A review of micronutrient deficiencies and analysis of maize contribution to nutrient requirements of women and children in Eastern and Southern Africa.

This paper reviews and analyses the importance of maize as staple food in Eastern and Southern Africa (E&SA) and contributes in understanding the nexus between maize nutritional composition and prevalence of micronutrient deficiencies (MNDs) in these regions. MNDs remain a major public health concern particularly for women and children, with calcium, iodine, iron, selenium, zinc, folate and vitamin A deficiencies being the most common. Estimates of their prevalence are among the highest in E&SA: iron-deficient anemia affected 26 to 31% of women of reproductive age, and deficiencies up to 53%, 36%, 66%, 75% and 62% for vitamin A, iodine, zinc, calcium and selenium, respectively, were measured in populations of these regions. Besides, these two regions show the highest worldwide maize per capita consumption (g/person/day) as main staple, with 157 in Eastern Africa and 267 in Southern Africa, including up to 444 in Lesotho. The analysis of food composition tables from these regions showed that 100 g of maize foods consumed by these populations could to some extent, contribute in satisfying dietary reference intakes (DRIs) of children and women in energy, proteins, carbohydrates, magnesium, zinc, vitamins B1 and B6. However, it provides very low supply of fats, calcium, sodium, selenium, vitamins C, A and E. The high occurrence of MNDs and considerable nutritional potential of maize consumed in E&SA can be explained by loss of nutrients due to processing practices, low food diversification and reduced nutrients bioavailability. Success cases of the main strategies to tackle the issue of MNDs in these regions by improving maize nutritional quality are discussed in this paper. Maize fortification was shown to improve nutrition and health outcomes of population. Increasing dietary diversity by complementing maize with other foods has improved nutrition through integration of micronutrient-rich foods in the diet. Mostly, biofortification has successfully contributed in reducing vitamin A and zinc deficiencies in rural communities more than nutrient supplementation, fortification and dietary diversity.

The role of bioactives in energy metabolism and metabolic syndrome.

Some food bioactives potentially exert anti-obesity effects. Anthocyanins (ACN), catechins, ß-glucan (BG) and n-3 long chain PUFA (LCPUFA) are among the most promising candidates and have been considered as a strategy for the development of functional foods counteracting body weight gain. At present, clinical trials, reviews and meta-analyses addressing anti-obesity effects of various bioactives or bioactive-rich foods show contradictory results. Abdominal obesity is an important criterion for metabolic syndrome (MetS) diagnosis along with glucose intolerance, dyslipidaemia and hypertension. Food bioactives are supposed to exert beneficial effects on these parameters, therefore representing alternative therapy approaches for the treatment of MetS. This review summarises outcomes on MetS biomarkers in recent clinical trials supplementing ACN, catechins, BG and n-3 LCPUFA, focusing mainly on anti-obesity effects. Overall, it is clear that the level of evidence for the effectiveness varies not only among the different bioactives but also among the different putative health benefits suggested for the same bioactive. Limited evidence may be due to the low number of controlled intervention trials or to inconsistencies in trial design, i.e. duration, dose and/or the method of bioactive supplementation (extracts, supplements, rich or enriched food). At present, the question 'Are bioactives effective in weight management and prevention of metabolic syndrome?' remains inconclusive. Thus, a common effort to harmonise the study design of intervention trials focusing on the most promising bioactive molecules is urgently needed to strengthen the evidence of their potential in the treatment of obesity, MetS and related diseases.

Brain structural correlates of obsessive-compulsive disorder with and without preceding stressful life events.

Objectives There is growing evidence supporting a role for stressful life events (SLEs) at obsessive-compulsive disorder (OCD) onset, but neurobiological correlates of such effect are not known. We evaluated regional grey matter (GM) changes associated with the presence/absence of SLEs at OCD onset. Methods One hundred and twenty-four OCD patients and 112 healthy controls were recruited. Patients were split into two groups according to the presence (n = 56) or absence (n = 68) of SLEs at disorder's onset. A structural magnetic resonance image was acquired for each participant and pre-processed with Statistical Parametric Mapping software (SPM8) to obtain a volume-modulated GM map. Between-group differences in sociodemographic, clinical and whole-brain regional GM volumes were assessed. Results SLEs were associated with female sex, later age at disorder's onset, more contamination/cleaning and less hoarding symptoms. In comparison with controls, patients without SLEs showed GM volume increases in bilateral dorsal putamen and the central tegmental tract of the brainstem. By contrast, patients with SLEs showed specific GM volume increases in the right anterior cerebellum. Conclusions Our findings support the idea that neuroanatomical alterations of OCD patients partially depend on the presence of SLEs at disorder's onset.

