Association of JC virus with tubulointerstitial nephritis in a renal allograft recipient

A renal allograft transplant patient with tubulointerstitial nephritis was examined for possible involvement of human polyomaviruses. Biopsy of the allograft kidney revealed inflammatory interstitial infiltration with tubulitis and typical inclusion bodies in the nucleus of the tubulo-epithelium. Glomeruli showed duplication and lamination of Bowman's capsule with enlargement of the parietal and visceral epithelia. Immunohistochemical analysis on the graft section using a JC virus (JCV) VP1 peptide-specific antibody showed positive staining. Paracrystalline arrays of naked viral particles with diameters of 40 nm were visualized in the nuclear inclusions under an electron microscope. Molecular examination using the polymerase chain reaction (PCR) and DNA sequencing revealed that the JCV was involved in the nephritis. The results indicated that JCV may be associated with tubulointerstitial nephritis.     

Siblings with congenital renal tubular acidosis and nerve deafness

Two siblings (a boy and a girl) had congenital renal tubular acidosis (RTA) with nephrocalcinosis. Hearing loss due to nerve deafness was diagnosed at 13 1/2 and 9 years of age, respectively. The parents, who are second cousins, are healthy. They have another boy who is unaffected. This is in accordance with an autosomal recessive gene. The association of RTA and deafness was first noted by Royer in 1967, and so far some 50 cases have been described. The literature is reviewed.     

Central role of lactic acidosis in cancer cell resistance to glucose deprivation-induced cell death

Solid tumours are dependent on glucose, but are generally glucose-deprived due to poor vascularization. Nevertheless, cancer cells can generally survive glucose deprivation better than their normal counterparts. Thus, to render cancer cells sensitive to glucose depletion may potentially provide an effective strategy for cancer intervention. We propose that lactic acidosis, a tumour microenvironment factor, may allow cancer cells to develop resistance to glucose deprivation-induced death, and that disruption of lactic acidosis may resume cancer cells' sensitivity to glucose depletion. Lactic acidosis, lactosis, or acidosis was generated by adding pure lactic acid, sodium lactate, or HCl to the culture medium. Cell death, cell cycle, autophagy, apoptosis, and gene expression profiling of the surviving cancer cells under glucose deprivation with lactic acidosis were determined. Under glucose deprivation without lactic acidosis, 90% of 4T1 cancer cells died within a single day; in a sharp contrast, under lactic acidosis, 90% of 4T1 cells died in a period of 10 days, with viable cells identified even 65 days after glucose was depleted. Upon glucose restoration, surviving cells resumed proliferation. Lactic acidosis also significantly extended survival of other cancer cells under glucose deprivation. G1/G0 arrest, autophagy induction, and apoptosis inhibition were tightly associated with lactic acidosis-mediated resistance to glucose deprivation. Lactosis alone had no effect on cell survival under glucose deprivation; acidosis alone can prolong cell survival time but is not as potent as lactic acidosis. Thus, the ability of cancer cells to resist glucose deprivation-induced cell death is conferred, at least in part, by lactic acidosis, and we envision that disrupting the lactic acidosis may resume the sensitivity of cancer cells to glucose deprivation.     

Acquired distal renal tubular acidosis in man

Summary Distal renal tubular acidosis (dRTA) may complicate renal transplantation, liver cirrhosis, and obstructive uropathy. Indeed, its occurrence may be an early clue to an episode of rejection of the graft or to obstructive uropathy. The mechanism in most patients with dRTA is impaired distal secretion of protons. In some patients, however, back leak of protons from tubular lumen to blood may abolish distal tubular ability to maintain urine to blood proton gradients. In patients with obstructive uropathy the spectrum of tubular acidosis is widened by the occurrence of additional defects in tubular secretion of potassium and impairment of hydrogen ion secretion secondary to hypoaldosteronism. Hyperkalemia is also seen in voltage dependent states such as following the administration of lithium and amiloride. Hyperkalemia per se is conducive to acidosis by a combination of extrarenal and several intrarenal mechanisms.     

