Myopathy with mitochondrial changes presenting as respiratory failure in two brothers.
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Biopsy, Needle↗
Biomedical subjects
J Mosquera
Publications and source records attributed to J Mosquera.
Erythrogenic toxin type B and its precursor isolated from nephritogenic streptococci induce leukocyte infiltration in normal rat kidneys.
BACKGROUND: Leukocyte infiltration is a common feature in renal biopsies from patients with acute poststreptococcal glomerulonephritis (APSGN). Cationic streptococcal erythrogenic toxin type B (ETB) and its precursor (ETBP) have been implicated in the pathogenesis of the disease, and the presence of ETB has been evidenced in renal biopsies from patients with APSGN. The present studies were performed to determine the effect of the ETBP and ETB on renal leukocyte infiltration and the mechanism(s) implicated in the phenomenon. METHODS: Male Sprague-Dawley rats were injected intrarenally with 100 microg of ETB or ETBP. Animals were sacrificed at 1, 6 and 24 h after injection and renal samples were studied by indirect immunofluorescence for the presence of leukocyte common antigen (LCA+) cells, C3, monocyte chemotactic protein-1 (MCP-1) and intercellular adhesion molecule-(ICAM-1), and by direct immunofluorescence for the presence of immunoglobulins. ETB and ETBP were tested for chemotactic effect and migration inhibition factor (MIF) activity by chemotaxis under agarose and agarose microdroplet methods, respectively. Streptococcal proteins were also tested for the capacity to induce MIF activity in rat glomerular cultures. To test for the influence of cationic charge on renal LCA+ cell infiltration, rats were injected with cationized ferritin or polyethyleneimine (PEI) and sacrificed 1 h later. RESULTS: An increased number of LCA+ cells was found in glomeruli and interstitial areas in ETB- or ETBP-injected animals. ETB and ETBP showed chemotactic and MIF activity on neutrophils and macrophages, and ETBP induced MIF activity in supernatants of glomerular cultures. Data obtained from C3, MCP-1, ICAM-1 or immunoglobulin renal staining in experimental animals were not significantly different when compared to control values. Cationized compounds failed to induce LCA+ cell infiltration; however, an increased number of glomerular LCA+ cells was observed after PEI perfusion. CONCLUSIONS: ETB and ETBP induce renal LCA+ cell infiltration during a short period after intrarenal injection, and this finding could be mediated by chemotactic and MIF activities. These observations could be relevant in the early events of pathogenesis of APSGN.
Animals↗
Evolution of virulence: a unified framework for coinfection and superinfection.
Models of the evolution of parasite virulence have focused on computing the evolutionarily stable level of virulence favored by tradeoffs within a host and by competition for hosts, and deriving conditions under which strains with different virulence levels can coexist. The results depend on the type of interaction between disease strains, such as single infection (immunity of infected individuals to other strains), coinfection (simultaneous infection by two strains), and superinfection (instantaneous takeover of host by the more virulent strain). We present a coinfection model with two strains and derive the superinfection model as the limit where individuals are rapidly removed from the doubly-infectious class. When derived in this way, the superinfection model includes not only the takeover of hosts infected by the less virulent strain, but new terms which take into account the possibility of increased mortality of doubly-infected individuals. Coinfection tends to favor higher virulence and support more coexistence than the single infection model, but the detailed results depend sensitively on two factors: (1) whether and how the model is near the superinfection limit, and (2) the shape of the coinfection function (the function describing the rate at which a more virulent strain can infect a host). If the superinfection limit arises due to rapid mortality of doubly-infected hosts, there is a region of uninvadable virulence levels rather than coexistence. When the coinfection function is discontinuous, as in many previous models, neither the coinfection model nor the superinfection limit can support an evolutionarily stable virulence level. Piecewise differentiable and differentiable coinfection functions produce qualitatively different results, and we propose that these more general cases should be used to study evolution of virulence when other mechanisms like space, population dynamics, and stochasticity interact.
Animals↗
A simple method to identify NBT-positive cells in isolated glomeruli.
BACKGROUND: Reactive oxygen radicals are probably involved in the pathogenesis of human and experimental models of renal disease, yet current methods are inadequate to quantify and identify the cells producing reactive oxygen radicals. METHODS AND RESULTS: We used the nitroblue tetrazolium reaction to determine superoxide anion production in glomerular cells in phorbol myristate-stimulated glomerular suspensions and in isolated glomeruli from rats with nephrotoxic nephritis, ureteral obstruction, and puromycin aminonucleoside nephrosis. We were also able to identify these nitroblue tetrazolium + cells using specific appropriate antibodies. When the technique was tested in conditions known to increase reactive oxygen radicals, as phorbol myristate-stimulated glomeruli and glomeruli from animals with nephrotoxic nephritis and ureteral obstruction, increased number of nitroblue tetrazolium + cells were found. These cells were identified as glomerular intrinsic cells (Thy-1 +) or infiltrating leukocytes (leukocyte common antigen + or antineutrophil +). CONCLUSION: This method may be useful to determine cells participating in glomerular damage induced by reactive oxygen radicals.