Impact of coeliac disease on dietary habits and quality of life.

BACKGROUND: Coeliac disease (CD) affects approximately 1% of the population in the UK and is managed by the life-long adherence to a strict gluten-free diet (GFD). Adhering to a GFD is practically difficult and not only affects dietary patterns, but also can affect many other aspects of daily life. The present study aimed to investigate the effect of CD and a GFD on dietary habits and quality of life of a cohort of adult biopsy diagnosed coeliac patients who reside in England. METHODS: The cohort was composed of 146 adult biopsy-diagnosed CD patients, who were all members of the Coeliac UK charity. Participants responded to a self-administered questionnaire considering dietary habits and quality of life. A food frequency questionnaire (FFQ) was used to assess dietary compliance. RESULTS: Generally, English CD patients reported to be in good physical and emotional health, although there were reports of anxiety and depression as a result of CD, most likely as a result of exclusion from social and leisure activities. The cohort reported high levels of dietary compliance (96%) which was supported by FFQ responses. However, there were reports of intentional gluten intake during social situations and when eating take-away foods. The FFQ revealed further examples of gluten ingestion, presumably unintentional, particularly through the consumption of breakfast cereals and starch-based sauces such as cheese sauce, custard and ketchup. CONCLUSIONS: The present study revealed that CD affects a wide range of daily activities and that gluten consumption may be more common than anticipated with possible consequences on health.

An unusual cause of acute renal failure in a kidney transplant recipient: salmonella enteritidis post-infectious glomerulonephritis.

BACKGROUND: Salmonella enteritidis-associated acute renal failure has often been described and is usually a result of dehydration or of rhabdomyolysis. A few cases of acute renal failure with glomerular syndrome, caused by S. enteritidis infection, have been reported in the literature, but none have been proven by histological findings. METHODS: Herein, we report on a case of S. enteritidis-related glomerulonephritis that occurred in a 42-year-old male transplant recipient. He was admitted with fever, signs of urinary infection, diarrhea, and nephritic syndrome, i.e. edema, hypertension, increase in serum creatinine, microscopic hematuria, proteinuria. His urine culture tested positive for S. enteritidis. RESULTS: Under light microscopy, the graft biopsy showed proliferative and exudative endocapillary glomerulonephritis. In addition, there was polymorphonuclear infiltration of the interstitium, and extra-capillary proliferation in one glomerulus. Immunofluorescence showed granular deposits of C3 in the mesangium. Electron microscopy showed electron-dense deposits typical of humps. He fully recovered on a double antibiotic therapy that included ofloxacin and amikacin. CONCLUSION: Although acute renal failure related to non-typhoidal Salmonella infections are often related to dehydration or rhabdomyolysis, this case report shows that it might also be related to immune complex-mediated glomerulonephritis manifesting as nephritic syndrome.

Altered middle lamella homogalacturonan and disrupted deposition of (1-->5)-alpha-L-arabinan in the pericarp of Cnr, a ripening mutant of tomato.

Cnr (colorless non-ripening) is a pleiotropic tomato (Lycopersicon esculentum) fruit ripening mutant with altered tissue properties including weaker cell-to-cell contacts in the pericarp (A.J. Thompson, M. Tor, C.S. Barry, J. Vrebalov, C. Orfila, M.C. Jarvis, J.J. Giovannoni, D. Grierson, G.B. Seymour [1999] Plant Physiol 120: 383-390). Whereas the genetic basis of the Cnr mutation is being identified by molecular analyses, here we report the identification of cell biological factors underlying the Cnr texture phenotype. In comparison with wild type, ripe-stage Cnr fruits have stronger, non-swollen cell walls (CW) throughout the pericarp and extensive intercellular space in the inner pericarp. Using electron energy loss spectroscopy imaging of calcium-binding capacity and anti-homogalacturonan (HG) antibody probes (PAM1 and JIM5) we demonstrate that maturation processes involving middle lamella HG are altered in Cnr fruit, resulting in the absence or a low level of HG-/calcium-based cell adhesion. We also demonstrate that the deposition of (1-->5)-alpha-L-arabinan is disrupted in Cnr pericarp CW and that this disruption occurs prior to fruit ripening. The relationship between the disruption of (1-->5)-alpha-L-arabinan deposition in pericarp CW and the Cnr phenotype is discussed.

