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Biomedical subjects

E Bartoli

Publications and source records attributed to E Bartoli.

At least 37 records · Page 2Linked to original sources
PubMed1999

Effect of eating on plasma radical-trapping antioxidant activity (TRAP) in patients with cirrhosis.

OBJECTIVES: To ascertain the effects of eating on plasma antioxidant capacity in patients with liver disease. DESIGN AND METHODS: Eighteen cirrhotic patients were compared to 18 age and sex-matched controls. TRAP was measured by a fluorometric assay after a 12 h fast, and 60, 120, and 180 min after the study participants had taken a drink formula food. RESULTS: In the fasting state, TRAP was higher in patients with alcoholic cirrhosis (847+/-39 micromol/L, mean +/- SEM) in comparison to patients with viral cirrhosis (653+/-41) and to controls (758+/-26) (p<0.005). In cirrhotic patients, TRAP did not change in the post-absorptive state. In controls, TRAP decreased progressively, to a value of 719+/-21 (p<0.02), and the AUC of the delta-values of TRAP and of plasma insulin showed an inverse correlation (r = -0.52, p<0.05). CONCLUSIONS: In normal subjects, but not in cirrhotics, TRAP decreases in the post-absorptive state, probably in relationship with the activation of metabolic pathways.

Antioxidants↗
PubMed1999

Lipoprotein(a) and apolipoprotein(a) isoforms and proteinuria in patients with moderate renal failure.

BACKGROUND: Atherosclerotic diseases are a major cause of death in patients with renal failure. Increased serum concentrations of lipoprotein(a) [Lp(a)] have been established as a genetically controlled risk factor for these diseases and have been demonstrated in patients with moderate renal failure, suggesting that this lipoprotein contributes to the increased cardiovascular risk seen in these patients. Variable alleles at the apolipoprotein(a) [apo(a)] gene locus are the main determinants of the serum Lp(a) level in the general population. The purpose of this study was to investigate apo(a) isoforms in patients with moderate renal failure and mild proteinuria (less than 1.0 g/day). METHODS: In 250 consecutive subjects recruited at a hypertension clinic, we assessed the renal function by 24-hour creatinine clearance, proteinuria, and microalbuminuria, as well as the prevalence of atherosclerotic disease, and we also measured apo(a) isoforms, serum albumin, and Lp(a) concentrations. RESULTS: Moderate impairment of renal function (creatinine clearance, 30 to 89 ml/min per 1.73 m2 of body surface area) was found in 97 patients. Lp(a) levels were significantly greater in patients with moderate renal failure (21.7+/-23.9 mg/dl) as compared with patients with normal renal function (15.6+/-16.4 mg/dl, P<0.001), and an inverse correlation was observed between log Lp(a) and creatinine clearance (r = -0.181, P <0.01). However, no difference was found in the frequency of low molecular weight apo(a) isoforms between patients with normal (25.5%) and impaired (27.8%) renal function. Only patients with the smallest size apo(a) isoforms exhibited significantly elevated levels of Lp(a), whereas the large-size isoforms had similar concentrations in patients with normal and impaired renal function. No significant relationship was found between serum Lp(a) and proteinuria. Clinical and laboratory evidence of one or more events attributed to atherosclerosis was found in 9.8% of patients with normal renal function and 25.8% of patients with moderate renal failure (P<0.001). CONCLUSIONS: These results indicate that renal failure per se or other genes beside the apo(a) gene locus are responsible for the elevation of serum Lp(a) levels in patients with moderate impairment of renal function. The elevation of Lp(a) levels occurs independently of the level of proteinuria and may contribute to the risk for atherosclerotic disease in these patients.

Adult↗
PubMed1999

Colorectal cancer screening in Italy: feasibility and cost-effectiveness in a model area.