肾移植受体血管的选择

为给肾移植血管端端吻合提供解剖学基础,本文观测了32具成年尸体的髂动脉系和肾动脉.通过前后两者口径的对比,一支型肾动脉和多支型肾动脉第一支可与髂内动脉干作对端吻合,二支型动脉,可先并合为与髂内动脉内径相近的一支,再与髂内动脉作端端吻合;三支型肾动脉,亦可合并成一支与髂内动脉干作对端吻合,也可合并其中二支,合并支与另支分别与髂内动脉前、后干作端端吻合,还可依其口径大小,其中二支分别与髂内动脉前、后干(或臀上动脉)端端吻合,另支与髂外动脉作端侧吻合.     

Mutational and functional analysis of SLC4A4 in a patient with proximal renal tubular acidosis

Permanent isolated proximal renal tubular acidosis (pRTA) with ocular abnormalities is a systemic disease with isolated pRTA, short stature and ocular abnormalities. We identified a novel homozygous deletion of nucleotide 2,311 adenine in the kidney type Na⁺/HCO₃^– cotransporter (kNBC1) cDNA in a patient with permanent isolated pRTA. This mutation is predicted to result in a frame shift at codon 721 forming a stop codon after 29 amino acids anomalously transcribed from the SLC4A4 gene. Cosegregation of this mutation with the disease was supported by heterozygosity in the parents of the affected patient. The absence of this mutation in 156 alleles of 78 normal individuals indicates that this mutation is related to the disease and is not a common DNA sequence polymorphism. When injected into Xenopus oocytes, the mutant cRNA failed to induce electrogenic transport activity. In addition, immunofluorescence and Western blot analysis failed to detect the expression of the full-length protein in mutant-injected oocytes. Our results expand the spectrum of kNBC1 mutations in permanent isolated pRTA with ocular abnormalities and increase our understanding of the renal tubular mechanism that is essential for acid-base homeostasis.     

Monocyte implication in renal allograft dysfunction

Macrophages are involved in the development and progression of kidney fibrosis. The aim of this study was to analyse the phenotype of circulating monocytes and their ability to predict kidney allograft dysfunction in living kidney transplant recipients. Whole blood samples from 25 kidney recipients and 17 donors were collected at five time‐points. Monocyte phenotype was analysed by flow cytometry, and interleukin (IL)‐10 and soluble CD163 by enzyme‐linked immunosorbent assay. One week after transplantation, surface CD163 and IL‐10 levels increased significantly from baseline [2·99 ± 1·38 mean fluorescence intensity (MFI) to 5·18 ± 2·42 MFI for CD163; 4·5 ± 1·46 pg/ml to 6·7 ± 2·5 pg/ml for IL‐10]. This CD163 increase correlated with 4‐month creatinine levels (r = 0·4394, P = 0·04). However, soluble CD163 decreased significantly from baseline at 1 week (797·11 ± 340·45 ng/ml to 576·50 ± 293·60 ng/ml). CD14⁺CD16^– monocytes increased at 4 months and correlated positively with creatinine levels at 12 and 24 months (r = 0·6348, P = 0·002 and r = 0·467, P = 0·028, respectively) and negatively with Modification of Diet in Renal Disease (MDRD) at 12 months (r = 0·6056, P = 0·003). At 4 months, IL‐10 decreased significantly (P = 0·008) and correlated positively with creatinine at 2 years (r = 0·68, P = 0·010) and with CD14⁺CD16^– monocytes at 4 months (r = 0·732, P = 0·004). At 24 h, levels of human leucocyte antigen D‐related declined from 12·12 ± 5·99 to 5·21 ± 3·84 and CD86 expression decreased from 2·76 ± 1·08 to 1·87 ± 0·95. Both markers recovered progressively until 12 months, when they decreased again. These results indicate that monitoring monocytes could be a promising new prognostic tool of graft dysfunction in renal transplant patients.     

Causality of parenchymal and vascular changes in rats with experimental thiamine deficiency encephalopathy

