and eicosapentaenoic acid) on Ox transport and the phosphorylation status of band 3 protein, which has been shown to mediate red blood cell Ox flux, were investigated. Preincubation of erythrocytes with AA induced a dose-dependent increase in the phosphorylation level of band 3 protein and an increase in transmembrane Ox self-exchange. In contrast, inhibitory effects on both parameters were observed after the incorporation of oleic and eicosapentaenoic acids. These data, together with previous observations of dietary effects on erythrocyte Ox transport and urinary Ox excretion, indicate that genetic and/or nutritional changes in membrane phospholipid fatty acid composition play a crucial role in modulating cellular Ox transport in idiopathic calcium Ox nephrolithiasis.

We have recently described heterogeneity in renal structure in non-insulin-dependent diabetic patients (NIDDM) with microalbuminuria (MA; defined as albumin excretion rate from 20 to 200 micrograms/min). Thus, at variance with IDDM patients, "typical" diabetic glomerulopathy by light microscopy is observed only in a third of NIDDM with MA (Category II, CII). Further, despite persistent MA, 30% of NIDDM have normal or near normal renal structure (Category I, CI). Another one-third shows "atypical" patterns of renal injury with absent or mild diabetic glomerular changes, associated with disproportionately severe tubulointerstitial lesions and/or arteriolar hyalinosis and global glomerular sclerosis (Category III, CIII). The aims of this study were to evaluate whether similar patterns of renal lesions could be confirmed in a larger group of NIDDM with MA and to investigate tubular function in order to understand the mechanisms underlying MA in NIDDM patients. Renal biopsies were performed in 53 NIDDM with MA. Categories I, II and III were found in 41%, 26% and 33% of NIDDM with MA, respectively. All 8 patients with proliferative diabetic retinopathy were in CII. We also studied the urinary daily excretion rate of alpha 1-microglobulin (alpha 1 m), a low molecular weight protein, which is a useful indicator of tubular function. alpha 1 m was markedly increased only in CII patients (CI vs. CII vs. CIII: 6.2 +/- 1.2 vs. 13.7 +/- 2.1 vs. 7.3 +/- 0.9 mg/day, ANOVA, P0.01). In conclusion, we confirm that there is heterogeneity in renal structure in NIDDM patients with MA. This heterogeneity is not due to renal diseases other than diabetes. Increased alpha 1 m and proliferative retinopathy are useful indicators of the subgroup of MA NIDDM patients with typical diabetic glomerulopathy. It is suggested that diabetic microangiopathy explains the simultaneous occurrence of typical diabetic glomerulopathy, proliferative retinopathy and tubular dysfunction in a subgroup of NIDDM patients with MA.

Heparin as a therapeutic option in glomerular disease In the late 1960s, Priscilla Kincaid-Smith first proposed the therapeutic use of heparin in nephrology based on the putative pathogenetic role of the coagulative cascade in acute kidney rejection and in rapidly progressive glomerulonephritis. Small series of anecdotal observation on patients treated with triple or quadruple therapy comprising heparin, or oral anticoagulants (the so-called Melbourne cocktail) were reported by Kincaid-Smith and others. At that time it was not clearly recognized that heparin has activities other than anticoagulation, so that oral anticoagulants were gradually substituted for heparin. The high frequency of side-effects and disappointing results gradually relegated heparin, anticoagulants, and the Melbourne cocktail to the nephrology museum [1], Recently there has been a renaissance in heparin with a novel rationale. Studies in 'non-immunological' models gave strong evidence that heparin and glycosaminoglycans are effective in ameliorating the natural progression of a number of nephropathies, puromycin and habu snake-venom-induced nephrosis [2,3], antiThyl.l experimental mesangioproliferative glomerulonephritis [4], glomerulosclerosis in the GH-transgenic mouse [5], and nephropathy in the streptozotocin (STZ)-induced diabetic rat [6-8]. Purkerson et al. demonstrated that progression of glomerulosclerosis in subtotally nephrectomized rats is prevented by heparin, but not by other anticoagulant drugs such as coumadin [9]. This was the first observation to support the idea that the renoprotective effect of heparin depends on mechanisms other than the coagulation cascade. It is now clear that anticoagulation is not needed for these actions of heparin. In fact, Diamond and Karnovsky [2] demonstrated that chronic aminoglycoside nephrosis is prevented by a non-anticoagulant heparin, and in the quite different model of subtotal nephrectomy, Purkerson et al. [10] showed that a chemically transformed heparin devoid of anticoagulant activity ameliorates the progression of renal disease in the same way as anticoagulant heparin. Finally, in the STZdiabetic rat, nephropathy is prevented by both modified heparins and a dermatan sulphate which are poor anticoagulants [6,7].