OBJECTIVE: To evaluate the feasibility and cost-effectiveness of screening programmes for colorectal cancer in Italy. DESIGN; We compared five types of programmes: annual faecal occult blood testing, sigmoidoscopy (every 5 years), faecal occult blood testing plus sigmoidoscopy (every 1 and 5 years), colonoscopy (every 10 years) (all in the age group 55-69 years, last examination at 70 years) and 'filter' colonoscopy. The latter had to be performed in persons at 50 years of age and repeated every 10 years until the age of 70. Costs for the tests and colon cancer care were paid by the Regional Health Office to the hospitals performing the procedures/treatments. SETTING: Data were applied to a small model area in northern Italy (Gemona, 80,000 inhabitants) with well-known demographic (age distribution) and epidemiological (colon cancer incidence) features. RESULTS: All-inclusive 10-year costs per screenee and per death prevented (in US dollars) were: 965 and 77,200 for faecal occult blood testing; 436 and 15,500 for sigmoidoscopy; 1521 and 35,000 for sigmoidoscopy plus faecal occult blood testing; 510 and 15,100 for colonoscopy; 510 and 14,000 for 'filter' colonoscopy. With 'filter' colonoscopy the programme required 870 colonoscopies per year, while with colonoscopy 13,700 colonoscopies were needed at time zero. CONCLUSIONS: In Italy, screening programmes based on sigmoidoscopy/colonoscopy are more cost effective than those based on faecal occult blood testing. 'Filter' colonoscopy at age 50 appears superior to the other types of endoscopy-based screening programmes because it utilizes, at any point in time, a much smaller fraction of available resources.

Colonic Neoplasms↗
PubMed1999

T cell receptor repertoire in B cell lymphoproliferative lesions in primary Sjögren's syndrome.

OBJECTIVE: Studies have analyzed T cell receptor (TCR)-Vbeta in benign, minor salivary or lacrimal gland, or kidney lesions in Sjögren's syndrome (SS). We investigated SS related lymphoproliferative lesions. METHODS: By "family" reverse transcriptase polymerase chain reaction, we studied the expression of 20 different TCR-Vbeta families in parotid lymphoproliferative lesions and peripheral blood lymphocytes (PBL) from 7 patients with primary SS, in PBL from 6 primary SS patients with no associated lymphoproliferative disorder, and in activated PBL from 2 healthy controls. T cell clonal expansion was investigated in 10 Vbeta families (i.e., the most expanded ones and those previously implicated in SS pathogenesis) by single strand conformation polymorphism (SSCP) analysis. Frozen sections from parotid gland specimens were tested by immunohistochemistry for the expansion of selected Vbeta families. Viral infection within the parotid lesions and serum autoantibody response were also studied. RESULTS: An unrestricted Vbeta pattern was observed. The most widely expressed Vbeta family in parotid lesions was Vbeta2, and Vbeta immunohistochemistry results were concordant with Vbeta mRNA findings. A similar pattern was observed in PBL, although the Vbeta2 family was expressed at lower levels. The parotid/PBL ratio was occasionally > 1.8-2.0 (indicative of local Vbeta overexpression) in different Vbeta families. T cell expansion proved to be largely polyclonal by SSCP analysis, and scattered T cell clonotypes were detected within different Vbeta families, with a different pattern from patient to patient. CONCLUSION: Our observations in SS related lymphoproliferative lesions largely reflect previous evidence in fully benign lesions. The pathogenetic events involved in autoimmune benign lesions in SS may then persist and play a role in SS related lymphoproliferative disorders. The link between the observed TCR-Vbeta repertoire and specific local triggering (auto)antigens remains to be elucidated.

Adult↗
PubMed1999

Tubular reabsorption and sodium excretion during urine reinfusion.

BACKGROUND: The mechanisms responsible for the natriuresis that follows urine reinfusion was investigated in rats by clearance and micropuncture techniques. METHODS: In each animal two urine reinfusion periods (R1 and R2) were performed and compared to a non-urine-reinfusion, saline infusion period (S) sandwiched between them. RESULTS: Switching from urine reinfusion to an equivalent rate of saline loading was followed by a fall in Na excretion from 1.9 +/- 0.5 to 0.5 +/- 0.2% of filtered load, p < 0.002. Urine osmolality rose, and urine to plasma inulin concentration ratio rose significantly from 73 +/- 14 to 147 +/- 21 (p < 0.002). The changes in GFR, SNGFR, absolute and percent proximal reabsorption could not account for these findings. A reduced Na excretion coupled to increased urine osmolality indicates enhanced transport along a segment responsible for the urinary concentrating mechanism. Thus the data can be interpreted then as due to enhanced reabsorption along the ascending limb of Henle's loop. These changes were reversed by reinstituting urine reinfusion after the S period. The consensual changes in Na+ and K+ excretion excluded an effect of urine reinfusion on the distal exchange site. There was a continuous fall in proximal reabsorption from R1 (76 +/- 3%) to S (69 +/- 3%) to R2 (62 +/- 5%) which was inversely correlated with the changes in hematocrit (R = 0.49, p < 0.026). This indicates that part of the late diuresis and natriuresis was due to volume expansion. An osmotic effect of reinfused urine solutes was suggested by a late rise in plasma osmolality, from 312 +/- 13 to 323 +/- 8 mOsm/kg. Osmotic diuresis could have exerted additive effects upon those of volume expansion, accounting for the late fall in proximal reabsorption. CONCLUSIONS: We conclude that the acute effects of urine reinfusion are due to changes in transport of solutes and permeability to water along distal tubular segments. The changes in plasma osmolality during the last period of the present acute experiments, suggest the possibility that solute retention may be linked to the chronic effects of urine reinfusion.

