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PubMed2003

A corresponding tyrosine residue in the C2/factor B type A domain is a hot spot in the decay acceleration of the complement C3 convertases.

The cleavage of C3 by the C3 convertases (C3bBb and C4b2a) determines whether complement activation proceeds. Dissociation (decay acceleration) of these central enzymes by the regulators decay-accelerating factor (DAF), complement receptor 1 (CR1), factor H, and C4-binding protein (C4BP) controls their function. In a previous investigation, we obtained evidence implicating the alpha4/5 region of the type A domain of Bb (especially Tyr338) in decay acceleration of C3bBb and proposed this site as a potential interaction point with DAF and long homologous repeat A of CR1. Because portions of only two DAF complement control protein domains (CCPs), CCP2 and CCP3, are necessary to mediate its decay of the CP C3 convertase (as opposed to portions of at least three CCPs in all other cases, e.g. CCPs 1-3 of CR1), DAF/C4b2a provides the simplest structural model for this reaction. Therefore, we examined the importance of the C2 alpha4/5 site on decay acceleration of C4b2a. Functional C4b2a complexes made with the C2 Y327A mutant, the C2 homolog to factor B Y338A, were highly resistant to DAF, C4BP, and long homologous repeat A of CR1, whereas C2 substitutions in two nearby residues (N324A and L328A) resulted in partial resistance. Our new findings indicate that the alpha4/5 region of C2a is critical to decay acceleration mediated by DAF, C4BP, and CR1 and suggest that decay acceleration of C4b2a and C3bBb requires interaction of the convertase alpha4/5 region with a CCP2/CCP3 site of DAF or structurally homologous sites of CR1 and C4BP.

Amino Acid Sequence↗
PubMed1986

Order of class III genes relative to HLA genes determined by the haplotype method.

The B18 C4A3 C4BQ0 BfF1 DR3 haplotype was found to be ideal for determining the order of C4 and Bf relative to HLA-B and DR by the haplotype method. All the copies of this haplotype are assumed to be derived from a single ancestral haplotype. Sixteen of the twenty-six BfF1-containing haplotypes carried all of the alleles from this "ancestral" haplotype. Most of the other BfF1-containing haplotypes could be derived from the "ancestral" haplotype by a single crossover event for one of the two possible gene orders. This suggests that B18 C4A3 C4BQ0 BfF1 DR3 is the sole source of the BfF1 allele. The uncommon C4 type on B18 C4A3 C4BQ0 BfF1 DR3 facilitates recognition of the BfF1-containing products of recombination between Bf and C4. One such recombinant haplotype was found which shows that the orientation of the class III genes is as follows: C4 is closest to HLA-B and Bf is closest to HLA-DR. This gene order is supported by all the earlier unequivocal results obtained using the haplotype method (Olaisen et al. 1983, Marshall et al. 1984a). Combining these results with the information on class III genes obtained from overlapping cosmid clones (Carroll et al. 1984) and earlier mapping studies (Robson and Lamm 1984) shows that HLA-B is telomeric to 21B. C4B, 21A, C4A, Bf and C2 then follow 21B in that order covering 120 kb. HLA-DR is located further toward the centromere.

Chromosome Mapping↗
PubMed1991

Immune adherence and clearance of hepatitis B surface Ag/Ab complexes is abnormal in patients with systemic lupus erythematosus (SLE).

Complement levels and complement receptor 1 (CR1) on erythrocytes (E) are reduced in systemic lupus erythematosus (SLE). To see whether these abnormalities are responsible for defective transport and elimination of immune complexes (IC) from the circulation, patients with active SLE (14) and normal volunteers (14) were injected with preformed IC (hepatitis B surface Ag/Ab). Two minutes after injection only 25.9 +/- 19.1% (mean +/- 1 s.d.) of the circulating IC were bound to E in the SLE patients as compared to 63 +/- 3.7% in the normal subjects (P = 0.0001). For SLE patients, the reduced immune adherence was best explained by a combination of complement depletion and low CR1 binding capacity (tau = 0.80, P = 0.0001). The disappearance of IC as estimated from the area under the elimination curve was faster in SLE than in controls (P = 0.02), and correlated with CR1 (tau = 0.54, P = 0.0001) and immune adherence observed in vivo (tau = 0.33, P = 0.013). Finally, immune adherence was absent and IC disappeared very rapidly in a patient with C2 deficiency and an SLE-like disease. These observations suggest that in SLE the defective immune adherence reaction might be responsible for the accelerated disappearance of IC from the circulation.