Animals↗
Apoptosis in proliferative glomerulonephritis: decreased apoptosis expression in lupus nephritis.
BACKGROUND: Apoptosis is a mechanism of cellular death involved in the deletion of cells in hyperplasic processes which has been observed in proliferative glomerulonephritis. Patients with systemic lupus erythematosus (SLE) are known to have defective apoptosis but there is scarce information about apoptosis in the renal lesions of this disease. The present studies were done to evaluate apoptosis in relation to the intensity of proliferation in several glomerulonephritis and the possible association between this relationship and the chronic histologic changes in lupus nephritis. METHODS: Studies were done in renal biopsies from 19 patients with lupus nephritis (types, IV, Va, Vb) classified with respect to chronicity and activity indexes, five patients with acute poststreptococcal glomerulonephritis, five with idiopathic mesangioproliferative glomerulonephritis, four with membranous glomerulonephritis, four with minimal-change nephrotic syndrome, and three patients with focal segmental sclerosis. Seven normal kidneys which could not be used for transplantation were used as a control group. Apoptosis was determined by in situ DNA nick-end labelling techniques and proliferating cells were identified with a monoclonal antibody antiproliferating cell nuclear antigen (PCNA). RESULTS: Decreased number of apoptotic cells and a high ratio of PCNA: apoptosis were observed in glomerulus and tubulointerstitium of patients with lupus nephritis when compared to other proliferative glomerulonephritis and controls. In lupus nephritis, glomerular apoptosis had a negative correlation with the chronicity index (r = -0.606 P = 0.005). The number of apoptotic cells in the glomeruli was not correlated with the number of PCNA positive cells in lupus nephritis, in contrast with a striking linear correlation observed in acute poststreptococcal nephritis (r = 0.925, P = 0.024), a disease with excellent prognosis. CONCLUSIONS: Apoptosis is decreased in proliferative lupus nephritis. Intense proliferation without increment in apoptosis (a high PCNA: apoptosis ratio) is a characteristic of lupus nephritis associated with chronic renal histological changes.
Adolescent↗
Histological evidence of neuraminidase involvement in acute nephritis: desialized leukocytes infiltrate the kidney in acute post-streptococcal glomerulonephritis.
Serum neuraminidase (NA, sialidase) activity has been demonstrated in acute poststreptococcal glomerulonephritis (APSGN) and implicated in the pathogenesis of the disease. Recent investigations show that neuraminidase-treated leukocytes accumulate preferentially in kidneys; therefore, we were interested in knowing if desialized cells infiltrate the kidney in APSGN. We first tested the capacity of peanut agglutinin lectin (PNA) to detect injected NA-treated leukocytes in the kidney of rats. NA-treated leukocytes were transfused and desialized cells were identified with fluorescein-conjugated peanut lectin (FITC-PNA) in renal tissue. PNA positive cells were identified in rat kidneys 3 hours after injection (glomeruli: 1.67 +/- 0.19 cells/g.c.s.; interstitium: 0.50 +/- 0.12 cells/int). Sections from available renal biopsy material of APSGN (n = 11), other glomerulonephritis (n = 28) and normal kidneys (n = 5) were double-stained with FITC-PNA and with monoclonal antibody to the CD11b molecule, which is expressed on polymorphonuclear and monocytes the main types of infiltrating cells during APSGN. Desialized (FITC-PNA positive) cells were found in the glomeruli (2.17 +/- SEM 0.22 cells per glomerular cross section, g.c.s.) and interstitium (0.61 +/- 0.15 cells per 0.0625 mm2, int) in all biopsies of APSGN. Only in 2 of 28 other glomerulonephritis showed desialized cells. More than 80% of the PNA positive cells in APSGN expressed the CD11b molecule and the infiltration was more intense in early biopsies. In conclusion, desialized leukocytes represent a significant part of the inflammatory infiltrate in APSGN. This finding gives support for a role of NA in the disease and provides clinical validation for a mechanism of renal cellular infiltration suggested by experimental observations.
Animals↗
Amyloid goitre: CT and MR findings.
