Tumor sólido pseudopapilar de páncreas: reporte de caso / Pseudopapilar solid tumor of pancreas: case Report

Resumen Introducción: El tumor sólido pseudopapilar del páncreas es una rara entidad que representa menos del 1% de las neoplasias pancreáticas. Suele presentarse en mujeres jóvenes y solo da síntomas de carácter compresivo una vez que alcanza un gran tamaño. Dado su comportamiento biológico incierto el tratamiento es la cirugía. Caso Clínico: Presentamos el caso de una mujer de 23 años con historia de 1 año de evolución de dolor epigástrico y baja de peso. El estudio imagenológico demostró una masa heterogénea sólida-quística dependiente de la cabeza del páncreas de aspecto neoplásico. Se realizó una biopsia incisional laparoscópica cuyo resultado fue de un tumor maligno indiferenciado, por lo que se optó por la resección quirúrgica. Se realizó una pancreatoduodenectomía abierta sin incidentes con un postoperatorio favorable. Los análisis histopatológicos e inmunohistoquímico fueron compatibles con un tumor sólido pseudopapilar de páncreas.

Introduction: The pseudopapillary solid tumor of the pancreas is a rare entity that represents less than 1% of pancreatic neoplasms. It usually occurs in young women and only gives symptoms of a compressive nature once it has reached a large size. Given its uncertain biological behavior, the treatment is surgery. Case Report: We present the case of a 23-year-old woman with a 1-year history of epigastric pain evolution and weight loss. The imaging study demonstrated a solid-cystic heterogeneous mass dependent on the head of the pancreas of neoplasic appearance. A laparoscopic incisional biopsy was performed, the result of which was an undifferentiated malignant tumor, which was why the surgical resection was chosen. An open pancreatoduodenectomy was performed without incident with a favorable post operative. Histopathological and immunohistochemical analyzes were compatible with a solid pseudopapillary tumor of the pancreas.

Early hyperglycemia: a risk factor for posttransplant diabetes mellitus among renal transplant recipients.

To ascertain the frequency, epidemiology, and risk factors of posttransplant diabetes mellitus (PTDM), a retrospective analysis of all first renal transplantations, without personal history of diabetes (DM) and with a follow up >or=6 months, was performed. All patients received methylprednisolone (0.5-1 g IV) immediately prior to surgery, followed by immunosuppression including steroids, cyclosporine, and azathioprine most frequently. Early hyperglycemia was defined as values >126 mg/dL during the first week after transplantation and DM by 2 blood glucose levels of >126 mg/dL after the first month of follow-up. Included were 163 patients, namely, 57.6% males and 66% recipients of a deceased donor and 12% with a first-degree family history of DM. Mean age at transplantation was 39 years (range, 17-70 years) with a mean follow-up of 64 months. Among the 163 total subjects, some developed PTDM with frequencies of 7.5%, 13%, and 23% at 1, 5, and 10 years, respectively. Among patients with a first-degree family history of DM, 37% developed PTDM compared with 14% of those without it (odds ratio [OR] = 3.6; P < .05). Early hyperglycemia was observed in 55/92 patients, 15 of whom developed PTDM. Among patients with PTDM, the frequency of early hyperglycemia was 87% compared with 54% among those who did not develop this complication (OR = 5.4; P < .05). We confirmed a high frequency of PTDM, identifying risk factors such as a first-degree family history of DM and the development of early hyperglycemia, which should be taken into account to increase our diagnostic sensitivity and improve therapeutic individualization among renal transplant patients.

[Bariatric surgery in patients with focal segmental glomerulosclerosis secondary to obesity]. / Cirugía bariátrica en pacientes con glomeruloesclerosis focal y segmentaria secundaria a obesidad.

2 cases of proteinuria in obese non-diabetic young males, both corresponding to focal segmental glomerulosclerosis are presented. Effective reduction of body weight by bariatric surgery was followed by sustained remission of proteinuria allowing significant reduction or total removal of blockers of the reninangiotensin- system.

Cirugía bariátrica en pacientes con glomeruloesclerosisfocal y segmentaria secundaria a obesidad / No disponible

Se presentan dos casos de proteinuria en jóvenes obesos no diabéticos, con histología de Glomeruloesclerosis Focaly Segmentaria (GFS). La efectiva reducción de peso corporal mediante cirugía bariátrica se siguió de una remisión sostenida de la proteinuria, permitiendo una significativa reducción o suspensión de las dosis de fármacos bloqueadores del sistema renina-angiotensina (AU)

2 cases of proteinuria in obese non-diabetic youngmales, both corresponding to focal segmental glomerulosclerosis are presented. Effective reduction of bodyweight by bariatric surgery was followed by sustained remission of proteinuria allowing significant reduction or total removal of blockers of the renin-angiotensinsystem (AU)

Ethnic differences in HLA antigens in Chilean donors and recipients: data from the National Renal Transplantation Program.