Nonstructural 3 protein of hepatitis C virus triggers an oxidative burst in human monocytes via activation of NADPH oxidase.

It has been shown that oxidative stress occurs in chronic hepatitis C. Release of reactive oxygen species (ROS) from sequestered phagocytes and activated resident macrophages represents the predominant component of oxidative stress in the liver. However, little is known about the ability of the monocyte to produce ROS in response to protein of hepatitis C virus. In this study, we investigated the ROS production in human monocytes stimulated by several viral proteins of hepatitis C virus. Human monocytes from healthy blood donors were incubated with recombinant viral protein: Core, NS3, NS4, and NS5. ROS production was measured by chemiluminescence. Only NS3 triggered ROS production in human monocytes. Generated ROS were mainly the anion superoxide. NS3 also induced a rapid and transient increase in intracellular calcium concentration measured by a video digital microscopy technique. By using different metabolic inhibitors, we showed that ROS production requires calcium influx, tyrosine kinases, and the stress-activated protein kinase, p38. The study of p47(PHOX) phosphorylation and translocation showed that NADPH oxidase was activated and involved in ROS production induced by NS3. In a second experiment, NS3 inhibited the oxidative burst induced by phorbol 12-myristate 13-acetate. These results indicate that NS3 activates NADPH oxidase and modulates ROS production, which may be involved in the natural history of hepatitis C infection.

Modulation of the degree and pattern of methyl-esterification of pectic homogalacturonan in plant cell walls. Implications for pectin methyl esterase action, matrix properties, and cell adhesion.

Homogalacturonan (HG) is a multifunctional pectic polysaccharide of the primary cell wall matrix of all land plants. HG is thought to be deposited in cell walls in a highly methyl-esterified form but can be subsequently de-esterified by wall-based pectin methyl esterases (PMEs) that have the capacity to remove methyl ester groups from HG. Plant PMEs typically occur in multigene families/isoforms, but the precise details of the functions of PMEs are far from clear. Most are thought to act in a processive or blockwise fashion resulting in domains of contiguous de-esterified galacturonic acid residues. Such de-esterified blocks of HG can be cross-linked by calcium resulting in gel formation and can contribute to intercellular adhesion. We demonstrate that, in addition to blockwise de-esterification, HG with a non-blockwise distribution of methyl esters is also an abundant feature of HG in primary plant cell walls. A partially methyl-esterified epitope of HG that is generated in greatest abundance by non-blockwise de-esterification is spatially regulated within the cell wall matrix and occurs at points of cell separation at intercellular spaces in parenchymatous tissues of pea and other angiosperms. Analysis of the properties of calcium-mediated gels formed from pectins containing HG domains with differing degrees and patterns of methyl-esterification indicated that HG with a non-blockwise pattern of methyl ester group distribution is likely to contribute distinct mechanical and porosity properties to the cell wall matrix. These findings have important implications for our understanding of both the action of pectin methyl esterases on matrix properties and mechanisms of intercellular adhesion and its loss in plants.

Increased cyclooxygenase-2 and 5-lipoxygenase activating protein expression in peritoneal macrophages during ovalbumin immunization of mice and cytosolic phospholipase A(2) activation after antigen challenge.

The present study investigates phenotypic and functional differentiation of peritoneal macrophages during ovalbumin-induced subcutaneous immunization of mice. For the first time we show that, in mouse peritoneal macrophages, ovalbumin immunization induces an increase in cyclooxygenase-2 (COX-2) and 5-lipoxygenase activating protein (FLAP) expression whereas it inhibits cytosolic phospholipase A(2) (cPLA2) expression. The study of arachidonic acid (AA) metabolism in peritoneal macrophages from control (cPM) and ovalbumin-immunized (iPM) mice shows that the reduced cPLA2 expression is correlated to a reduced basal AA metabolism, but is not a limiting factor for the opsonized zymosan-, PMA-, or A23187-triggered AA metabolism. We also show that in vitro ovalbumin challenge induces, only in iPM, cPLA2 activation through phosphorylation of serine residues, via a mechanism involving MAP kinases, and through increased intracellular calcium concentrations, leading to eicosanoid production. In parallel, we report that, in peritoneal macrophages, ovalbumin immunization induces the expression of CD23, the low affinity receptor for IgEs known for its involvement in allergic diseases. Thus, the modified expression of the enzymes involved in AA metabolism and the difference of response of cPM and iPM toward the antigen are important elements to understand the underlying mechanisms of ovalbumin-induced allergic responses.