Two cases of amyloid goitre presented as an enlarged thyroid mass with cystic components. Solid parts of the goitre showed high attenuation on computed tomography (CT) and moderate hypointensity on T1 and T2-weighted images. Fine needle aspiration was negative for amyloid, but pathological studies of surgical specimens demonstrated amyloid infiltration of the thyroid interstitium and regressive colloid cysts. In a patient at risk for systemic amyloidosis, thyroid enlargement with a cystic component suggests amyloid goitre. In this case, needle biopsies should be directed to solid areas of the mass because amyloid material may not be present in the cysts.
Adult↗
Neuraminidase promotes neutrophil, lymphocyte and macrophage infiltration in the normal rat kidney.
Neuraminidase (NA) is an enzyme produced by several microorganisms, which is capable of liberating sialic acid from glycoproteins and modifying cellular adhesion mechanisms. NA is considered a virulence factor in some bacterial species and has been implicated in the pathogenesis of acute poststreptococcal glomerulonephritis, a disease in which glomerular leukocyte infiltration is a prominent feature. We examined the effect of NA on kidney infiltration by neutrophils (PMN), T lymphocytes (TL) and monocyte-macrophages (MM). Intravenous injection of NA resulted in an early increase in the number of PMN (1 hr, 3.42 +/- 0.19 cells/cgs, mean +/- SEM; 3 hr, 3.63 +/- 0.13; 6 hr, 2.9 +/- 0.24; controls, 1.53 +/- 0.18; P < 0.001) and MM (1 hr, 3.49 +/- 0.16; 3 hr, 4.02 +/- 0.2; 6 hr, 3.88 +/- 0.27; controls 1.43 +/- 0.14; P < 0.001) in the glomeruli, while TL increased later (24 hr, 2.29 +/- 0.14; 48 hr, 2.4 +/- 0.2; 72 hr, 2.16 +/- 0.15; controls 0.7 +/- 0.07; P < 0.001). PMN and TL were also increased in the interstitium (up to ninefold for PMN and up to threefold for TL). Following i.v. injection of 51Cr-labeled NA-treated leukocytes, renal radioactive uptake was significantly increased at all times tested (percent radioactivity/gram of tissue after PMN injection, 3 hr, 5.57 +/- 0.46, mean +/- SEM; 12 hr, 5.38 +/- 0.77; 60 hr, 6.51 +/- 1.1; controls, 1.26 +/- 0.17, 1.75 +/- 0.25, and 2.46 +/- 0.08, respectively; P < 0.001 in each case.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Nutritional status and cutaneous leishmaniasis in rural Ecuadorian children.
The relationship between nutritional status and cutaneous leishmaniasis (CL) was evaluated in 230 children living in a rural subtropical rainforest in Northwest Ecuador. One-third of the subjects had evidence of either current (13 per cent) or past CL infection (21 per cent). Subjects with current (4.71 +/- 0.44 mg) or previous disease (4.29 +/- 0.35 mg) had lower mean daily dietary iron intakes than non-infected children (5.45 +/- 0.2 mg; chi 2 = 0.048), but not energy, protein, or other micronutrients. The low dietary iron intake data was corroborated by the reduced mean haemoglobin values observed in children with current (11.7 +/- 0.3 mg/dL) or past infection (11.3 +/- 0.2 mg/dL) compared to non-infected subjects (12.7 +/- 0.15 mg/dL; F-ratio = 17.0, P < 0.0001). Mean hematocrit values were also lower in the two infected groups (37.4 +/- 0.9 per cent and 37.4 +/- 0.6 per cent v. 39.5 +/- 0.5 per cent; F-ratio = 4.23, P = 0.0175). Furthermore, they were more likely to suffer from iron-deficiency anaemia than their non-infected counterparts (chi 2 = 4.64, P = 0.03). However, the children with active disease accounted for most of the excess risk for anemia (Fisher's exact test P = 0.009; OR = 10.0, exact 95 per cent CI = 1.37-111.8). Finally, growth stunting (< -2SD height-for-age) was more common in subjects with current (54 per cent) or past infection (51 per cent) compared to those without CL history (31 per cent; chi 2 = 8.03, P = 0.004).(ABSTRACT TRUNCATED AT 250 WORDS)
Anemia, Iron-Deficiency↗
Kaposi sarcoma involving bone in an HIV negative patient.
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Bone Neoplasms↗
Target dependence of central rapidity Lambda production in sulfur-nucleus collisions at 200 GeV/c per nucleon.
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Journal Article↗
[Role of complement in experimental glomerulonephritis].