Adolescent↗
PubMed1999

Complement-dependent accumulation and degradation of platelets in the lung and liver induced by injection of lipopolysaccharides.

We found unique behaviors among platelets within a few minutes of the intravenous injection of lipopolysaccharide (LPS) into mice. Platelets accumulated primarily in the liver at lower doses of LPS, but at higher doses they accumulated largely in the lungs. When the platelets accumulated in these organs were degraded, there was a rapid anaphylactoid shock. The platelet response depended on the strain of mouse and on the source of LPS. Of various LPSs tested, the LPS from the smooth type of Klebsiella O3 (KO3-S LPS) was the most potent at inducing the platelet response and shock. K-76 monocarboxylic acid, an inhibitor of complement C5, effectively prevented the KO3-S LPS-induced degradation (but not accumulation) of platelets and the ensuing rapid shock in BALB/c mice. Moreover, in DBA/2 mice (which are deficient in complement C5), platelets accumulated in the lungs and liver in response to KO3-S LPS but soon returned to the circulation without degradation, and there was no rapid shock. The LPS from the rough type of KO3 induced an accumulation of platelets in the liver and lungs but not a degradation of platelets. On the basis of these results and those reported by other investigators, we propose that in the platelet response to LPS, the lectin pathway to form C3 convertase from C4 and C2 is involved in the rapid accumulation of platelets in the liver and lungs and that the pathway from C5 to C9 is involved in the destruction of platelets and the consequent anaphylactoid shock.

Anaphylaxis↗
PubMed2002

Synthesis of factor D by gastric cancer-derived cell lines.

Synthesis of complement components in vitro by four human gastric cancer-derived cell lines, MKN28, MKN74, MKN45 and KATO-III, was studied. When these cells were cultured for 3 days without addition of any stimulator, 0.94 +/- 0.49, 2.10 +/- 0.59, 7.29 +/- 5.94 and 2.47+/- 1.34 ng of factor D/10(6) cells were detected in supernatants of MKN28, MKN74, MKN45 and KATO-III, respectively. Factor D production by these cells was reversibly inhibited by the presence of cycloheximide. Factors B, C3 and C2 were also detected in protein-free culture medium of these cell lines. Addition of tumour necrosis factor (TNF) to culture enhanced C3 and factor B secretion but depressed C2 secretion, without any distinct effect on factor D secretion. Since all cell lines tested secreted significant amounts of factor D without addition of any stimulator in medium, it is possible that factor D may be synthesized by gastric epithelial cells physiologically and constitutively. From a quantitative analysis of factor D secretion by these cells, factor D secreted by gastric tissue is likely to contribute to the factor D level in circulating blood. The possible mechanism of participation of complement system in inflammation of gastric epithelium was proposed. Thus, the present study may be significant for clarification of the mode of extrahepatic complement synthesis participating in mucosal immunity.

Adenocarcinoma↗
PubMed2005

Measurement of ribose carbon chemical shift tensors for A-form RNA by liquid crystal NMR spectroscopy.

Incomplete motional averaging of chemical shift anisotropy upon weak alignment of nucleic acids and proteins in a magnetic field results in small changes in chemical shift. Knowledge of nucleus-specific chemical shift (CS) tensor magnitudes and orientations is necessary to take full advantage of these measurements in biomolecular structure determination. We report the determination by liquid crystal NMR of the CS tensors for all ribose carbons in A-form helical RNA, using a series of novel 3D NMR pulse sequences for accurate and resolved measurement of the ribose (13)C chemical shifts. The orientation of the riboses relative to the rhombic alignment tensor of the molecule studied, a stem-loop sequence corresponding to helix-35 of 23S rRNA, is known from an extensive set of residual dipolar couplings (RDC), previously used to refine its structure. Singular-value-decomposition fits of the chemical shift changes to this structure, or alternatively to a database of helical RNA X-ray structures, provide the CS tensor for each type of carbon. Quantum chemical calculations complement the experimental results and confirm that the most shielded tensor component lies approximately along the local carbon-oxygen bond axis in all cases and that shielding anisotropy for C3' and C4' is much larger than for C1' and C2', with C5' being intermediate.

