Influence of continuity of care on self-management ability and quality of life in outpatient maintenance hemodialysis patients.

INTRODUCTION: The objective of this study was to evaluate the effect of continuity of care on self-management ability and quality of life (QOL) in patients undergoing maintenance hemodialysis (MHD). METHODS: One hundred patients were randomly assigned to the observation group and the control group. In the observation group, patients received a 12-month continuity of care. In the control group, patients were given with routine nursing. Evaluate the patients' self-management ability and QOL between two groups 1 week before discharge and 6 and 12 months outpatient MHD. RESULTS: Observation group had higher Hemodialysis Self-Management Instrument (HD-SMI) scores and Kidney Disease Quality of Life-Short Form (KDQOL-SF™) scores than control group at 6 and 12 months outpatient MHD. But patients in observation group had a much lower systolic blood pressure than those in control group at 12 months outpatient MHD. CONCLUSIONS: Our study suggested that continuity of care in the form of online education, telephone visit, and outpatient visit could improve self-management ability and QOL of patients undergoing MHD.

sPLA2-IB and PLA2R mediate insufficient autophagy and contribute to podocyte injury in idiopathic membranous nephropathy by activation of the p38MAPK/mTOR/ULK1ser757 signaling pathway.

Secretory phospholipase A2 group IB (sPLA2-IB) and M-type phospholipase A2 receptor (PLA2R) are closely associated with proteinuria in idiopathic membranous nephropathy (IMN). Podocytes constitute an important component of glomerular filtration, and high basal autophagy is indispensable for podocyte function. The current study aimed to analyze the relationship between sPLA2-IB and podocyte autophagy in IMN and determine whether sPLA2-IB mediates abnormal autophagy regulation in podocytes. The serum sPLA2-IB level and podocyte autophagy were detected, and clinical data were collected from IMN patients with different proteinuria levels. Then, the effects of sPLA2-IB on autophagy signaling pathways were evaluated in cultured human podocytes treated with sPLA2-IB, rapamycin, p38 inhibition, and PLA2R-siRNA in vitro. We found that IMN patients with nephrotic-range proteinuria have a significantly higher level of sPLA2-IB and fewer autophagosomes than those with non-nephrotic-range proteinuria. In vitro sPLA2-IB-induced insufficient autophagy in podocytes and promoted podocyte injury via activation of the mTOR/ULK1ser757 signaling pathway. Moreover, inhibition of p38 MAPK evidently abrogated sPLA2-IB-induced autophagy and the activation of mTOR/ULK1ser757 . Additionally, PLA2R silencing demonstrated that sPLA2-IB-induced abnormal autophagy was also PLA2R-dependent. In conclusion, the results revealed that sPLA2-IB downregulated autophagy and contributed to podocyte injury via PLA2R though activation of the p38MAPK/mTOR/ULK1ser757 signaling pathway.

Effects of Probiotics on Malnutrition and Health-Related Quality of Life in Patients Undergoing Peritoneal Dialysis: A Randomized Controlled Trial.

OBJECTIVE: Alterations in the gut microbiota and host responses have been implicated in the progression of end-stage renal disease, increased cardiovascular risk, uremic toxicity, and inflammation. The purpose of this study was to evaluate the clinical efficacy of probiotics on malnutrition and health-related quality of life in patients undergoing peritoneal dialysis (PD). DESIGN AND METHODS: A total of 116 patients undergoing PD were randomly divided into an intervention group (n = 58) and a control group (n = 58). The intervention group received a daily dose of probiotics (1 × 109 CFU/day, i.e., 2 capsules, tid) for 2 months, while the control group did not receive probiotics during the same period. Biochemical indicators, physical measurements, and scores on the SF-36 were measured before and 2 months after the intervention. RESULTS: A total of 98 patients completed the study (50 in the intervention group and 48 in the control group). Among patients receiving probiotics, the levels of high-sensitivity C-reactive protein and interleukin-6 decreased after 2 months of treatment, while the serum albumin levels, upper arm circumference, and triceps skinfold thickness increased significantly. The probiotic group had higher scores on the physical functioning and social functioning domains than the control group after 2 months. CONCLUSIONS: Probiotics could significantly decrease the serum levels of high-sensitivity C-reactive protein and interleukin-6 and increase the serum albumin levels, upper arm circumference, and triceps skinfold thickness in patients undergoing PD. As a result, malnutrition and health-related quality of life partially improved after probiotic supplementation in patients undergoing PD.

Circular RNA expression profiles and features in NAFLD mice: a study using RNA-seq data.