To describe HLA antigen distribution, looking for possible markers of renal disease in Mapuche and non-Mapuche people in the renal transplantation program, we reviewed data from 1297 histocompatibility studies of the Chilean national renal transplantation program (421 donors and 876 recipients), performed between 2000 and 2005. Mapuche people were classified according to their family surnames. The most frequent antigens found among the total Chilean population were A2 (48%), A19 (33%), B16 (33%), B35 (26%), DR4 (38%), and DR6 (28%), without significant differences between donors and recipients. Among the 114 individuals (9%) classified as Mapuche, the most frequent antigens were A28 (49%), A2 (44%), B16 (63%), B35 (24%), DR4 (48%), and DR8 (30%), with A28/B16/DR4 as the most common haplotype. In contrast, A28, B16, DR4, and DR8 were significantly more frequent in Mapuche compared with non-Mapuche people. B8 was significantly more frequent in Mapuche recipients than in non-Mapuche recipients and Mapuche donors. The higher frequency of some HLA antigens in Mapuche people was confirmed, possibly corresponding to ethnic markers. The special concentration of B8 among Mapuche recipients might represent a genetic factor predisposing to chronic renal disease in this human group.

Renal transplantation in Mapuche people.

Previous studies have demonstrated higher concentrations of some histocompatibility antigens in Mapuche people compared with non-Mapuche Chileans in the renal transplantation program. With the aim of evaluating whether those antigenic differences might induce differences in the outcomes of renal transplantation among patients belonging to that ethnic group, we reviewed HLA studies and at least 6 months follow-up of all patients with a first kidney transplant between 1980 and 2006. The 248 patients had a mean age of 37.6 years, 40% were females, and 48% had living related donors. The mean kidney follow-up was 90 months and patient follow-up was 106 months. Thirty-nine patients (16%) were classified as Mapuche, according to their surnames, including 16 women with overall mean age of 34.5 years, and 14 had been transplanted from a living related donor. Mapuche patients received organs with better HLA matching expressed as number of identities (3.4 +/- 0.1 versus 2.8 +/- 0.1 among non-Mapuche; P < .05), and the proportion receiving organs with > or = 3 compatibilities was significantly higher (Mapuche 38% versus non-Mapuche 22%; P < .05). Kaplan-Meier survival curves showed nonsignificant differences in kidney survival: 86% at 5 years and 68% at 10 years in Mapuche; and 83% and 65%, respectively, for non-Mapuche. Patient survival rates were 97% at 5 years and 86% at 10 years in the Mapuche group versus 91% and 79%, respectively, in the non-Mapuche group; both results were not significantly different. Our results showed similar outcomes of kidney and patient survivals among Mapuche people even when they received organs with better HLA matches.

Gremlin: a novel mediator of epithelial mesenchymal transition and fibrosis in chronic allograft nephropathy.

BACKGROUND: Chronic allograft nephropathy (CAN) is the most frequent cause of chronic dysfunction and late loss of renal allografts. Epithelial mesenchymal transition (EMT) has been identified as responsible for the presence of activated interstitial fibroblasts (myofibroblasts) and transforming growth factor beta (TGF-beta)/Smad is the key signaling mediator. It has been proposed that the bone morphogenetic protein 7 (BMP-7) antagonist, Gremlin, could participate in EMT, as a downstream mediator of TGF-beta. METHODS: We evaluated 33 renal allograft biopsies, 16 of which showed CAN, versus 17 controls. By in situ hybridization we studied the expression of TGF-beta and Gremlin mRNA. Gremlin, BMP-7, E-cadherin, and alpha-smooth muscle actin (alpha-SMA) proteins were evaluated by immunohistochemistry and Smad3 activation by Southwestern. In cultured human tubuloepithelial cells (HK2 cell line), Gremlin induction by TGF-beta was studied by confocal microscopy. RESULTS: Among renal biopsies of transplanted patients with CAN, we detected up-regulation of TGF-beta in colocalization with Gremlin (RNA and protein), mainly in areas of tubulointerstitial fibrosis. In the same tubules, we observed decreased expression of E-cadherin and induction of vimentin and alpha-SMA. BMP-7 was significantly decreased in the CAN biopsies. In addition, HK2 stimulated with TGF-beta (1 ng/mL) induced Gremlin production at 72 hours. CONCLUSION: We postulated that Gremlin is a downstream mediator of TGF-beta, suggesting a role for Gremlin in EMT observed in CAN.