Spatial regulation of pectic polysaccharides in relation to pit fields in cell walls of tomato fruit pericarp.

Scanning electron microscopic examination of intact tomato (Lycopersicon esculentum) pericarp and isolated pericarp cell walls revealed pit fields and associated radiating ridges on the inner face of cell walls. In regions of the cell wall away from pit fields, equivalent ridges occurred in parallel arrays. Treatment of isolated cell walls with a calcium chelator resulted in the loss of these ridges, indicating that they contain homogalacturonan-rich pectic polysaccharides. Immunolabeling procedures confirmed that pit fields and associated radiating ridges contained homogalacturonan. Epitopes of the side chains of pectic polysaccharides were not located in the same regions as homogalacturonan and were spatially regulated in relation to pit fields. A (1-->4)-beta-galactan epitope was absent from cell walls in regions of pit fields. A (1-->5)-alpha-arabinan epitope occurred most abundantly at the inner face of cell walls in regions surrounding the pit fields.

Reactive oxygen intermediates and eicosanoid production by kupffer cells and infiltrated macrophages in acute and chronic liver injury induced in rats by CCl4.

OBJECTIVE AND DESIGN: The aim of the present study was to characterize during acute and chronic liver injury induced by CCl4, macrophage phenotypes and whether a change in reactive oxygen intermediates (ROI) and eicosanoids production by Kupffer cells (KC) was observed. MATERIAL AND METHODS: Liver steato-necrosis and cirrhosis were induced in rats after 3 weeks and 9 weeks of CCl4 intoxication, respectively. Monocytes and tissue macrophages were identified by immunohistochemical study using monoclonal antibodies ED-1 and tissue macrophages using the antibody ED-2. The release of ROI and eicosanoids in response to the phorbol ester TPA (protein kinase activator) and to the calcium ionophore A23187 was assessed in cultivated cells. RESULTS: As compared to healthy controls, livers of rats with steato-necrosis or cirrhosis exhibited a significant increase of ED-1 and ED-2 positive cells. Only KC from rats with liver steato-necrosis were found to have higher A23187, TPA + A23187 or opsonized zymosan induced ROI production than healthy controls (p < 0.01). After TPA + A23187 or opsonized zymosan stimulation, KC from both rats with steato-necrosis or cirrhosis produced more TxB2 and leukotrienes and less PGE2 as compared to healthy controls (p <0.05). CONCLUSIONS: These results suggest an influx of monocytes into the liver during acute and chronic injury induced by CCl4. Functional changes of this inflammatory infiltrate have been demonstrated with an increase of ROI production only in the early stage of liver injury whereas a rise in KC leukotriene production and an imbalance between cytoprotective and cytotoxic prostanoids were observed at all stages of liver disease.

Expression of TNF-alpha and immunohistochemical distribution of hepatic macrophage surface markers in carbon tetrachloride-induced chronic liver injury in rats.

In liver injury induced by carbon tetrachloride, secondary hepatic injury occurs from inflammatory processes originating from products released by activated Kupffer cells, which play a central role in hepatic inflammation. The purpose of our study was to demonstrate, in rats, the relationships between a function of the hepatic macrophages, TNF-alpha production and the state of activation of these cells, characterized by their phenotype, in the different phases of the process and development of fibrosis in a carbon tetrachloride-induced cirrhosis model. The immunohistochemical localization of proinflammatory cytokine TNF-alpha and surface surface makers (ED1 and ED2) was studied in hepatitis and cirrhosis in response to 3 and 9 weeks ingestion of carbon tetrachloride. After carbon tetrachloride ingestion, accompanying the increased necrosis, immunohistochemical analysis of liver tissue sections demonstrated the significantly increased number of cells expressing ED1, ED2 and TNF-alpha, compared to normal. The number of cells expressing the surface phenotypic markers of liver macrophages increased and this change was concomitantly associated with an increased cellular expression of TNF-alpha. Local macrophage proliferation and influx of newly recruited blood monocytes resulted in an increase of the macrophage population. The populational changes involved difference in functional activity and enhanced TNF-alpha expression. This cytokine expressed in the carbon tetrachloride-induced inflammatory process is associated with the development of fibrosis and may contribute to disease severity.