Animals↗
PubMed1998

Increased serum lipoprotein(a) levels in patients with early renal failure.

BACKGROUND: Elevated serum lipoprotein(a) levels have been found in patients with end-stage renal disease and in patients undergoing dialysis, suggesting that this lipoprotein contributes to the increased cardiovascular risk seen in these patients. It is not known whether lipoprotein(a) levels are elevated in the early phases of renal disease. OBJECTIVE: To evaluate levels of lipoprotein(a) and other lipids and the prevalence of atherosclerotic disease in patients with early renal failure. DESIGN: Cross-sectional study. SETTING: Hypertension clinic of a university medical center. PATIENTS: 257 patients with normal renal function and 160 patients with early impairment of renal function (creatinine clearance, 30 to 89 mL/min per 1.73 m2 of body surface area). MEASUREMENTS: Renal function was assessed by 24-hour creatinine clearance, proteinuria, and microalbuminuria. Cardiovascular disease status was also assessed. Serum lipoprotein(a), lipids, apolipoproteins, and apolipoprotein(a) isoforms were measured. RESULTS: Age, blood pressure, and serum lipoprotein(a) levels were greater in patients with early renal failure than in those with normal renal function and were independently associated with the presence of decreased creatinine clearance. Serum lipoprotein(a) and creatinine clearance were inversely correlated. The prevalence of coronary artery, cerebrovascular, and peripheral vascular disease was greater in patients with early renal failure than in those with normal renal function. The frequency distribution of apolipoprotein(a) isoforms was similar in patients with normal and those with impaired renal function. CONCLUSIONS: Serum lipoprotein(a) levels are elevated in patients with early impairment of renal function and are associated with greater prevalence of cardiovascular disease. An inverse correlation between serum lipoprotein(a) level and creatinine clearance and a frequency distribution of apolipoprotein(a) isoforms similar to that of normal patients point to decreased renal catabolism as a probable mechanism of lipoprotein(a) elevation in patients with early renal failure.

Adult↗
PubMed1998

The site of action of furosemide.

To establish whether furosemide (F) acts on the proximal tubule beside the thick ascending limb of Henle's loop, we reviewed the data from 55 rats studied before and during the i.v. infusion of 10 mg kg-1 of furosemide. These animals were the object of previously published studies. SNGFR was 42.6+/-1.1 nl min-1 during baseline conditions (B), 42.7 nl min-1 during F (P>0.9). In 151 paired last proximal tubular samples, percentage reabsorption was 71.72 before and 71.72% after F (P=1.0). In 64 paired early distal tubular samples, percent reabsorption fell from 86% in B to 78% during F (P<0.0001). During F, the urine flow rate expressed as a percentage of GFR (24+/-2%) was significantly correlated (R=0.52, P<0.0001) with the percent delivery of filtrate out of the proximal tubule (26+/-3%). These data demonstrate that, even at this very high dosage, F does not act on the proximal tubule. It inhibits transport on the ascending limb of Henle's loop. By allowing the delivery of isotonic tubular fluid to the distal tubule, it causes a fall in volume absorption along the early distal convolution in proportion to its baseline water permeability. It increases urine flow by abolishing the interstitial hypertonicity and, consequently, the osmotically driven solvent flow across the distal epithelium and collecting ducts. Therefore the urine flow rate during F closely approximates volume delivery out of the proximal tubule.

Animals↗
PubMed1998

The effect of reducing proximal tubular fluid delivery on the rate of filtration of single nephrons.