Modulation of renal kallikrein by a high potassium diet in rats with intense proteinuria.

Injury of the renal tubulointerstitial compartment is recognized to play an important role in hypertension. Its damage may in turn, impair the activity of vasodepressor systems, like the kallikrein-kinin, in blood pressure regulation. The overload proteinuria model induces tubulointerstitial injury with activation of the renin-angiotensin system, but renal kallikrein and the development of hypertension have not received special attention. Sprague-Dawley rats received seven intraperitoneal doses of bovine serum albumin (BSA) 2 g/day under normosodic diet and were hydrated ad libitum. A second group received a high potassium diet to stimulate kallikrein production during the previous four weeks and while under BSA administration. A third one received potassium and BSA in the same schedule, but with the kinin B2 receptor antagonist, HOE140, added during the protein load phase. A control group received seven saline injections. Kallikrein protein was detected by immune labeling on renal sections and enzymatic activity in the urine. The BSA group showed massive proteinuria followed by intense tubulointerstitial damage. Blood pressure increased after the third dose in BSA animals, remaining elevated throughout the experiment, associated with significant reductions in renal expression and urinary activity of kallikrein, compared with controls. An inverse correlation was found between blood pressure and immunohistochemistry and urinary activity of kallikrein. Potassium induced a significant increase in both urinary activity and renal kallikrein expression, associated with significant reduction in blood pressure. The HOE140 antagonist blunted the antihypertensive effect of kallikrein stimulation in proteinuric rats. Loss of renal kallikrein, produced by tubulointerstitial injury, may participate in the pathogenesis of the hypertension observed in this model.

No gender-associated differences of cyclosporine pharmacokinetics in stable renal transplant patients treated with diltiazem.

Cytochrome-P450 enzymes metabolize cyclosporine both in the liver and in the intestinal wall. Diltiazem, by competitive inhibition of these enzymes, may increase the absorption and the bioavailability of cyclosporine. Some evidence points to a higher activity of some specific enzymes in women, such as CYP3A, that may influence differences in cyclosporine pharmacokinetics. We examined possible gender-associated differences in pharmacokinetic profiles of cyclosporine in 19 stable renal transplant recipients cotreated with diltiazem. Ten women and nine men, chronically using diltiazem associated with cyclosporine, azathioprine, and prednisone were randomly assigned to an 8-week period of continued controlled treatment with diltiazem (10 patients) or a wash-out period discontinuing diltiazem (nine patients). At the end of this period, the time-concentration curves of cyclosporine in the first 4 hours were performed after a single dose of cyclosporine. Thereafter, a cross-over between groups was performed, and time-concentration curves repeated. A specific RIA was used to measure cyclosporine concentrations. Comparisons between male and female patients in doses of cyclosporine and other pharmacokinetics parameters (C(0), C(2), AUC(0-4)), with or without diltiazem, did not show any difference related to gender. The association of diltiazem allowed a similar degree of reduction in Neoral dosage in male and female patients (21%). No changes in serum creatinine, blood urea nitrogen, potassium, uric acid, or blood pressure, or other adverse event were observed during the study. In these groups of patients, gender was not an important factor to be considered when diltiazem is added to cyclosporine therapy.

Human leukocyte antigens in indigenous (mapuche) people in a regional renal transplantation program in chile.

An active regional transplantation program established in the southern region of Chile has allowed the incorporation of ethnic minorities particularly Mapuche living in this geographic area in the development of a histocompatibility database. To identify possible differences in the human leukocyte (HLA) antigen distribution in Chilean Mapuche compared with non-Mapuche, we reviewed 442 HLA tissue-typing studies. Seventy-eight of 309 recipients (25%) and 18 of 133 donors (13%) were Mapuche. Among recipients, Mapuche people showed a significantly higher frequency of the HLA antigens, A28, B16, DR4, and DR8, and a lower one for A19, B15, and DR1 (P < .05) compared with non-Mapuche individuals. A particularly higher frequency of the haplotype A28, -B16, -DR4 was also evidenced in Mapuche. Besides, these recipients showed a higher frequency of the allele -DR4 when compared with Mapuche donors. A greater frequency of some histocompatibility antigens in patients with chronic renal disease might be attributed to allelic concentration due to a high index of endogamy, but a possible association with the development of progressive renal disease cannot be ignored, especially when a higher prevalence of DR4 was observed among Mapuche recipients.

