[Urinary excretion of microproteins during essential arterial hypertension].
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Biomedical subjects
Publications and source records attributed to B Baggio.
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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.
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.
BACKGROUND: Ischemic nephropathy is an important cause of renal failure in western countries. Subclinical renal function abnormalities may exist in patients with extrarenal atherosclerosis, and may precede the onset of overt ischemic nephropathy. METHODS: To assess the impact of extrarenal atherosclerosis on the kidney, we evaluated renal function in 89 subjects with differing degrees of peripheral atherosclerosis, without manifest clinical or laboratory signs of ischemic nephropathy and renovascular hypertension. All laboratory testing, ultrasonography with Doppler analysis for the localization of peripheral vascular disease (carotid and lower limb arteries), and non-invasive evaluation of renal function by radionuclide studies of renal plasma flow (MAG3 clearance) and glomerular filtration (DTPA clearance), as well as total, LDL and HDL cholesterol, and triglycerides were determined; smoking habit was recorded. By combining sonographic data on arterial tree stenosis (ATS), the subjects were grouped according to the atherosclerotic vascular damage (ATS involvement). RESULTS: Despite no change in plasma creatinine and DTPA clearance (from 91.58+/-26.53 mL/min/1.73 m2 to 93.47+/-24.82), MAG3 clearance progressively declined with the severity of vascular damage (from 244.86+/-60.60 mL/min/1.73 m2 to 173.59+/-58.74). Stepwise multiple regression analysis indicated that MAG3 clearance was best explained by ATS involvement (standardized beta coefficient -0.40; p<0.001), smoking habit (-0.34; p= 0.004), and serum LDL-cholesterol (-0.24; p<0.035). CONCLUSIONS: The renal hemodynamic profile in atherosclerotic patients might constitute functional evidence of the silent phase of ischemic renal disease. The findings suggest that renal function should be carefully assessed in patients with extrarenal atherosclerosis, particularly in those with classic cardiovascular risk factors.
The subcellular localization of renin and kallikrein in rat kidney cortex homogenate was investigated using both differential and density gradient centrifugation techniques. Highest specific activity of renin was found in the heavy mitochondrial fraction. Mitochondrial localization of renin was further supported by the behaviour of succinic dehydrogenase. By differential centrifugation, highest specific activity of kallikrein was found in the light mitochondrial fraction, while by density gradient centrifugation kallikrein was almost completely recovered in the lysosomal fraction. Lysosomal localization of kallikrein is further supported by the behaviour of acid phosphatase. The different subcellular localizations of renin and kallikrein are confirmed and the suggestion that kallikrein is located in the lysosomes is advanced.
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The role of polyunsaturated fatty acids in renal fibrosis. Several studies suggest a close relationship between polyunsaturated fatty acids (PUFA) and renal inflammation and fibrosis, which are crucial stages in chronic kidney disease (CKD). Beneficial effects of n-3 PUFA on the course of experimental and human nephropathies have been reported. PUFA can ameliorate chronic, progressive renal injury beyond the simple reduction of serum lipid levels. These pleiotropic effects of PUFA are due to their properties of interfering with the synthesis of a variety of inflammatory factors and events, through effects related both to the modulation of the balance of n-6 and n-3-derived eicosanoids and to direct action on the cellular production of the major cytokine mediators of inflammation and on endothelium function. The mechanisms by which PUFA can favorably interfere with some stages in renal fibrosis processes, such as mesangial cell activation and proliferation and extracellular matrix protein synthesis, include the regulation of some pro-inflammatory cytokine production, renin and nitric oxide (NO) systems and peroxisome proliferator-activated receptor gene expression. An optimal n-6/n-3 PUFA ratio dietary intake could offer new therapeutic strategies aimed at interrupting the irreversible process of renal fibrosis and ameliorating chronic renal injury. However, further experimental, epidemiological and clinical investigations are needed to confirm the role of PUFA in the renal fibrosis pathway and the natural history of chronic nephropathies.
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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.
Acute intravenous infusion of fructose was given to 30 normal subjects and 27 normo-uricemic patients affected by psoriasis, 12 with cutaneous involvement only and 15 with psoriatic arthritis. Serum uric acid was measured before and after infusion. A significantly lower increase in serum uric acid levels was found in psoriatic patients in comparison to controls, and the increase rate appeared to be significant only in controls. Moreover, the overall fructose-induced hyperuricemia was significantly lower in the group of patients with psoriatic arthritis than in normal subjects. Since the fructose-induced increase of serum uric acid is most probably achieved by an augmented turnover of preformed purine nucleotides, it is suggested that in normouricemic patients with psoriasis the "pool" of purine nucleotides is lower than normal. Such a condition seems to be more evident in psoriatic arthritis.
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