Anisotropy↗
PubMed2006

Synthesis and hybridization studies of 2'-amino-alpha-L-LNA and tetracyclic "locked LNA".

A convergent route to a new class of locked nucleic acids, i.e., 2'-amino-alpha-L-LNA, has been developed. The optimized synthetic route to the corresponding phosphoramidite building block of thymine proceeds in 4% overall yield over 15 steps from the starting diol. Crucial synthetic steps include (a) introduction of a C2-azido group prior to nucleobase coupling, (b) Vorbrüggen glycosylation primarily affording the desired alpha-anomer, (c) separation of alpha-L-ribo- and beta-L-ribo-configured bicyclic nucleosides, and (d) selection of a suitable protecting group to avoid intramolecular Michael addition of the C2'-amino group onto the C6-position. Incorporation of a 2'-amino-alpha-L-LNA monomer into oligodeoxyribonucleotides results in modest changes in thermal stability with complementary DNA, whereas significant increases in thermal stability are observed with RNA complements along with excellent Watson-Crick discrimination. These results, along with the flexibility of the synthetic strategy allowing chemoselective N2'-functionalization at a late stage, render 2'-amino-alpha-L-LNA a promising building block for nucleic acid based nanobiotechnology and therapeutics. A slight modification in strategy facilitated the synthesis of the corresponding phosphoramidite building blocks of Michael adducts, which due to their tetracyclic skeletons exhibit a conformationally restricted furanose ring and glycosidic torsion angle (anti-range). Incorporation of such a "locked LNA" monomer into oligodeoxyribonucleotides results in large decreases in thermal affinity toward DNA/RNA complements.

Molecular Structure↗
PubMed2004

Fine needle aspiration cytology of benign breast disease. Markers of apoptosis and proliferation.

Aim of the study was to compare the fine needle aspiration cytology findings of benign breast lesions with incidence of proliferation markers and apoptosis. This study included 37 patients with palpable breast lumps, referred for USG guided FNA. FNAC were prospectively classified as C2-benign, C4-suspicious of malignancy, and C5-malignant. The specimens were simultaneously stained for Ki-67, MPM2, Bcl2 and P53. The diagnoses in group-C2 were following: simple cyst, multiple cysts, simple cyst with apocrine metaplasia, inflammatory cyst, benign dysplasia (BD) and benign solid tumors. The final diagnoses, after histopathological verification, in cases of primary classification as C4 and C5 were as follow: proliferative fibroadenoma (FAp) and breas cancer, respectively. Great majority of C2/BD aspirates were negative for proliferative antigens Ki-67 and PCNA. These antigens were detected in part of benign solid tumors, as anticipated in suspicious solid tumor, and in all of cancer aspirates. Bcl-2 immunopositive cells were detected approximately in one quarter of C2/BD, nearly in half of C2 solid tumors and in one C4/FAp. Most of diagnosed specimens were P53-negative. Immunocytodetection of Ki67, MPM2, Bcl2, P53 might be promising, supportive method in the classification of benign breast lesions. FNAC increases the reliability of diagnosis when complemented by immunocytochemical staining. It could be helpful procedure of establishing more accurately the biology of these lesions and possibly serve as an essential factor in clinical follow-up. Nevertheless, further study on larger group of patients comparing cytological and histopathological diagnosis is required to estimate reliability of its predictive value.

Adult↗
PubMed1986

Genetic markers in rheumatoid arthritis.

Genetic as well as environmental factors are believed to be of importance in the etiology of rheumatoid arthritis (RA). There are a number of previous studies of genetic markers in RA, but so far no genetic linkage and only a few associations have been found. Of the associations only one (with the HLA antigen DR4) appears to be well documented. In most previous association studies the patients have not been divided according to sex and family history of RA. In this investigation the HLA antigens A, B and DR and five serum protein systems (Bf, C3, Pi, Hp and Tf) were studied in patients with erosive RA, from northern Sweden. Special attention was paid to variations in the strength of associations according to sex and family history of polyarthritis. The following results were found: The frequency of the HLA antigen B27 was significantly increased in the North-Swedish population (16.6%) and among patients with a family history of polyarthritis (42.6%). In agreement with previous investigations a significantly increased frequency of the DR4 antigen was found in the RA patients. In the properdin factor B (Bf) system the S phenotype was found to be significantly increased in male patients and in patients with a family history of polyarthritis, a more severe form of RA and high titres of rheumatoid factor. No significant differences with respect to phenotype or gene frequencies were found in the C3 complement system. Thus, the association between RA and C3 found in previous investigations was not confirmed. A significant increase of rare alpha-1-antitrypsin (Pi) types (MS, MZ, MF and SZ) was found among RA patients. However, the increase concerned mainly Z heterozygotes and was more strongly pronounced among male patients. In the haptoglobin system a significant increase of the Hp2 gene and the Hp2-2 type was found among patients with a family history of polyarthritis, more pronounced among males. A significant increase of the transferrin gene C2 and of the C2 type was found among male RA patients, more pronounced among patients with a family history of polyarthritis. In 6 out of 8 gene loci studied significant associations were found, which is in agreement with a multifactorial etiology of RA.(ABSTRACT TRUNCATED AT 400 WORDS)