The rate of delivery of tubular fluid from the proximal tubule (PT) is thought to reset nephron filtration rate (SNGFR). In micropuncture experiments in rats we tested this hypothesis by reducing the efflux from the PT by simultaneously "double collecting" (DC) tubular fluid from the early distal tubule (DT) and from the last convolution of the PT of the same nephrons. SNGFR measured by total collection of tubular fluid was 34 +/- 3 nl/min at the DT and 34 +/- 3 nl/min at the PT (p > 0.97, n = 42). The simultaneous collection from proximal and distal sampling site was performed between these two paired measurements. It yielded an average SNGFR of 40 +/- 3 nl/min (p < 0.02). This may be due to the collection, at the distal site, of the extra amount of inulin stored between distal and proximal pipette, prior to starting the aspiration of tubular fluid. Since this error would decrease in longer collections, the difference in SNGFR between single and double collections was plotted against the duration of collections. In fact it was negatively correlated with the sampling time (p < 0.01), indicating no difference in SNGFRs for collections > 4 minutes. Reduction and complete interruption of the delivery of native proximal tubular fluid to the Macula Densa does not seem to influence the measurement of SNGFR. Filtration rate is not significantly different when measured within few minutes at the DT and PT of the same nephrons.

Animals↗
PubMed1998

Portal vein thrombosis in hepatocellular carcinoma: age and sex distribution in an autopsy study.

The purpose of this work was to investigate the prevalence, associated features and effect on survival of portal vein thrombosis (PVT) complicating hepatocellular carcinoma (HCC). The autopsy data of a series of 72 consecutive patients (57 male, 15 female) with HCC were reviewed. PVT was found in 32/72 patients (44%), and tended to be more common in female patients (10/15 versus 22/57, P = 0.052). Stratifying the data according to gender, it appeared that the mean age of patients with PVT compared to those without was greater in woman (71.9 +/- 5.9 versus 63.2 +/- 6.9 years, P = 0.024) and younger in men (58.8 +/- 8.9 versus 66.0 +/- 9.9 years, P = 0.007). When PVT was present, it was more likely that a definite diagnosis of HCC had been obtained before autopsy (P = 0.0001) and that death had been caused by bleeding complications (P = 0.007). Median survival times were similar, irrespective of the presence of PVT. During the natural history of HCC, PVT occurs in a substantial proportion of patients. Hormonal factors may have a permissive role in thrombus formation or neoplastic vascular invasion. Although in the presence of PVT a diagnosis of HCC is rarely missed and bleeding complications are likely to occur, patient survival does not seem to be significantly affected.

Age Factors↗
PubMed1998

High prevalence of infection with hepatitis G virus in patients with hepatic and extrahepatic malignancies.

BACKGROUND/AIMS: The pathogenic role of hepatitis G virus, the recently discovered blood-borne agent, is controversial. Our aim was to ascertain the prevalence of hepatitis G virus infection in hepatic and in extrahepatic malignancies. METHODS: We studied 166 Italian patients (112 male, 54 female, mean age 61.8+/-9.3, mean+/-SD, range 34-85). One hundred and eighteen had cirrhosis, which was complicated by hepatocellular carcinoma in 66 cases. Forty-eight patients had extra-hepatic malignancies. Circulating HGV RNA was detected by reverse transcriptase-polymerase chain reaction (RT-PCR) of both the nonstructural-3 and 5'noncoding regions of the hepatitis G virus genome. Antibodies to the E2 protein of hepatitis G virus were detected by means of an enzyme-linked immunosorbent assay. RESULTS: Ongoing HGV infection was detected in 30/66 (46%) patients with hepatocellular carcinoma, 12/52 (23%) patients with cirrhosis, and 14/48 (29%) patients with extrahepatic malignancies (p<0.05). Evidence of exposure to hepatitis G virus (detection of either HGV RNA or anti-E2 antibodies) was found in 46% of patients with cirrhosis, 66% of patients with hepatocellular carcinoma, and 39% of patients with extrahepatic malignancies. Serum HGV RNA positivity was associated with a hematocrit value < or = 0.35 and with history of exposure to blood products (p<0.005). CONCLUSIONS: Ongoing hepatitis G virus infection is detected at a very high rate in patients with hepatocellular carcinoma, but is also fairly common in extrahepatic malignancies. Hepatitis G virus infection in these patients is likely to originate from exposure to blood products, and to persist because of deficient immune surveillance.

Adult↗
PubMed1998

Factors associated with serum HCV RNA positivity in anti-HCV antibody positive intravenous drug users.