The aim of the study was to assess the relation between the waist to hips ratio (WHR) and the distribution of adipose tissue in visceral or subcutaneous site through the use of CAT. Results are expressed as the ratio of visceral to subcutaneous adipose tissue area (VSR). A total of 61 patients were randomly selected for inclusion in the study. Contrary to normal weight subjects, obese patients did not reveal significant correlations between the two ratios. Following multi-variant analysis in normal weight subjects, WHR appeared to be influenced by sex, BMI and VSR. In patients with prevalently visceral adiposity WHR was determined by sex and VSR, whereas in patients with prevalently subcutaneous adiposity it was influenced by BMI alone. In conclusion, the significant correlations between WHR and tomographic indices of adipose tissue distribution reported in the literature are not present in all types of patient, and in particular are not found in obese patients and normal weight subjects with prevalently subcutaneous adiposity.

Compensatory renal hypertrophy has been induced in rats by uninephrectomy. Tissue kallicrein concentration of the remaining kidney was evaluated 5, 10, 15 and 20 days after operation. The previously removed kidneys were used as controls. In the hypertrophic kidney the kallicrein increases progressively up to 20 days after uninephrectomy. Since kallicrein generates kinins, potent vasodilators, it is suggested that the increase in renal blood flow observed after uninephrectomy might be promoted by an overproduction of kinins.

Tamm-Horsfall (TH) mucoprotein has been suggested to play a lithogenetic role in calcium-oxalate nephrolithiasis. However it is still debated whether it promotes or inhibits crystal growth and aggregation. To make clear the role played by this mucoprotein, we have carried out the following experiments: 1) the urinary excretion of TH has been evaluated by radial immunodiffusion in 27 recurrent idiopathic CaOx stone formers and in 35 controls; 2) in a metastable solution of CaOx the effect of TH addition on crystal growth has been monitored; 3) in whole urine the effect of TH addition on crystal aggregation has been assayed by an aggregometer. Urinary excretion of TH is significantly lower in stone formers. TH does not seem to promote crystal growth, while it is effective on crystal aggregation. These data seem to suggest that the reduced excretion of TH in nephrolithiasis may be a lithogenic risk factor.

We studied prostaglandins and kallikrein urinary excretion in 14 children with acute poststreptococcal glomerulonephritis within 48 hours of hospital admission (period A), and again, 4-6 weeks later, when they were clinically recovered (period B). Seventeen apparently healthy children were studied as controls. The results (mean +/- SEM) indicate that PGE2 urinary excretion (ng/kg/day) was diminished during both periods of study (control group = 2.06 +/- 0.43, patients = period A 0.91 +/- 0.28 [P less than 0.02], period B 0.92 +/- 0.21 [P less than 0.02]). PGF2 alpha urinary excretion (ng/kg/day) was also suppressed during period A, but not during period B when large individual variability existed (control group = 7.10 +/- 1.07, patients period A 3.56 +/- 0.66 [P less than 0.001], period B 10.51 +/- 5.01 [NS]). Kallikrein urinary excretion (EU/kg/day) was also depressed during the acute phase and remained low during convalescence (control group = 0.492 +/- 0.1, patients period A 0.143 +/- 0.044 [P less than 0.001], period B 0.265 +/- 0.093 [P less than 0.02]). There was no difference in PGE/PGF ratio between controls and patients in the periods of study (control 0.328 +/- 0.055, period A 0.395 +/- 0.144, period B 0.384 +/- 0.128). Urine volume (ml/day) was lower in period A (582 +/- 75.8) but comparable in period B (1020 +/- 140.2) and control children (1210 +/- 80.2). No correlation could be found between the urinary excretion of PGE2, PGF2 alpha and kallikrein with any of the following parameters: urinary or serum sodium and potassium, serum or urinary osmolality, Cosm, urine flow, plasma renin activity, plasma or urinary aldosterone, hypertension or fluid retention.(ABSTRACT TRUNCATED AT 250 WORDS)

The effect of up to 6months antibacterial treatment on both urine culture and the presence of antibody-coated bacteria in the urinary sediment was examined in 15 patients with upper urinary-tract infection. At the end of the sixth month all the patients had sterile urine, while about one half still demonstrated antibody-coated bacteria in their sediment. Such a finding strongly suggests that urine culture is "per se" insufficient to exclude the presence of bacteria in the renal parenchyma, and that the evaluation of antibody-coated bacteria might be a better way to watch the effect of treatment in upper urinary-tract infections.