Arthritis, Rheumatoid↗
PubMed1988

Biosynthesis of complement factor P (properdin) by the human pre-monocyte cell line (U-937).

The human monocyte-like cell line, U-937, is known to differentiate into macrophage-like cells following stimulation with phorbol myristate acetate (PMA) or interferon-gamma (IFN-gamma). The activated cells have been reported to have enhanced capacity to synthesize C2, C3, Factors B and H. Here, U-937 cells were used as a model system to investigate the effects of immunomodulatory agents on the biosynthesis of Factor P by monocytoid cells. Non-stimulated U-937 cells progressively secreted increasing amounts of Factor P over a 72-hr culture period. The secreted Factor P was hemolytically active. The daily production of Factor P was nearly linear (approx. 2.1 +/- 0.2 ng/10(6) cells; mean +/- SEM). Factor P synthesis was reversibly inhibited by cycloheximide indicating de novo synthesis. Both secreted Factor P and Factor P in normal plasma contained Factor P of heterogeneous molecular sizes and eluted from Sephacryl S-300 gel filtration column as a broad peak (mol. wt 250-800 kDa). The synthesis of Factor P by U-937 cells was augmented 1.8-, 2.1- and 2.5-fold respectively following induction with PMA (30 ng/ml), IFN-gamma (100 U/ml) and LPS (0.1 microgram/ml). Metabolic labeling of U-937 cells and autoradiograms of SDS-PAGE analysis of Factor P immunoprecipitates demonstrated a 54 kDa band in the culture supernate, co-migrating with purified 125I Factor P. Intracellular Factor P however had an apparent mol. wt that was 4000 kDa smaller than secreted Factor P. Thus U-937 cells synthesize a precursor Factor P subunit polypeptide chain which undergoes post-synthetic glycosylation and polymerization to give rise to the oligomers characteristic of native Factor P in fresh plasma. Our data also demonstrate that Factor P synthesis by monocytic cells can be enhanced by immunomodulatory factors or mediators that are generally found at sites of inflammation and immune response.

Cell Line↗
PubMed1986

A molecular mechanism for the activation of the first component of complement by immune complexes.

The proposed activation mechanism is based upon several key concepts, including the "S"-structure for the folding of the C1r2C1s2 tetramer among the C1q arms [Poon, et al., J. molec. Biol. 168, 563-577 (1983)]; the locations of the catalytic domains on the tetramer and the resulting functional relevance of the "S"-structure [Colomb et al., Phil. Trans. R. Soc. B306, 282-292 (1984)]; the structure of C1-inhibitor [Odermatt et al., FEBS Lett. 131, 283-289 (1981)]; and the control of C1 activation by C1-inhibitor [Ziccardi, J. Immun. 128, 2505-2508 (1982)]. The proposed activation mechanism has four main features: steric exclusion of C1-inhibitor from C1 when it binds to an immune complex; signal generation through multivalent binding of the C1q heads to an irregularly-arranged cluster of antibody Fc regions, and signal transmission through the movement of the stiff C1q arms about their semi-flexible joints, causing distortion of the symmetrical cone of C1q arms; induction of rapid activation by a shift in equilibrium favoring the autocatalytic conformation of C1r2C1s2; and release of the activated C1s from the C1q arms, so that the ends of the tetramer are free for interaction with C4 and C2 and C1-inhibitor, and the C1q subcomponent becomes more flexible, allowing access of C1-inhibitor to C1r.