The causality of vascular and parenchymal damage to the central nervous system (CNS) was examined In rats with thiamine deficiency. Male Sprague Dawley rats were divided Into two groups; one was given a thiamlne-deficient diet ODD) and Injected Intraperitoneally with 10μg/100g bodyweight pyrithlamine (PT) In order to analyze morpho-metrically the topographical and sequential relationship between vascular and parenchymal changes and vase dilatation, and the other was given a TDD and 50 μg/100 g bodyweight PT in order to determine hemorrhagic sites using serial dons. Histological examination showed that sponglotic change occurred selectively in the Interior colllculus (100%) from day 19, and thereafter In the thalamus (95%), mammlllary body (50%) and nuclei olivaris and vestlbularls of the pons (25%), with or without hemorrhage. Simultaneously, glycogen accumulation was also observed In these regions at a frequency similar to that of hemorrhage. Ultrastructurally, however, hydroplc swelling of astrocytic and neuronal processes without glycogen accumulation was observed as early as day 9 In the inferior cofliculus, at which time an Increase of glial fibrillary acldic protein-positive processes was also recognized. The Superior colllculus was completely spared. From day 22 vasodilatation of the Inferior colliculus occurred, concomltantly with bodyweight loss and neurological symptoms. Twenty-two examined hemorrhages, which occurred in the thalamus and Inferior colliculus, were distributed along the arterioles or capillarles on the arterial side. In conclusion, the morphological CNS changes caused by thiamine deficiency with administration of low-dose PT in rats begin as hydropic swelling of neuronal and astrocytic processes, followed by hemorrhage and, thereafter, by vasodllatatlon. The predilectlon for hemorrhage on the arterial side without parenchymal changes suggests that petechial hemorrhage Is not simply secondary to parenchymal changes, but Is due to hemadynamlc change resulting from thlamfne deficiency-Induced vascular dysfunction.     

A distinct mitochondrial myopathy,lactic acidosis and sideroblastic anemia (MLASA) phenotype associates with YARS2 mutations

Nuclear‐encoded disorders of mitochondrial translation are clinically and genetically heterogeneous. Genetic causes include defects of mitochondrial aminoacyl‐tRNA synthetases, and factors required for initiation, elongation and termination of protein synthesis as well as ribosome recycling. We report on a new case of myopathy, lactic acidosis and sideroblastic anemia (MLASA) syndrome caused by defective mitochondrial tyrosyl aminoacylation. The patient presented at 1 year with anemia initially attributed to iron deficiency. Bone marrow aspirate at 5 years revealed ringed sideroblasts but transfusion dependency did not occur until 11 years. Other clinical features included lactic acidosis, poor weight gain, hypertrophic cardiomyopathy and severe myopathy leading to respiratory failure necessitating ventilatory support. Long‐range PCR excluded mitochondrial DNA rearrangements. Clinical diagnosis of MLASA prompted direct sequence analysis of the YARS2 gene encoding the mitochondrial tyrosyl‐tRNA synthetase, which revealed homozygosity for a known pathogenic mutation, c.156C>G;p.F52L. Comparison with four previously reported cases demonstrated remarkable clinical homogeneity. First line investigation of MLASA should include direct sequence analysis of YARS2 and PUS1 (encoding a tRNA modification factor) rather than muscle biopsy. Early genetic diagnosis is essential for counseling and to facilitate appropriate supportive therapy. Reasons for segregation of specific clinical phenotypes with particular mitochondrial aminoacyl tRNA‐synthetase defects remain unknown. © 2013 Wiley Periodicals, Inc.     

Natural killer-cell activity in cyclosporine-treated renal allograft recipients

We prospectively studied natural killer (NK)-cell activity in 16 cyclosporine-treated renal transplant recipients. NK function remained intact in the group as a whole in the initial 6 months following transplantation. The percentage of CD16-positive cells within the peripheral blood mononuclear-cell population was highly correlated with NK activity both prior to and following transplantation in the absence of rejection. During rejection, the correlation was poor. A marked increase in NK activity occurred during 9 of 12 rejection episodes; similar increases in NK activity were rarely observed in the absence of rejection. Significant infiltrates of NK cells, as determined by expression of CD16, were not demonstrated in stained biopsy specimens obtained from rejecting allografts. Pretransplant NK activity did not predict clinical outcome of the allograft. Our results indicate that NK cells are activated during allograft rejection in cyclosporinetreated patients, but their exact role in the rejection process is unknown.     