Correlation Between C2 and AUC(0-4) in Renal Transplant Patients Treated With Diltiazem.

BACKGROUND: The area-under-the-curve (AUC) of cyclosporine (CsA) reflects exposure to the drug, but this monitoring strategy is time-consuming and not cost-effective. Recently, it has been suggested that the concentration at 2 hours after dosing (C2) shows the best correlation with AUC. The C2 has been replacing the trough measurement (C0) to monitor CsA therapy, but in patients receiving diltiazem there is not much information about this issue. We investigated the correlations between C2 and C0 with absorption AUC over the first 4 hours (AUC(0-4)) in renal stable transplant patients receiving CsA therapy with or without diltiazem. PATIENTS AND METHODS: Ten patients (five men) of ages 23 to 68 years and 6 to 84 months after transplantation, were randomly assigned to an 8-week initial period of either diltiazem washout or controlled treatment with diltiazem. Time-concentration curves of cyclosporine were performed at the end of this period using a specific RIA measurement of blood samples. Thereafter, a crossover of the groups was performed and after another 8 weeks, a second curve was obtained. Drugs that change the pharmacokinetics of cyclosporine or diltiazem were not allowed. RESULTS: The cyclosporine daily dose was lower with diltiazem (173 +/- 4 mg vs 213 +/- 4 mg, P = .002), but despite a dose reduction of only 19% +/- 1.5%, there was a trend to a larger AUC/dose (28 +/- 5 ng x h/mL x mg vs 17 +/- 2 ng x h/mL x mg, P = .1) and a trend to an increased C2 when treatment included diltiazem (1035 +/- 156 ng/mL vs 652 +/- 126 ng/mL, P = NS). Moreover, we confirmed that C2 showed the best correlation with AUC(0-4), (r = 0.7, P = .04), a correlation that improved with diltiazem (r = 0.9, P < .002). CONCLUSION: C2 is the point that correlates best with AUC(0-4) with or without diltiazem. C2 in the presence of diltiazem was associated with a stronger, more significant correlation with AUC(0-4).

Valsartan-induced hematocrit changes in renal transplant patients.

BACKGROUND: Angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor type 1 blockers (ARB) are frequently prescribed for renal transplant patients. The main reasons for their use are that their antihypertensive and antifibrogenic effects may prevent chronic renal allograft dysfunction, potentially improving transplant survival. Furthermore, ACE and ARB have been used to reduce the hematocrit in patients with posttransplant erythrocytosis. We evaluated the effects of the ARB valsartan on the evolution of hematocrit in stable renal transplant patients treated with cyclosporine (CsA), azathioprine (Aza), and prednisone. PATIENTS AND METHODS: Twenty-six stable renal transplant patients treated with valsartan 80 mg/d orally were followed for 6 months. Evaluations were performed prior to as well as at 3 and 6 months following the initiation of valsartan. RESULTS: The hematocrit levels decreased significantly at 3 months (46.1 +/- 7.3 vs 39.9 +/- 5.8 ; P < .0001) in patients with a normal hematocrit, namely a level over 38%, with no further reduction at 6 months. In recipients with an hematocrit less than 38%, there was no significant reduction, either at 3 or 6 months follow-up. Valsartan was well tolerated without significant side effects. CONCLUSION: We postulate that inhibition of the proerythropoietic effects of angiotensin II and/or the reduction in hypoxia within the renal tubulointerstitium as well as the vasodilator effects on the efferent arterioles, represent possible mechanisms for the reduction and stabilization of the hematocrit in stable renal transplant patients.

Tubular NF-kappaB and AP-1 activation in human proteinuric renal disease.