Study of the association between major histocompatibility complex class II genes and the response to interferon alpha in patients with chronic hepatitis C infection.

OBJECTIVE: The aim of the study was to determine the influence of HLA class II genes on the response to interferon-alpha (IFN-alpha) in patients with chronic hepatitis C. METHODS: The distribution of HLA DRB1 and DQB1 alleles was assessed in 170 caucasoïd patients treated with IFN-alpha for chronic hepatitis C. 50 patients had a long term sustained response to treatment whereas 120 patients were nonresponders. RESULTS: Female sex, non-1 HCV genotype particularly genotype 2 and pretreatment low serum HCV RNA level were associated with long-term sustained response to IFN-alpha. A trend towards a higher prevalence of DRB1*07 allele in non responders than in patients with sustained response (45% vs. 28%, odds ratio 2.1; P < 0.05) on the one hand and of DQB1*06 allele in HCV genotype 1 patients with sustained response than in HCV genotype 1 nonresponders (75% vs 27.3%, odds ration 7.9; P < 0.02) on the other hand, were observed. However, none of these two differences remained significant after Bonferroni's correction. CONCLUSION: Accordingly, we conclude that the response to IFN-alpha therapy is more tightly related to virus factors than to host's HLA class II genes.

Molecular and genetic characterization of a novel pleiotropic tomato-ripening mutant

In this paper we describe a novel, dominant pleiotropic tomato (Lycopersicon esculentum)-ripening mutation, Cnr (colorless nonripening). This mutant occurred spontaneously in a commercial population. Cnr has a phenotype that is quite distinct from that of the other pleiotropic tomato-ripening mutants and is characterized by fruit that show greatly reduced ethylene production, an inhibition of softening, a yellow skin, and a nonpigmented pericarp. The ripening-related biosynthesis of carotenoid pigments was abolished in the pericarp tissue. The pericarp also showed a significant reduction in cell-to-cell adhesion, with cell separation occurring when blocks of tissue were incubated in water alone. The mutant phenotype was not reversed by exposure to exogenous ethylene. Crosses with other mutant lines and the use of a restriction fragment length polymorphism marker demonstrated that Cnr was not allelic with the pleiotropic ripening mutants nor, alc, rin, Nr, Gr, and Nr-2. The gene has been mapped to the top of chromosome 2, also indicating that it is distinct from the other pleiotropic ripening mutants. We undertook the molecular characterization of Cnr by examining the expression of a panel of ripening-related genes in the presence and absence of exogenous ethylene. The pattern of gene expression in Cnr was related to, but differed from, that of several of the other well-characterized mutants. We discuss here the possible relationships among nor, Cnr, and rin in a putative ripening signal cascade.

IgA nephropathy complicating diabetic glomerulosclerosis.

A retrospective study was done on 66 diabetic patients who had renal biopsies performed during 1979-1994. This review shows 10 patients who presented IgA nephropathy associated with diabetic nephropathy. Six patients had insulin-dependent diabetes mellitus and 4 patients non-insulin-dependent diabetes mellitus. All patients presented with proteinuria and 7 had hematuria. Four patients presented with renal impairment. Histologic evaluation disclosed the presence of thickened glomerular basement membranes and increased mesangial matrix in all cases, associated with nodular sclerosis in 8 cases. By immunofluorescence, diffuse mesangial IgA deposits were observed in all cases. The high incidence of the coexistence of IgA nephropathy and diabetes seems not merely coincidental. Structural and/or functional abnormalities of the glomerular basement membranes might facilitate the development of immune complex glomerular diseases. In patients with diabetes, the appearance of urinary abnormalities and/or deterioration in renal function altered the clinical history of diabetic nephropathy. The disorders are clinically suggestive of the presence of nondiabetic renal disease and raised the possibility of another pathogenetic mechanism.

Immunocytochemical characterization of lung macrophage surface phenotypes and expression of cytokines in acute experimental silicosis in mice.