The complement system is composed by 26 plasmatic proteins. The activation of either the classical or alternative complement pathway leads to the formation of the membrane attack complex C5b-C9 (MAC) which is capable of producing damage of the cellular membrane. MAC has been identified in renal biopsies from human and experimental, immune and nonimmune renal diseases, but it has not been possible to demonstrate any enzymatic activity on the glomerular basement membrane components (GBM). MAC can produce a lytic or a nonlytic effect on renal cells depending upon the dose used. The lytic effect in vitro has been demonstrated in epithelial, mesangial and endothelial cells, whereas the lytic effect in vivo has been described in a model of acute glomerulonephritis produced by the administration of monoclonal antibody anti-Thy 1.1. which reacts with mesangial cells. The nonlytic effect of MAC on renal cells is characterized by alterations in cell metabolism which can lead the production of prostaglandins, type IV collagen, reactive oxygen species, and a growth factor resembling interleukin I which can contribute to glomerular damage, to the modification of the filtration barrier permeability and hemodynamic changes in experimental glomerulonephritis. The effector mechanisms by which the complement system participates in the pathogenesis of glomerulonephritis are different in the various experimental models of nephritis. In nephrotoxic nephritis the complement pathway participates at least in 3 different ways: a) complement-neutrophil mediated injury, b) MAC dependent mechanism and c) producing hemodynamic alterations. In acute serum sickness the complement system beyond C2 is not necessary for the development of proteinuria and glomerular inflammation, but the MAC assembly seems to be important for the formation of large deposits. In the chronic serum sickness model, the complement system participates in the early proteinuria as well as in the histological expression of the disease. In the heterologous phase of Heymann's nephritis, the proteinuria is complement dependent whereas in the autologous phase the damage depends upon cellular mediated immunity. In passive Heymann's nephritis the complement system and particularly MAC, has a central role for the histological lesion of the epithelial cell as well as in the proteinuria. In conclusion, the complement system can mediate renal damage by the following mechanism: a) Releasing chemotactic factors which result in neutrophil recruitment and neutrophil mediated glomerular damage.(ABSTRACT TRUNCATED AT 400 WORDS)
Animals↗
Fish oil dietary supplementation reduces Ia expression in rat and mouse peritoneal macrophages.
Preliminary studies suggest that administration of fish oil fatty acids may be beneficial in several immunological diseases; therefore, we studied the effect of fish oil dietary supplementation on the expression of Ia in stimulated murine peritoneal macrophages. Rats (n = 19) and mice (n = 27) on standard rodent feeding were separated in experimental (E) and control (C) groups that received fish oil or saline solution, respectively, daily for 4 weeks by esophageal gavage. Cholesterol serum levels were significantly lowered by fish oil (E vs C, P less than 0.01). E and C groups were injected intraperitoneally with Listeria monocytogenes (LM) and peritoneal cells were harvested 4 and 7 days after infection. Decreased expression of Ia induced by LM was found in rats (C = 49.68 +/- 5.09%, E = 16.95 +/- 4.3%, P less than 0.01) and mice (C = 47.38 +/- 7.63%, E = 26.66 +/- 1.92%, P less than 0.01). Animals with a more pronounced depression of serum cholesterol (reduction of 44.04 +/- 1.52% of baseline levels) had more depression of Ia expression (6.47 +/- 1.22%, P less than 0.001 vs control). Reduction of Ia expression was not related to PGE2 production by peritoneal cells. Reduction of Ia expression by fish oil could induce down-regulation of antigen presentation and alloreactivity.
Animals↗
Migration inhibition factor in acute serum sickness nephritis.
Monocytes have been demonstrated to play an important role in acute serum sickness (AcSS) nephritis. Because accumulation of monocytes within the glomeruli could be the result of local lymphokine production, we studied migration inhibition factor (MIF) activity in supernatants from glomerular cultures, analyzed its temporal relationship with monocyte and lymphocyte accumulation, and tested the effect of anti-T lymphocyte monoclonal antibody on local MIF production. AcSS was induced in 12 rabbits, and one additional rabbit had antigen elimination without proteinuria. Single nephrectomy was performed at the time of antigen elimination in all animals; the remaining kidney was removed four days (4 rabbits) or 14 days afterwards (5 rabbits). In glomerular cross sections (gcs), lymphocytes were identified using monoclonal antibody M108, and monocytes by nonspecific esterase stain (ES). MIF activity was determined in supernatants of cultures of isolated glomeruli by the agarose microdroplet method. Peak of MIF activity (84.3 +/- 2.6%, SEM) was observed the first day of proteinuria in association with peak of lymphocyte infiltration (1.15 +/- 0.1 lymphocytes/gcs) and monocyte infiltration (2.4 +/- 0.3 mean ES score/gcs). MIF activity diminished by day 4 (66.0 +/- 6.3%) and reached control levels by day 14 (12.8 +/- 3.2%). There was a significant correlation between lymphocyte infiltration and MIF activity (r = 0.776, P less than 0.0001) as well as between MIF activity and monocyte accumulation (r = 0.858, P less than 0.0001). In five additional rabbits with AcSS, glomeruli were isolated, treated successively with M108 and normal rabbit serum, and supernatants harvested from 24-hour cultures were tested for MIF activity.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Intrarenal manometry in the diagnosis of acute rejection superimposed on acute tubular necrosis in renal transplantation.