Serum hepatitis C virus (HCV) RNA, HCV genotypes and liver function tests were evaluated in a series of 189 unselected, consecutive anti-HCV positive intravenous drug users (IVDUs). Serum HCV RNA was detected in 106/189 patients. Abnormal liver function tests were associated with alcohol abuse, but not with the presence of serum HCV RNA. Among 109 patients retested after a mean follow-up of 21 months, 41 were intermittently serum HCV RNA positive. Patients persistently negative had more commonly a past history of acute hepatitis. A history of prostitution and/or a pattern of abuse involving >30 injections per week were related to infection by genotype 3a. In conclusion, serum HCV RNA is either transiently or persistently detectable in most anti-HCV positive IVDUs, but bears no association with abnormal liver biochemistry. Infection by HCV-3a is more common in IVDUs with more deviant life styles. In those cases where serum HCV RNA is found repeatedly negative, HCV infection may have been cleared, possibly through an episode of acute hepatitis.

Adult↗
PubMed1998

Hyperglycemia-induced circulating ICAM-1 increase in diabetes mellitus: the possible role of oxidative stress.

ICAM-1 is one of the most important intercellular adhesion molecules involved in atherogenesis. Previous studies reported increased circulating ICAM-1 plasma levels in NIDDM patients with or without vascular complications. It has been suggested that an acute increase of plasma glucose may produce an oxidative stress in man, and in vitro studies have demonstrated that high glucose and free radicals induce cellular expression of ICAM-1. In this study, three different experiments were performed in nine NIDDM patients and in seven matched healthy controls: oral glucose tolerance test, antioxidant glutathione i.v. administration for two h, oral glucose tolerance test plus glutathione i.v. administration. Blood samples were drawn at -15 min and every 30 min from 0 to 180 min. During the oral glucose tolerance test, circulating ICAM-1 plasma levels significantly increased in both diabetic and normal subjects. Glutathione administration during the oral glucose tolerance test abolished this phenomenon. Glutathione administered alone significantly decreased circulating ICAM-1 plasma levels in diabetic patients, while no effect was observed in the normal subjects. These data suggest that hyperglycemia may induce an increase of circulating ICAM-1 plasma levels through an oxidative stress, and that the antioxidant glutathione counterbalances this effect. These data support the hypothesis of a causal relationship linking hyperglycemia, oxidative stress and atherogenesis in diabetes mellitus.

Aged↗
PubMed1998

Effects of BQ-123 on systemic and renal hemodynamic responses to endothelin-1 in the rat split hydronephrotic kidney.

OBJECTIVE: To assess the site of action of endothelin-1 in vessels of different sizes in the kidney in vivo and investigate the function of endothelin A (ET(A)) receptors in mediating renal and systemic vasoconstriction. DESIGN: The luminal diameters of different vessels were measured and glomerular blood flow in cortical glomeruli was determined by intravital videomicroscopy in the split hydronephrotic kidney of anesthetized female Wistar rats. METHODS: The rats were infused with endothelin-1 (40 pmol/kg per min) with or without pretreatment with the selective ET(A)-receptor antagonist BQ-123 (0.5 mg/kg). Aortic clamping was used to control renal blood pressure during the endothelin-1 infusion. RESULTS: Exogenous endothelin-1 induced a significant rise (30+/-3%) in mean arterial pressure and a marked, long-lasting fall in glomerular blood flow (53+/-3%) related to reduction of the inner diameter of arcuate (-30%), interlobular arteries (-33%) and afferent arterioles (-17%). Aortic clamping to normalize renal blood pressure did not attenuate the vasoconstriction and reduction in glomerular blood flow. Pretreatment with BQ-123 significantly reduced both the endothelin-1-induced rise in mean arterial pressure (12+/-1%) and the fall in glomerular blood flow (-23+/-11%). BQ-123 blunted the response to endothelin-1 in arcuate (-12%), interlobular (-11%) and afferent vessels (-5%). Acetylcholine and nitroprusside completely reversed the vasoconstriction in BQ-123-pretreated animals. CONCLUSIONS: BQ-123 largely prevented the hemodynamic effects of exogenously administered endothelin-1. Our direct in-vivo techniques showed that ET(A) receptors are, at least in part, involved in endothelin-1 -mediated vasoconstriction in the rat kidney, and support the hypothesis that ET(A) receptors may help to control arterial pressure in anesthetized rats.

Animals↗
PubMed1998

Contribution of endothelin receptors in renal microvessels in acute cyclosporine-mediated vasoconstriction in rats.