BACKGROUND: Nuclear factor-kappaB (NF-kappaB) and activated protein-1 (AP-1) are transcription factors that regulate many genes involved in the progression of renal disease. Recent data have shown that NF-kappaB is activated in tubules and glomeruli in various experimental models of renal injury. In vitro studies also suggest that proteinuria could be an important NF-kappaB activator. We therefore approached the idea that NF-kappaB may be an indicator of renal damage progression. METHODS: Paraffin-embedded renal biopsy specimens from 34 patients with intense proteinuria [14 with minimal change disease (MCD) and 20 with idiopathic membranous nephropathy (MN)] and from 7 patients with minimal or no proteinuria (IgA nephropathy) were studied by Southwestern histochemistry for the in situ detection of activated transcription factors NF-kappaB and AP-1. In addition, by immunohistochemistry, we performed staining for the NF-kappaB subunits (p50 and p65) and AP-1 subunits (c-fos, c-jun). By immunohistochemistry and/or in situ hybridization, the expression of some chemokines [monocyte chemoattractant protein-1 (MCP-1), RANTES, osteopontin (OPN)] and profibrogenic cytokines [transforming growth factor-beta (TGF-beta)], whose genes are regulated by NF-kappaB and/or AP-1, were studied further. RESULTS: NF-kappaB was detected mainly in the tubules of proteinuric patients, but rarely in nonproteinuric IgA nephropathy (IgAN) patients. In addition, there was a significant relationship between the intensity of proteinuria and NF-kappaB activation in MCD (r = 0.64, P = 0.01) and MN patients (r = 0.64, P < 0.01). Unexpectedly, patients with MCD had a significantly higher NF-kappaB tubular activation than those with MN (P < 0.01). To assess whether there was a different composition of NF-kappaB protein components, immunostaining was performed for the NF-kappaB subunits p50 and p65. However, no differences were noted between MCD and MN patients. In those patients, there was a lower tubular activation of AP-1 compared with NF-kappaB. Moreover, a strong correlation in the expression of both transcription factors was observed only in MN (r = 0.7, P = 0.004). Patients with progressive MN had an overexpression of MCP-1, RANTES, OPN, and TGF-beta, mainly in the proximal tubules, while no significant expression was found in MCD patients. CONCLUSIONS: On the whole, our results show that a tubular overactivation of NF-kappaB and AP-1 and a simultaneous up-regulation of certain proinflammatory and profibrogenic genes are markers of progressive renal disease in humans. Increased activation of solely NF-kappaB and/or AP-1 may merely indicate the response of tubular renal cells to injury.

Overexpression of chemokines, fibrogenic cytokines, and myofibroblasts in human membranous nephropathy.

UNLABELLED: Overexpression of chemokines, fibrogenic cytokines, and myofibroblasts in human membranous nephropathy. BACKGROUND: Proteinuria plays a central role in the progression of glomerular disease, and there is growing evidence suggesting that it may determine tubular cell activation with release of chemokines and fibrogenic factors, leading to interstitial inflammatory reaction. However, most studies on this subject have been performed in experimental models, and the experience in human kidney biopsies has been scarce. We analyzed the tissue sections of patients with idiopathic membranous nephropathy (IMN), a noninflammatory glomerular disease that may follow a progressive disease with heavy persistent proteinuria, interstitial cell infiltration, and decline of renal function. METHODS: Paraffin-embedded biopsy specimens from 25 patients with IMN (13 progressive and 12 nonprogressive) were retrospectively studied by immunohistochemistry [monocyte chemoattractant protein-1 (MCP-1), regulated on activation normal T-cell expressed and secreted chemokine (RANTES), osteopontin (OPN), platelet-derived growth factor-BB (PD-GF-BB)] and in situ hybridization [MCP-1, RANTES, PDGF-BB, transforming growth factor-beta1 (TGF-beta1)]. Moreover, we studied the presence of myofibroblasts, which were identified by the expression of alpha-smooth muscle actin (alpha-SMA), the monocytes/macrophages (CD68-positive cells), and T-cell infiltration (CD4+ and CD8+ cells). All of the patients were nephrotic and without treatment at time of the biopsy. RESULTS: A strong up-regulation of MCP-1, RANTES, and OPN expression was observed, mainly in tubular epithelial cells, with a significant major intensity in the progressive IMN patients. A strong correlation between the mRNA expression and the corresponding protein was noted. The presence of these chemokines and OPN was associated with interstitial cell infiltration. TGF-beta and PDGF were also up-regulated, mainly in tubular epithelial cells, with a stronger expression in the progressive IMN, and an association with the presence of myofibroblasts was found. CONCLUSIONS: Patients with severe proteinuria and progressive IMN have an overexpression in tubular epithelial cells of the chemokines MCP-1, RANTES, and OPN and the profibrogenic cytokines PDGF-BB and TGF-beta. Because this up-regulation was associated with an interstitial accumulation of mononuclear cells and an increase in myofibroblastic activity, it is suggested that those mediators are potential predictors of progression in IMN. Finally, based on experimental data and the findings of this article, we speculate that severe proteinuria is the main factor responsible for the up-regulation of these factors in tubular epithelial cells.