In our experience, idiopathic calcium-oxalate (CaOx) nephrolithiasis is generally associated with an increased oxalate self-exchange (SE) in red blood cells (RBC) (1). This anomaly seems to be related to an altered state of phosphorylation of the anion carrier (band-3 protein) (2). We also have evidence that some glycosaminoglycans (GAG) can inhibit band-3 phosphorylation and normalize oxalate SE (3). In view of these findings, and because of the possibility that the cellular transport defect could also be present in other cell lines, we have set up a clinical trial to check the effects of orally-administered GAG on lithogenic factors.

Prolonged muscular exercise stimulates glucose uptake by the working muscles themselves. The mechanism of this phenomenon is at present unclear. It has been proposed that the kallikrein-kinin-prostaglandin system plays a role in the physiological regulation of muscular glucose metabolism during exercise. Since bradykinin can stimulate phospholipase A2, a key enzymatic step in prostaglandin synthesis, phospholipase A2 activity was assayed in rats at rest and in rats compelled to swim for 60 minutes. The physiological significance of an increase in muscular phospholipase A2 activity is not clear. Since bradykinin can stimulate both muscular glucose uptake and phospholipase A2 activity, it is possible that the increased activity of this enzyme is involved in the exercise-induced increase of muscular glucose uptake. Phospholipase A2 activity was strongly increased in the exercising rat muscles. A small but significant increase in phospholipase A2 activity was observed in the heart, whereas no variation in activity was demonstrated in either the kidney or the liver of exercising rats. These findings strongly indicate that prolonged exercise increases muscular phospholipase A2 activity only in the muscle and heart. This phenomenon appears to be strongly related to muscular contraction, since other stress situations such as cold exposure did not modify phospholipase A2 activity. Our data are in agreement with the hypothesis of a possible involvement of prostaglandins in the priming action of insulin on glucose uptake during muscular work.

The echocardiographic features of the left ventricle of 37 obese women (body mass index above 30) and 37 lean controls, matched for sex, age, height and blood pressure levels, were studied. Twenty-six patients in each group were hypertensive. The normotensive obese patients did not show any differences, comparing to the normotensive controls; on the contrary, the hypertensive obese patients had higher left ventricular mass (LVM), stroke volume and cardiac output (CO), and lower total peripheral resistance (TPR) than the hypertensive controls. A positive correlation was found between the LVM and the CO (r = 0.57, P less than 0.01) in hypertensive obese patients, and between the relative wall thickenss (h/r, that is the ratio between the left ventricular wall thickness and the left ventricular radius) and TPR (r = 0.64, P less than 0.01) in the hypertensive controls. It is concluded that obesity per se does not determine left ventricular hypertrophy in women; however, when obesity is associated with arterial hypertension, a distinct pattern of hypertrophy, characterized by high CO and low TPR, develops.

Oxalate with calcium forms the most-common crystal salt in the majority of calculi formed within the urinary tract. These ions are present in an equal molar ratio in the crystals of calcium oxalate monohydrate and calcium oxalate dihydrate. The greatest crystalline mass from a solution supersaturated with calcium oxalate is made when these ions are present at equal molar concentrations. In normal urine, the ratio between the molar concentration of calcium and oxalate is usually greater than 3:1 and often 5:1 or greater. Thus, increases in the calcium concentration would be expected to have a lesser effect on supersaturation and crystalline mass than increases in the oxalate concentration, making oxalate concentration a major determinant in the formation of calcium oxalate stones within the urinary tract (1–3).

The occurrence of mild hyperoxaluria “idiopathic” calciumoxalate (CaOx) stone disease has been stressed recently1,2 It is thought to be due to a higher than normal intestinal absorption of oxalate3,4, although abnormal renal handling of the ion cannot be ruled out. The underlying mechanism of both these abnormalities might involve a defect in the cellular transport of oxalate. To test this hypothesis, we have compared the rates of oxalate transport in red blood cells (RBC) in “idiopathic” CaOx stone forming patients and normal subjects. The results of this study are reported here.