BACKGROUND: Nonalcoholic fatty liver disease (NAFLD) is primarily characterized by the hepatic cholesterol accumulation. Circular RNA (circRNA), one of noncoding RNA, involves in many liver diseases progression. However, no recent studies on circRNA expression profiles in NAFLD have been reported previously. METHODS: A NAFLD mouse model was constructed by providing high-fat diet (HFD) for 32 weeks. The circRNAs expression profile in normal mice and NAFLD mice were determined using high-output RNA sequencing method and bioinformatics methods, while the differentially expressed circRNAs were confirmed using Sanger sequencing and qRT-PCR. The circRNA-miRNA network was also predicted. The biological functions of circRNAs were annotated by Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG). RESULTS: The results demonstrated the successful construction of NAFLD mice model by immunohistology and serology assay. In total, 93 dysregulated circRNAs were observed, including 57 upregulated circRNAs and 36 downregulated circRNAs, in the NAFLD group. The circRNA-miRNA network revealed the complex interaction between circRNAs and its potential miRNA targets in NAFLD. The characteristic of tissue-specific expression in circRNA was demonstrated. The differentially expressed circRNAs with important biological function were also annotated using GO and KEGG. Both DDAH1 and VAV3 genes were found to be associated with the NAFLD development. CONCLUSIONS: Taken together, this study demonstrated the circRNAs expression profile and features in NAFLD, which may provide potential biological markers for the pathogenesis of NAFLD.

Emodin ameliorates renal injury in BXSB mice by modulating TNF-α/ICAM-1.

The purpose of the present study was to explore the effects of emodin on renal injury in a BXSB mouse model of lupus and its mechanisms. BXSB mice were fed different concentrations of emodin (0, 5, 10 and 20 mg/kg.d), and the levels of intercellular adhesion molecule-1 (ICAM-1), tumor necrosis factor-α (TNF-α) and fibronectin (FN) levels in the glomeruli and serum levels of the anti-dsDNA antibody were determined. Mesangial cells (MCs) were cultured in vitro, and IgG-type anti-dsDNA antibody and/or emodin were added to the MC culture supernatant. In addition, TNF-α small interfering RNA (siRNA) was transfected into MCs to explore the mechanism of action of emodin. The results showed that the mice fed emodin presented decreases in the urinary protein content and glomerular TNF-α, ICAM-1 and FN levels (P<0.05). Moreover, the urine protein, TNF-α, ICAM-1 and FN levels were decreased in a dose-dependent manner (P<0.05). In vitro, the anti-dsDNA antibody group exhibited increased levels of ICAM-1 and TNF-α (P<0.05), and the anti-dsDNA antibody group showed myofibroblast-like structural changes. The aforementioned indexes were decreased in the emodin group (P<0.05), and the extent of transdifferentiation was significantly reduced. Moreover, the level of ICAM-1 decreased with the down-regulation of TNF-α (P<0.05). Emodin reduced the urine protein levels and serum levels of the anti-dsDNA antibody in a mouse model of lupus nephritis (LN). The underlying mechanism may be related to decreased levels of TNF-α, ICAM-1 and FN and the inhibition of dsDNA antibody-induced MC damage.

sPLA2-IB Level Correlates with Hyperlipidemia and the Prognosis of Idiopathic Membranous Nephropathy.

Recent studies suggested that serum secretory phospholipase A2 group IB (sPLA2-IB) was increased in idiopathic membranous nephropathy (IMN). However, the interference of high lipemia on the sPLA2-IB levels was not taken into account in these studies. The present study aimed to investigate the correlation between sPLA2-IB and lipemia, and the clinical merit of sPLA2-IB in the prediction of prognosis of IMN patients. A total of 64 IMN patients, 39 immunoglobulin A nephropathy (IgAN) patients and 64 healthy controls were included in the study. The levels of serum sPLA2-IB, lipemia and proteinuria were measured. Fifty IMN patients were followed up for 6 months. Pathologic stages were made for all IgAN and IMN patients. The results showed that the levels of serum sPLA2-IB, cholesterol and low-density lipoprotein cholesterol (LDL-C) were significantly higher, and the levels of albumin and high-density lipoprotein cholesterol (HDL-C) were significantly lower in IMN patients than in healthy controls and IgAN patients. Serum sPLA2-IB levels were also found to be higher in IgAN patients than in heathy controls, but the association of serum sPLA2-IB levels with proteinuria, cholesterol and albumin was only shown in IMN patients. Antibody against M-type receptor for secretory phospholipase A2 (PLA2R1) was positive in 81.3% IMN patients. Glomerular sPLA2-IB deposition, podocyte fused processes, and density deposition on thickened basement membrane were seen in IMN patients, but not in IgAN patients. IMN patients with lower sPLA2-IB and proteinuria levels were found to have better outcome after the 6-month follow-up. In IMN patients, sPLA2-IB levels were significantly increased in both serum and renal tissue. In conclusion, serum sPLA2-IB was closely correlated with proteinuria, albumin and cholesterol, and IMN patients with lower sPLA2-IB levels were more likely to achieve a better outcome.

Excessive arachidonic acid induced actin bunching remodeling and podocyte injury via a PKA-c-Abl dependent pathway.