The expression of the surface phenotypical profile and the cytokines TNF-alpha and IL-1beta from murine lung macrophages was studied in parenchymal lung tissue and bronchoalveolar fluid of mice, over a 2-week period, following a single intratracheal instillation of silica. The acute inflammatory reaction, confirmed by a significant augmentation of four times the control values of the number of macrophages recovered by lavage from experimental animals, was followed by organized granulomas in the interstitium. The immunohistochemical analysis of lung tissue sections after silica instillation demonstrated the increased alveolar and interstitial tissue expression of all surface antigens and cytokines studied, mainly Mac-1, F4/80 antigens, TNF-alpha and IL-1beta, which were occasionally observed in normal uninjected and saline-treated mice. These findings show that, after silica instillation, the expression of surface phenotypical markers of lung macrophages increased, and this change was concomitantly associated with an increased expression of the cytokines TNF-alpha and IL-1beta. These changes support the conclusion that an influx of the newly recruited and activated macrophage population, with a different phenotype, is induced by treatment during inflammation. The populational changes involve difference in functional activity and enhance TNF-alpha and IL-1beta expression. These cytokines, produced in the silicosis-induced inflammatory process, are associated with the development of fibrosis and may contribute to disease severity.

Reactive oxygen intermediates as regulators of TNF-alpha production in rat lung inflammation induced by silica.

Exposure to mineral dusts such as silica has been associated with progressive pulmonary inflammation and fibrosis. There is evidence that the release of reactive oxygen intermediates (ROI) and cytokines by alveolar macrophages (AM) is involved in lung injury associated with silica exposure. However, the chronology and relationship between these two mediators are poorly understood. In this study, an animal model of silicosis has been used, allowing simultaneous follow-up of lung histopathologic state, AM TNF-alpha production at the protein (biologic assay) and mRNA (reverse transcriptase-PCR) levels, and the release of ROI (luminol-dependent chemiluminescence), after bronchoalveolar lavages. In particular, it has been shown that intratracheal instillation of silica (50 mg/kg) in rats led to fibrosis characterized by cellular interstitial infiltrates with granulomas, and in AM, it led to 1) an early and continuous increase in 12-O-tetradecanoylphorbol-13-acetate- or zymosan-triggered ROI production (days 1, 3, 14, and 28 post-treatment), and 2) a rise of TNF-alpha mRNA expression and protein secretion on days 3 and 14. A free radical scavenger pretreatment (N-ter-butyl-alpha-phenylnitrone) reversed lung histopathologic changes and decreased AM ROI production and TNF-alpha expression at the level of mRNA. These findings suggest that ROI production is an important primary event determining the silica-induced inflammatory process. ROI may act in an autocrine or paracrine manner and regulate TNF-alpha production by a mechanism promoting gene expression. The critical role of this cytokine in the pathogenesis of silicosis was confirmed by anti-TNF-alpha Ab treatment.

Henoch-Schönlein purpura and membranoproliferative-like glomerulonephritis.

A 17-year-old man presented Henoch-Schönlein purpura with renal impairment, nephrotic syndrome needing transitory hemodialysis and hematuria. By light microscopy, the renal biopsy revealed membranoproliferative-like lesion associated with massive subendothelial deposits, some subepithelial deposits, hyalin thrombi and intracapillary neutrophils. By immunofluorescence, intense nodular and segmental deposits of IgG, IgM, IgA, C3, fibrinogen and C1q were found to be present in the intracapillary area and the mesangium. By electron microscopy, large subendothelial and rare subepithelial deposits were observed. A skin biopsy demonstrated leukocytoclastic skin vasculitis with IgA deposits in the arterial walls. Treatment with corticosteroids resulted in return renal to normal renal function but persistent proteinuria and hematuria. A second renal biopsy, performed after 2 months, showed a marked decrease in lesions and deposits. Fifteen months later, the patient presented normal serum creatinine level but proteinuria and hematuria persisted. At this time, a third renal biopsy was performed and showed segmental mesangial sclerosis and the decrease of disappearance of deposits. Two years after the first hospitalization, no abnormal serum creatinine or urinalysis were present. This report describes a detailed study of a case presented with Henoch-Schönlein purpura and morphologic features consistent with membranoproliferative-like lesion, who recovered normal renal function and urinalysis; repeat biopsies performed at intervals of 2 months and 1 year confirmed the disappearance of mesangial proliferation, double contours and deposits.