The effects of digoxin have been studied on PRA of 11 hypertensive patients treated with a single oral administration of the glycoside or submitted to a prolonged treatment. The experiments performed with a single oral administration (0,5 mg) showed that digoxin induces a significant decrease of the hyperreninemic response induced by furosemide. This effect of digoxin develops very quickly and is well evident when plasma levels of the glycoside are still low. However, in the patients pretreated with a beta blocker, digoxin was completely ineffective in preventing the response to furosemide. In view of the results, the hypothesis is put forward that digoxin mainly acts at renal level through an antiadrenergic activity.

In order to obtain new insights into the relevance of inhibitors in whole urine by focusing on their reciprocal interactions, a statistical approach was followed in 35 controls and 27 calcium oxalate (CaOx) recurrent idiopathic stone formers. The inhibiting activity of CaOx crystal growth and the most widely accepted inhibitors (glycosaminoglycans, citrate, magnesium, pyrophosphate), stone constituents (calcium, oxalate, phosphate, urate) and other normal urinary substances were evaluated. It was seen that the inhibitors played a very small role in total inhibiting activity. On the other hand, considering other normal urinary constituents, almost all the inhibiting power of urine on crystal growth could be explained.

During the school year 1974-75 serum cholesterol has been evaluated in the whole school population (520 subjects, 268 males and 252 females, age ranging from 6 to 14 years) of Saccolongo, a village which is about 20 kilometers from Padova (Italy) and serum triglycerides have been further evaluated in a random population of 161 subjects (90 males and 71 females, age ranging from 6 to 11 years). Serum cholesterol values did not show any significant difference between males and females. Analysis of serum cholesterol in the various age groups revealed that it was significantly higher in females at age 6 (t = 2.2296; p less than 0.05). A significant reduction in serum cholesterol values has been found at age 11 both in males (t = 4.7810; p less than 0.001) and in females (t = 5.6134; p less than 0.001). Serum cholesterol and triglycerides values did not correlate (r = 0.404). Serum triglycerides were higher in girls than in boys (t = 2.1360; p less than 0.05). Analysis of the serum triglycerides values in the various age groups were constant in males (F = 0.4161) and inconstant in females (F = 3.8844; p less than 0.01) where age groups 8 (t = 3.5127; p less than 0.005) and 11 (t = 3.5238; p less than 0.005) showed higher than normal values.

To evaluate a possible interaction between coagulation factors, inflammation, and immunological disorders in the pathogenesis of glomerulonephritis (G.N.) factor VIII clotting activity (VIII:C), related-antigen (VIIIR:AG), urinary fibrinogen degradation products (F.D.P.) excretion and cyclic nucleotides (cAMP) in 21 patients affected by chronic G.N. with normal renal function, was investigated. These patients were followed-up for two years. For the assay of factor VIII:C, a factor VIII deficient plasma was used. Factor VIIIR:AG were assayed by rocket electroimmunodiffusion in agarose gel, urinary F.D.P. by Thrombo-Wellcotest and cAMP by radioimmunoassay. The same tests were performed in 25 healthy controls. Patients' clotting activity, measured at first admission, showed a significant decrease in comparison with the values obtained at the end of the follow-up period (t=-2.61 p

We have evaluated the effects of dextrofenfluramine treatment on body weight control during a 90 day period, in obese patients on a calorie-restricted diet. The weight loss in dextrofenfluramine-treated patients was significantly higher than in placebo group. The rate of weight loss was linear up to the end of the trial in d-fenfluramine patients. Neural disturbances (vertigo, headache, depression) were the most frequent side effects observed in both the d-fenfluramine and in the placebo-treated groups, without significant differences between the groups. A total number of 23 patients in the dextrofenfluramine group and 20 patients in the placebo group complained side effects. Six patients (five in the d-fenfluramine group and one in the placebo group) discontinued the treatment, due to the side effects. No modifications of the biochemical parameters considered (fasting blood glucose, bilirubin, alkaline phosphatase, creatinine, blood cell counts, asparate-amino transferase (AST), alanine-amino transferase (ALT), total plasma and HDL cholesterol, and triglycerides) were observed at the end of the trial. A significant reduction of total serum cholesterol was observed in both groups at the end of the period of treatment. In conclusion, dextrafenfluramine was proved to be in short term trials an effective and safe tool in overweight control in obese patients.