Antigen-Antibody Complex↗
PubMed1988

A factor activating complement via the alternative pathway in the supernatants of B cell lines transformed by Epstein-Barr virus and in sera obtained from patients with systemic lupus erythematosus.

Serum factors activating the alternative pathway of the complement (APC) were detected in 5 of 14 patients with systemic lupus erythematosus (SLE). Epstein-Barr virus (EBV)-transformed B cell lines were subsequently established from these patients and 6 of these produced factors capable of activating the APC. Using a limiting dilution technique, we obtained a clone which was producing a factor activating the APC (AF); by affinity column fractionation and polyacrylamide gel electrophoresis, the AF was found to have heavy and light chains comparable to those of normal human IgG. Normal human serum exhibited C3 split products (demonstrated by immunoelectrophoresis) in the presence of AF and under conditions permitting activation of the APC. Sera devoid of factor B, but not of C2 and C4, failed to catabolize C3 in the presence of AF. The AF failed to stabilize erythrocyte-bound C3bBb or C4b2a convertases, indicating that it was not a nephritic-factor-like molecule. We conclude that IgG molecules present in the sera and produced by EBV-transformed B cell lines from patients with SLE are apparently responsible, at least partially, for complement consumption in these patients.

B-Lymphocytes↗
PubMed1983

Redox potential dependence of photophosphorylation and electron transfer in continuous illumination of Rhodopseudomonas sphaeroides chromatophores.

The dependence on redox potential (Eh) of the steady-state photophosphorylation rate in chromatophores of Rhodopseudomonas sphaeroides Ga was measured using slowly equilibrating (and hence less interfering) redox mediators. The remaining interference of the mediators was taken into account by extrapolating to zero mediator concentration. The extents of cytochrome redox reactions (in the presence of antimycin) and of the carotenoid shift were similarly measured. The redox titration of cytochrome c oxidation is consistent with a requirement for prior cytochrome c2 reduction and prior Q1 (primary electron acceptor) oxidation, while the titration of cytochrome b reduction is consistent with a requirement for prior (BChl)2 reduction and prior cytochrome b560 oxidation. The steady-state carotenoid shift extent is a much more broadly peaked function of Eh than is the extent following a single-turnover flash, indicating that the transmembrane electrical potential difference can be built up to significant levels by minimal rates of electron flow. The photophosphorylation rate, in contrast, is much more strongly Eh dependent, supporting the concept of a threshold membrane energization below which phosphorylation cannot occur. Earlier work by others showing a requirement for equilibrium cytochrome c2 reduction and Q1 oxidation is clearly confirmed. A much greater enhancement in phosphorylation rate was found at low Eh than has heretofore been reported. This threefold enhancement is discussed in relation to the equilibrium redox states of the ubiquinone-10 complement of the chromatophore membrane.

Bacterial Chromatophores↗
PubMed1980

The role of specific antibody in alternative complement pathway-mediated opsonophagocytosis of type III, group B Streptococcus.

The native capsular polysaccharide antigen of type III, group B Streptococcus contains a terminal sialic acid residue on each repeating unit that masks all end-group galactopyranose residues and prevents alternative pathway complement activation by adult human sera in the absence of type-specific antibody. The critical role of the sialic acid residues in allowing the organism to evade activating the alternative complement pathway was shown when neuraminidase treatment of the organism converted the bacteria to activators of the alternative pathway as assessed in agammaglobulinemic serum. The requirement for specific antibody in permitting alternative pathway activation by the fully sialated bacteria was shown when sera that contained low levels of specific antibody failed to activate this pathway, and when prior absorption of serum that contained higher type-specific antibody levels with the capsular antigen failed to activate this pathway. The use of C2-deficient sera showed that the calssical pathway was not required for antibody-dependent alternative pathway activation. The use of isotonic, pH 7.5, veronal-NaCl buffer that contained 1% gelatin and that was supplemented to 4 mM Mg++ and 16 mM EGTA and adjusted to pH 7.5 (MgEGTA) ruled out the participation of the C1-bypass pathway. The presence of sialic acid on the bacterial surface is one means of evading an important mechanism of natural immunity, namely activation of complement by the alternative pathway. Only specific antibody, i.e., acquired immunity, can overcome this virulence factor.

Antibodies, Bacterial↗
PubMed1978

Requirements for the solubilization of immune aggregates by complement. The role of the classical pathway.