慢性肾功能衰竭患者血液透析发生院内感染的临床分析

目的分析慢性肾功能衰竭患者血液透析发生院内感染的临床特点以及相关危险因素。方法回顾性分析2005年5月至2010年5月期间在我院长期行血液透析的383例患者的相关临床资料,将其中160例患者出现了不同程度的院内感染设为感染组,223例患者未出现院内感染为未感染组。结果血液透析患者发生院内感染的发生率为41.78%,其中以肺部感染最为常见;感染组与未感染组患者之间的相关临床指标相比较,年龄、住院天数、是否左心衰、是否有糖尿病、是否存在低蛋白血症、插管时间以及C反应蛋白具有统计学差异（P〈0.05或0.01）,而性别、血肌酐、甘油三脂不具有统计学差异（P〉0.05）。结论对于长期血液透析患者,我们应该控制好各个危险因素,规范化管理防治院内感染的相关制度,对患者采取正规的营养支持、纠正贫血、抗感染等支持治疗,及时的作相关病原学检查,严防滥用抗生素。     

间α胰蛋白酶抑制剂水平反映肾移植慢性排斥反应

背景：目前,肾移植病理学检查仍为移植肾慢性排斥反应的“金标准”,但肾移植程序性活检在中国尚难以普及,且存在一定的风险;由于诸多原因,使患者慢性排斥反应早期因未及时发现而错失治疗时机。 目的：观察肾移植慢性排斥反应大鼠血浆中间α胰蛋白酶抑制剂的水平。 方法：实验以正常雄性Wistar大鼠为供体,正常雄性SD大鼠为受体进行肾移植。移植后分为慢性排斥反应组和正常肾移植组。慢性排斥反应组受体于移植前3 d起,每日给予腹腔注射环孢素A微乳化剂2 mg/kg,正常肾移植组则每日给予环孢素A微乳化剂腹腔注射5 mg/kg。 结果与结论：移植后4,6,8,10,12周,Western blot检测结果显示,与移植前1周相比,正常肾移植组和慢性排斥反应组间α胰蛋白酶抑制剂蛋白表达量明显降低(P < 0.01)。移植后第4,6周,慢性排斥反应组间α胰蛋白酶抑制剂蛋白表达高于正常肾移植组(P < 0.01),而在8,10,12周低于正常肾移植组(P < 0.01)。慢性排斥反应组血浆间α胰蛋白酶抑制剂呈时间依赖性下降(P < 0.01)。结果证实,大鼠肾移植后出现慢性排斥反应时,血浆α胰蛋白酶抑制剂水平显著下调。间α胰蛋白酶抑制剂水平变化与肾移植慢性排斥反应关系密切,可为肾移植后慢性排异反应的预测提供参考依据。     

Variable sources of Bk virus in renal allograft recipients

BK virus is the causative agent of polyomavirus-associated nephropathy, a major cause of kidney transplant failure affecting 1%-10% of recipients. Previous studies that investigated the viral source on the kidney recipient pointed that the donor is implicated in the origin of human polyomavirus BK (BKPyV) infection in recipients, but giving the low genetic variability of BKPyV this subject is still controversial. The aim of this study was to determine if BKPyV replicating in kidney recipients after transplantation is always originated from the donor. Urine and blood samples from 68 pairs of living donors and kidney recipients who underwent renal transplantation from August 2010-September 2011 were screened for BKPyV by real time polymerase chain reaction. Only three recipients presented viremia. When both donors and recipients were BKPyV positive, a larger fragment of VP1 region was obtained and sequenced to determine the level of similarity between them. A phylogenetic tree was built for the 12 pairs of sequences obtained from urine and high level of similarity among all sequences was observed, indicating that homology inferences for donor and recipient viruses must be cautiously interpreted. However, a close inspection on the donor-recipient pairs sequences revealed that 3 of 12 pairs presented considerably different viruses and 4 of 12 presented mixed infection, indicating that the source of BKPyV infection is not exclusively derived from the donor. We report that about 60% of the renal recipients shed BKPyV genetically distinct from the donor, confronting the accepted concept that the donor is the main source of recipients’ infection.     

TNF-alpha and TGF-beta1 gene polymorphisms and renal allograft rejection in Koreans