Anticardiolipin antibodies in acute poststreptococcal glomerulonephritis and streptococcal impetigo.

Anticardiolipin (aCL) antibodies have been described in diverse clinical situations, linked to the risk of thrombosis in different vascular locations. They have been rarely studied in renal diseases, and occasionally they have been associated with glomerular thrombosis. We analyzed the incidence of aCL (isotypes IgG, IgA, and IgM) in samples, taken during the acute phase of the disease, from 27 well-documented patients having acute poststreptococcal glomerulonephritis. Twelve cases were positive on IgG testing, 1 case on IgA testing only, and no one was positive on IgM testing. A serological follow-up was performed with a second sample taken about 7 months later, for the patients initially positive on IgG testing showing persistence in 9. Clinical variables during the acute phase and after a follow-up period of 25 (range 6-89) months were analyzed for possible associations with the presence of these antibodies, but non was significantly related. Renal histopathological investigation did not reveal particular findings in the aCL-positive patients, and glomerular thrombosis was not found in any case. In addition, serum samples from 12 streptococcal impetigo patients without renal involvement were analyzed, showing similar incidence (4 positive on IgG testing, 1 of them positive on IgM testing as well, and no one positive on IgA testing) and titers of aCL antibodies. We conclude that the presence of aCL antibodies in acute poststreptococcal glomerulonephritis may be a marginal immunological phenomenon unrelated to the glomerular disease, triggered by the streptococcal infection.

Anticardiolipin antibodies in classic pediatric hemolytic-uremic syndrome: a possible pathogenic role.

Anticardiolipin (aCL) antibodies have been associated with thrombocytopenia, hemolytic anemia and an increased risk of thrombosis in different vascular locations, even in the absence of lupus. The classic hemolytic-uremic syndrome is a postinfectious acute renal failure characterized by hemolytic anemia, thrombocytopenia and the presence of widespread glomerular thrombosis in the kidney, with pathogenic mechanisms that remain to be identified. In order to establish the frequency of aCL antibodies in this syndrome and to identify a possible role in the pathogenesis and clinical manifestations, 17 patients were studied during the reactant phase of the disease looking for an association between the presence of aCL antibodies (isotypes IgG, IgA and IgM) and the main clinical variables of the syndrome. In 8 patients IgG aCL was present, 2 patients had IgM aCL, and 1 had IgA antibodies on the solid-phase ELISA aCL assays, but no association could be demonstrated with the clinical variables studied. Although it might correspond to an epiphenomenon related to the triggering intestinal infection, a pathogenic role cannot be discarded and additional studies should be performed.

Incidence and studies on antigenic specificities of antineutrophil-cytoplasmic autoantibodies (ANCA) in poststreptococcal glomerulonephritis.

Sera from 210 patients with Acute Poststreptococcal Glomerulonephritis (APSGN) and 14 patients with streptococcal impetigo without glomerular disease were tested for the presence of IgG-ANCA using an indirect immunofluorescence assay (IIF) on ethanol fixed normal human neutrophils. In the group of nephritic patients, ANCA were detected by IIF in 9% (18 out of 210 cases) in an atypical diffuse cytoplasmic pattern (a-ANCA) in 14 cases and in a (p-ANCA) perinuclear staining in the remaining 4 cases. Longitudinal studies performed on six IIF positive patients, showed persistence of the phenomenon for up to six months, without relationship with activity of disease. No patient with streptococcal impetigo showed positivity on the IIF assay. Positive sera were analyzed on ELISA plates for their IgG reactivity against specific purified ANCA antigens: Proteinase-3 (PR3), Myeloperoxidase (MPO). Cathepsin-G and Bactericidal/Permeability Increasing Protein (BPI). Anti-MPO antibodies were present in 4 cases (3 a-ANCA and 1 p-ANCA). No reactivity was identified against PR-3, BPI and Catepsin-G in any of the samples. The presence of ANCA was significantly associated with a more severe glomerular disease as assessed by the serum creatinine and the crescents formation. Further studies are required to identify other antigenic specificities of these autoantibodies. Their absence in the streptococcal impetigo control group might suggest that their presence in APSGN could play some pathogenic role in kidney disease.