In this paper we examine the role of the classical pathway in the complement-mediated solubilization of immune precipitates (CRA). Serum reagents were depleted of the alternative pathway components properdin and factor D. Both depleted reagents lack CRA although they have almost intact hemolytic activity. Also, immune complexes were not solubilized when incubated with high concentrations of the classical pathway components (C1, C4, C2, and C3. We conclude that CRA is not mediated by the classical pathway alone. Activation of the classical pathway by the immune aggregates greatly enhances CRA. The effect of the classical pathway is to deposit C3b on the antigen-antibody lattice and promote the assembly of a lattice-associated, properdin-dependent C3-convertase. Although C3, C4, and properdin were detected on complexes solubilized by serum in the presence of Ca++ and Mg++, only C3 and properdin were found on the complexes when Ca++ had been chelated by ethylene glycol-bis-(beta-aminoethyl ether), N,N'-tetraacetic acid. In both situations the aggregates were capable of converting C5 in the fluid phase. However, no C5 was found on the solubilized complexes. These findings suggest that in contrast to nascent C3b and C4b, nascent C5-9 lacks binding affinity for immune aggregates.

Antigen-Antibody Complex↗
PubMed1999

[Activation mechanism of the complement system].

Complement is an activation system designed for the elimination of pathogens and is activated in three ways, i.e. the classical, alternative and newly discovered lectin pathways. The classical pathway is initiated by the binding of C1 to immune complexes, whereas the alternative pathway is activated by pathogens themselves without involvement of immune complexes. Upon binding of MBL (mannose-binding lectin) to certain carbohydrates on pathogens, the lectin pathway is activated by two C1r/C1s-like serine proteases termed MASP-1 and MASP-2, which are associated with MBL. As a result, C4, C2 and C3 are activated. The lectin pathway plays a crucial role in innate immunity both in vertebrates and in invertebrates. The mechanism underlying lectin pathway activation remains unsolved. From an evolutional point of view, the classical and lectin pathways are closely related.

Animals↗
PubMed1999

Isocitrate lyase of Ashbya gossypii--transcriptional regulation and peroxisomal localization.

The isocitrate lyase-encoding gene AgICL1 from the filamentous hemiascomycete Ashbya gossypii was isolated by heterologous complementation of a Saccharomyces cerevisiae icl1d mutant. The open reading frame of 1680 bp encoded a protein of 560 amino acids with a calculated molecular weight of 62584. Disruption of the AgICL1 gene led to complete loss of AgIcl1p activity and inability to grow on oleic acid as sole carbon source. Compartmentation of AgIcl1p in peroxisomes was demonstrated both by Percoll density gradient centrifugation and by immunogold labeling of ultrathin sections using specific antibodies. This fitted with the peroxisomal targeting signal AKL predicted from the C-terminal DNA sequence. Northern blot analysis with mycelium grown on different carbon sources as well as AgICL1 promoter replacement with the constitutive AgTEF promoter revealed a regulation at the transcriptional level. AgICL1 was subject to glucose repression, derepressed by glycerol, partially induced by the C2 compounds ethanol and acetate, and fully induced by soybean oil.

Acetates↗
PubMed1976

Recurrence of membranoproliferative glomerulonephritis following kidney transplantation. Serum complement component studies.

Sixteen patients with membranoproliferative glomerulonephritis who required kidney transplantation because of renal failure were evaluated for evidence of recurrence of the original disease by serologic and morphologic studies. Of the 12 patients with transplant tissue available for study, seven showed membranoproliferative glomerulonephritis by light morphology. Four of these seven also had hypocomplementemia, and this hypocomplementemia was characterized by decreased serum CH50, C3 beta1A or C3-C9 but norma serum C1, C4 and C2 by hemolytic assay. Immunofluorescent microscopy demonstrated more intense glomerular deposition of C3 and properdin in the hypocomplementemic patients. Ultrastructural studies demonstrated intramembranous deposits typical of dense deposit disease in one patient who also had marked hypocomplementemia. One patient who had two transplant biopsies and persistent hypocomplementemia showed progression from predominantly mesangial glomerular changes to both capillary wall and mesangial abnormalities. This study has shown a high rate of recurrence of membranoproliferative glomerulonephritis in the transplanted kidneys. A high death rate was noted in persistently hypocomplementemic patients. The serum C profile in hypcomplementemic patients who received translants was similar to that seen before transplantation, but the signficance of this finding remains unknown.

Adolescent↗