This study was performed in order to evaluate the association of tumour necrosis factor-alpha (TNF-alpha) and transforming growth factor-beta1 (TGF-beta1) gene polymorphisms with renal allograft rejection in Koreans. Five TNF-alpha (-1031T/C, -863C/A, -857C/T, -308G/A and -238G/A) and two TGF-beta1 (codon 10 T/C and codon 25 G/C) single-nucleotide polymorphism (SNP) sites were studied by using polymerase chain reaction (PCR) single-strand conformation polymorphism and PCR restriction fragment length polymorphism methods in 100 controls and 164 patients. The patients underwent renal transplantation, having one or more Human leukocyte antigen (HLA)-A, HLA-B and HLA-DR antigens mismatched with their donors. For the TGF-beta1 gene, we also studied the polymorphism of donors. The allele frequencies of each SNP site in controls were not different from those of patients. The frequency of TNF-alpha high-producer genotype, -308GA, and TGF-beta1 lower (intermediate)-producer genotype, codon 10 CC and codon 25 GG, were significantly higher in patients with recurrent acute rejection episodes (REs), compared to those in patients with no or one RE. The highest risk group for developing recurrent REs showed the combination of TNF-alpha high- and TGF-beta1 lower-producer genotypes. Analysis of chronic renal allograft dysfunction (CRAD) revealed that TGF-beta1 high-producer genotype of donors, codon 10 TT/TC and codon 25 GG, is associated with CRAD especially in patients with recurrent REs. The highest risk group for developing CRAD showed the combination of recipient's TNF-alpha high- and donor's TGF-beta1 high-producer genotypes. These results would be useful for predicting high-risk group for acute rejection or CRAD in renal transplantation.     

Biallelic variants in WARS2 encoding mitochondrial tryptophanyl‐tRNA synthase in six individuals with mitochondrial encephalopathy

Mitochondrial protein synthesis involves an intricate interplay between mitochondrial DNA encoded RNAs and nuclear DNA encoded proteins, such as ribosomal proteins and aminoacyl‐tRNA synthases. Eukaryotic cells contain 17 mitochondria‐specific aminoacyl‐tRNA synthases. WARS2 encodes mitochondrial tryptophanyl‐tRNA synthase (mtTrpRS), a homodimeric class Ic enzyme (mitochondrial tryptophan‐tRNA ligase; EC 6.1.1.2). Here, we report six individuals from five families presenting with either severe neonatal onset lactic acidosis, encephalomyopathy and early death or a later onset, more attenuated course of disease with predominating intellectual disability. Respiratory chain enzymes were usually normal in muscle and fibroblasts, while a severe combined respiratory chain deficiency was found in the liver of a severely affected individual. Exome sequencing revealed rare biallelic variants in WARS2 in all affected individuals. An increase of uncharged mitochondrial tRNA^Trp and a decrease of mtTrpRS protein content were found in fibroblasts of affected individuals. We hereby define the clinical, neuroradiological, and metabolic phenotype of WARS2 defects. This confidently implicates that mutations in WARS2 cause mitochondrial disease with a broad spectrum of clinical presentation.     

Anion exchanger 1 mutations associated with distal renal tubular acidosis in the Thai population

We have previously demonstrated that compound heterozygous (SAO/G701D) and homozygous (G701D/G701D) mutations of the anion exchanger 1 (AE1) gene, encoding erythroid and kidney AE1 proteins, cause autosomal recessive distal renal tubular acidosis (AR dRTA) in Thai patients. It is thus of interest to examine the prevalence of these mutations in the Thai population. The SAO and G701D mutations were examined in 844 individuals from north, northeast, central, and south Thailand. Other reported mutations including R602H, V850, and A858D were also examined in some groups of subjects. The SAO mutation was common in the southern Thai population; its heterozygote frequency was 7/206 and estimated allele frequency 1.70%. However, this mutation was not observed in populations of three other regions of Thailand. In contrast, the G701D mutation was not found in the southern population but was observed in the northern, northeastern, and central populations, with heterozygote frequencies of 1/216, 3/205, and 1/217, and estimated allele frequencies of 0.23%, 0.73%, and 0.23%, respectively. The higher allele frequency of the G701D mutation in the northeastern Thai population corresponds to our previous finding that all Thai patients with AR dRTA attributable to homozygous G701D mutation originate from this population. This suggests that the G701D allele that is observed in this region might arise in northeastern Thailand. The presence of patients with compound heterozygous SAO/G701D in southern Thailand and Malaysia and their apparently absence in northeastern Thailand indicate that the G701D allele may have migrated to the southern peninsular region where SAO is common, resulting in pathogenic allelic interaction.     