We used fine-needle intrarenal manometry as a guide for detection of acute rejection superimposed on protracted oliguric acute tubular necrosis occurring in the postoperative course of human renal transplantation. We followed intrarenal pressure (IRP) in 31 patients who received 32 renal transplants, 12 from living related donors and 20 from cadaveric donors. There were 19 rejection episodes and 10 episodes of transient cyclosporin A (CyA) nephrotoxicity. Nine patients had posttransplant acute renal failure. Levels of IRP (mmHg) in acute rejection were (mean +/- SD) 48.6 +/- 11.1, significantly higher (p less than 0.001) than the levels in CyA nephrotoxicity (28.2 +/- 5.21), acute tubular necrosis (24.5 +/- 5.5) and normal functioning grafts (26.4 +/- 6.63). Antirejection treatment was associated with return to normal of IRP after 10 days. Intrarenal manometry was performed routinely ever 2-3 days in patients who had postoperative acute renal failure. Increments in IRP were detected on the 7-10th postoperative day in 7 patients who had 10-25 days of post-transplant oliguria. Renal biopsy findings were compatible with acute rejection, and the patients responded to intravenous bolus of steroids. We suggest that fine-needle intrarenal manometry is a reliable test for the detection of acute rejection in circumstances when traditional parameters of altered renal function cannot be evaluated.
Acute Kidney Injury↗
Extracellular neuraminidase production of streptococci associated with acute nephritis.
The possibility that streptococcal neuraminidase has a pathogenic role in acute poststreptococcal glomerulonephritis is reviewed. Experimental and clinical evidence suggesting autologous immune phenomena and anti-Ig reactivity in this disease is discussed. Neuraminidase may also induce sialic acid depletion that would be expected to result in changes of the electrical charge in the immune complex as well as in the glomerular polyanion filtration barrier. The nature of these changes will facilitate penetrability of material with nephritogenic potential. Neuraminidase production was detected in the majority of streptococcal isolates obtained from patients with glomerulonephritis and the best substrate for screening purposes appears to be bovine submaxillary gland mucin. On the basis of available evidence, it is suggested that the development of glomerulonephritis after streptococcal infection probably does not depend on neuraminidase production by the bacteria; however, this enzyme may be responsible for the anti-Ig reactivity demonstrated in some patients and thereby influence the course of the disease.
Acute Disease↗
[Giant retroperitoneal lipoma in a child].
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Child, Preschool↗
Increased apoptosis in acute puromycin aminonucleoside nephrosis.
Acute puromycin aminonucleoside nephrosis (PAN) in rats is characterized by heavy proteinuria associated with renal hypercellularity. The role of apoptosis in the resolution of renal hypercellularity was investigated in PAN. To study the participation of apoptosis in PAN, renal tissues were collected from nephrotic and control rats on weeks 1, 2 and 7 after a single puromycin aminonucleoside injection. Apoptosis was evaluated by light and electron microscopy. Apoptotic DNA fragmentation was detected by TUNEL staining. Renal tissues were also evaluated by the presence of leukocyte common antigen (LCA), ED1 (macrophages) and proliferating cell nuclear antigen (PCNA) with corresponding monoclonal antibodies. An increased number of apoptotic (TUNEL+) cells was observed in the glomerulus at week 1. Electron microscopy analysis showed glomerular apoptosis mainly in endothelial cells. In the interstitium and tubules, increased apoptosis was observed at weeks 1 and 2. Increased apoptosis was accompanied with increased LCA+, ED1+ and PCNA+ cells in the interstitium and with increased PCNA+ cells in tubules. There was a high significant correlation between the number of apoptotic cells and the number of interstitial LCA+, ED1+ and PCNA+ cells. Tubular PCNA expression was correlated with tubular apoptosis. We also observed significant correlation between glomerular, interstitial and tubular apoptosis with proteinuria during the nephrosis. Double staining analysis showed that about 13% of interstitial or tubular apoptotic cells were positive for PCNA. All these values returned to normal by week 7. These results indicate that apoptosis is involved in the repairing process of this disease model.
Acute Disease↗