Cyclosporine A (CsA), a widely used immunosuppressive agent, causes renal vasoconstriction and systemic hypertension. Recent data suggest that the renal effect of CsA is possibly mediated by endothelin (ET). We investigated the effects of CsA on renal microvessels and the efficacy of ETA or ETA/ETB receptor antagonists in ameliorating CsA effects in the hydronephrotic rat kidney. Infusion of CsA (30 mg.kg-1) induced a transient increase (20%) in mean arterial pressure (MAP) and a sustained reduction (85%) in glomerular blood flow (GBF) due to preferential constriction of the arcuate artery (39%) and the proximal segment of the interlobular artery (23%). Under basal conditions the ETA receptor antagonist BQ-123 had marginal effects consisting of reduction in MAP, rise in GBF and dilation of preglomerular vessels. The non-selective ETA/ETB receptor antagonist PD 145065 also reduced MAP, but tended to decrease GBF and constrict large preglomerular vessels. The difference in effects of the two antagonists indicated that under basal conditions ETB blockade constricts large preglomerular vessels and reduces GBF. After BQ-123 or PD 145065, the constriction of large preglomerular vessels and reduction in GBF induced by CsA was attenuated by about 50%, but the rise in MAP was not influenced. Our data indicate that a sizable part of renal vasoconstriction due to CsA is mediated via ET production in large preglomerular arteries and can be avoided by the blockade of ETA receptors. Additional blockade of ETB receptors does not attenuate the CsA effects further, possibly because ETB receptors mediate both vasoconstriction and dilation.

Animals↗
PubMed1998

Proximal reabsorption with changing tubular fluid inflow in rat nephrons.

The relative contribution of intraluminal versus peritubular factors in mediating glomerulo-tubular balance (GTB) is still controversial. We modulated the load of tubular fluid to the proximal tubule of single nephrons of rats by injecting oil into the efferent arteries (EAO). In fifty nephrons the changes in reabsorption induced by obstruction occurred in the same direction as, and were significantly correlated with, the simultaneous changes in single nephron glomerular filtration rate (SNGFR) (y = -0.54 + 0.92x, R = 0.91, P < 0.0001). In an additional set of thirty-nine nephrons the load of tubular fluid was changed, during EAO, by partial collection from Bowman's space or from the early proximal convolution. Thus, the rate of tubular fluid delivery along the proximal tubule was changed in an experimental situation that prevented any modification in the oncotic pressure of peritubular capillaries. The changes in proximal deliveries during this experimental condition were significantly correlated with those during reabsorption (y = -2.87 + 0.71x, R = 0.82, P < 0.0001). These data demonstrate that GTB is fully expressed even when the native peritubular environment is kept constant while the rate of perfusion of proximal tubular segments with native tubular fluid is changed.

Absorption↗
PubMed1998

Helicobacter pylori infection and autoimmune processes: an emerging field of study.

Evidence is accumulating that Helicobacter pylori infection may be closely associated with autoimmunity. However, whether autoimmunity plays a causal role in the pathogenesis of some of the diseases attributed to this bacterium or whether it is rather an epiphenomenon remains to be determined. In this brief review, a summary is made of current knowledge regarding the potential general mechanisms by which Helicobacter pylori causes mucosal damage. A review is then made of the evidence linking this bacterium to the production of different gastric autoantibodies. Finally, the reported association between Helicobacter pylori infection and some known autoimmune diseases is discussed. Although the data are still not sufficiently complete to draw definite conclusions, autoimmunity appears to be an important aspect of this infection and will certainly become a major field of study in the next few years.

Antigens, Bacterial↗
PubMed1998

Clinical assessment of renal vascular involvement and clinical-pathological correlations.

The renal vascular involvement of systemic diseases can be of embolic, thrombotic or inflammatory nature. Occlusion of proximal arterial vessels results in a dissociation between the rapid progression of renal failure, and the urinary abnormalities. Urine examination can be nearly normal and non revealing, except for a loss in maximal concentrating ability. In contrast, inflammatory changes of distal vessels are variably transmitted to the glomeruli, resulting in proteinuria, variable hematuria associated to mixed abnormalities of the urinary sediment. In diffuse vascular involvement acute renal failure can supervene, difficult to distinguish from that of diffuse glomerulonephritides. Most systemic vasculitides, mainly those of SLE, microscopic polyangiitis, Henoch-Schoenlein purpura and that of Wegener granulomatosis cause a clinical picture either of acute, rapidly progressive glomerulonephritis, or of a nephritic syndrome. The vasculitides affecting small arteries, capillaries and venules can result in a clinical-histopathologic picture closely mimicking that of acute tubule-interstitial disease. A thorough evaluation of the clinical picture, of the degree and progression of renal failure, of urine analysis, and clinically guided biopsies of the appropriate tissues can lead to differentiation of the different diseases and precocious diagnosis and effective treatment.

Journal Article↗