Homozygous and compound heterozygous mutations in the ATP6V1B1 gene in patients with renal tubular acidosis and sensorineural hearing loss

Mohebbi N, Vargas‐Poussou R, Hegemann SCA, Schuknecht B, Kistler AD, Wüthrich RP, Wagner CA. Homozygous and compound heterozygous mutations in the ATP6V1B1 gene in patients with renal tubular acidosis and sensorineural hearing loss. Distal renal tubular acidosis (dRTA) is characterized by the inability to excrete acid in the renal collecting ducts resulting in inappropriately alkaline urine and hyperchloremic (normal anion gap) metabolic acidosis in the context of a normal (or near‐normal) glomerular filtration rate. Inborn dRTA can be due to autosomal dominant or recessive gene defects. Clinical symptoms vary from mild acidosis, incidental detection of kidney stones or renal tract calcification to severe findings such as failure to thrive, severe metabolic acidosis, and nephrocalcinosis. The majority of patients with recessive dRTA present with sensorineural hearing loss (SNHL). Few cases with abnormal widening of the vestibular aqueduct have been described with dRTA. Mutations in three different genes have been identified, namely SLC4A1, ATP6V1B1, and ATP6V0A4. Patients with mutations in the ATP6V1B1 proton pump subunit develop dRTA and in most of the cases sensorineural hearing loss early in childhood. We present two patients from two different and non‐consanguineous families with dRTA and SNHL. Direct sequencing of the ATP6V1B1 gene revealed that one patient harbors two homozygous mutations and the other one is a compound heterozygous. To our knowledge, this is the first case in the literature describing homozygosity in the same dRTA gene on both alleles.     

The primary hereditary form of distal renal tubular acidosis: clinical and genetic studies in 60-member kindred

A distal (type 1) renal tubular acidosis (RTA-1) has been studied in 60 of 69 living members of a large family "HK" and two unrelated small families. The "HK" family, including 28 RTA-1 subjects, presents the first large family with only primary RTA-1 reported to date. The genetic situation in this family confirms the autosomal dominant transmission of the hereditary primary RTA-1 suggested previously on the basis of a few small families. Our data show that, in contrast to the secondary hereditary form, RTA-1 in its primary hereditary form is always complete and often tolerated (asymptomatic). It occurs in non-hypercalciuric families with no clinical variants observed in family members without RTA-1. In our series some clinical abnormalities commonly associated with RTA-1, such as nephrocalcinosis and growth retardation, appeared only in three cases among offspring when both parents were affected. The appearance of such abnormalities, taken as consequences of chronic acidosis in RTA-1, could be favored by the genetic background and/or the homozygosity for the RTA-1 gene. Linkage studies between RTA-1 and 10 genetic markers have been carried out. Results show that only ABO, MNS, GM and RH loci are informative for linkage analysis and none of these loci can be suggested as linked to RTA-1 locus.     

Functional vulnerability of developing central nervous system to maternal thiamine deficiencies in the rat

Thiamine deficiency (B1 vitamin) was induced during three periods of rat central nervous system (CNS) ontogenesis. Females were fed a thiamine deficient diet such that developing offspring were exposed either to pre-, peri-, or postnatal thiamine deficiency. To control the effects of undernourishment generated by different thiamine deficiencies, every treatment group had its own pair-fed control pup from a non drug-treated but undernourished dam. Seven different developmental abilities (exploratory activity, emotional reaction, hind paws lifting reflex, wire grasping times, crawling and leap execution latencies, and nociception) were recorded in the offspring from the 10th to the 45th postnatal day. The vulnerability of developing brain to the specific lack of B1 vitamin increases from prenatal (28%) to perinatal (43%) and postnatal periods (57%).     

Fate of full‐house immunofluorescence staining in renal allograft: A case report

Here, we report the case of a patient with renal allograft with full‐house immunofluorescence staining in the zero‐hour biopsy. Full‐house immunofluorescence staining is a well‐known characteristic of lupus nephritis. Previous studies have reported patients with full‐house immunofluorescence staining, but without other symptoms or serological findings; this condition is referred to as full‐house nephropathy. We identified only one case out of 2203 zero‐hour biopsies over 13 years. Zero‐hour biopsy presented no glomerular changes but showed full‐house immunofluorescence staining. Electron microscopy revealed a nonorganized electron‐dense deposit mainly in the mesangial lesion. Systemic lupus erythematosus (SLE)‐associated antibodies were negative, and complement deficiency was not observed in the donor patients. Deposition of immunoglobulin and complement levels markedly decreased within 1–3 years post transplantation. Neither donor nor recipient developed clinical or biological features of SLE; they showed good renal prognosis.