Recent studies have shown that serum secretory phospholipase A2 group IB (sPLA2-IB) is associated with proteinuric kidney diseases and plays a pivotal role in podocyte injury via its natural receptor. Arachidonic acid (AA), as a major metabolite of sPLA2-IB, regulates the actin bungling remodeling and contributes to the podocyte injury. However, the underlying mechanism of AA in the regulation of podocyte actin remodeling and human podocyte injury is unclear. Here, we reported that AA induced F-actin cytoskeletal ring formation and promoted protein kinase A (PKA), nephrin and c-Abl phosphorylation. Moreover, AA promoted c-Abl translocation from the nucleus to the cytoplasm and increased the recruitment of c-Abl to p-nephrin by the interaction between them. H89 (PKA inhibitor) provided protection against AA-induced F-actin bunching remodeling, down-regulated nephrin phosphorylation, and suppressed the c-Abl translocation and activation. STI571 (c-Abl inhibitor) also improved the AA associated F-actin bunching remodeling. In addition, H89 and STI571 both alleviated apoptosis and adhesion damage of podocyte. These results indicate that an excess of AA treatment is detrimental to the podocyte actin cytoskeleton and promotes podocyte injury due to the activation of PKA-c-Abl signaling.

Novel conservative treatment for peritoneal dialysis-related hydrothorax: Two case reports.

BACKGROUND: Peritoneal dialysis (PD) is an important renal replacement therapy for patients with end-stage renal disease. PD-related hydrothorax is a rare but serious complication in PD patients, produced by the movement of peritoneal dialysate through pleuroperitoneal fistulas. In previous reports, patients with hydrothorax secondary to PD were usually recommended to discontinue PD and transfer to hemodialysis (HD). Herein, we describe another method of managing this complication-with an adjusted PD prescription and continuous drainage of pleural effusion, patients could continue PD without recurrence of hydrothorax. CASE SUMMARY: In this report, we present the medical records of 2 patients with hydrothorax secondary to PD. We recommended intermittent PD with continuous drainage of pleural effusion. A type 18Ga soft catheter was placed to drain pleural effusion. Ultrasound-guided thoracentesis was performed, and the soft catheter was placed in the pleural cavity for a long period (3 mo and 2 mo, respectively). The pleural catheter was removed when no fluid was drained from the pleural cavity. After several months, pleuroperitoneal fistulas were closed in both patients and PD was continued. These patients did not transfer to HD, had no recurrence of hydrothorax and were still treated with PD after 1 year. CONCLUSION: These 2 case reports show that continuous drainage of pleural effusion with an 18Ga soft catheter is a useful method for hydrothorax secondary to PD.

Serum anti-phospholipase A2 receptor (PLA2R) antibody detected at diagnosis as a predictor for clinical remission in patients with primary membranous nephropathy: a meta-analysis.

BACKGROUND: The diagnostic value of serum M-type phospholipase A2 receptor antibody (sPLA2R-ab) expression in patients with primary membranous nephropathy (PMN) has been established. However, the association between sPLA2R-ab and clinical remission remains uncertain. METHODS: We systematically searched the literature for clinical trials regarding the correlation between sPLA2R-ab expression and clinical remission of PMN patients. Meta-analysis was performed to determine this association. Subgroup analysis, funnel plots, and sensitivity analysis were also performed to investigate heterogeneity or bias. RESULTS: A total of 11 trials involving 824 patients were included. Patients with positive sPLA2R-ab had a poor clinical remission rate (RR = 0.76, 95%CI 0.68-0.86, P < 0.0001; I2 = 39%), a higher titer of sPLA2R-ab had a lower chance of clinical remission (RR = 0.72, 95%CI 0.59-0.87, P = 0.0006; I2 = 42%),and a higher risk of renal failure (RR = 4.85, 95% CI, 1.83-12.85, P = 0.002; I2 = 0%), without affecting relapse (RR = 0.97, 95% CI, 0.55-1.70; P = 0.92, I2 = 0%). Subgroup analysis by treatment strategies, assay methods, ethnicity, gender, renal function, the approach of ruling out SMN, and the ratio of patients with nephrotic-range proteinuria at baseline showed no significant association between these factors with the prognostic value of sPLA2R-ab for PMN patients. No significant publication bias was found. CONCLUSION: This meta-analysis adds to the evidence for current guidelines that sPLA2R-ab acts as not only a diagnostic marker but also a pivotal predictor for clinical remission. Therefore, sPLA2R-ab can be considered as a prognostic factor for stratifying PMN patients.

Ggnbp2 Is Essential for Pregnancy Success via Regulation of Mouse Trophoblast Stem Cell Proliferation and Differentiation.

The Ggnbp2 null mutant embryos died in utero between Embryonic Days 13.5 to 15.5 with dysmorphic placentae, characterized by excessive nonvascular cell nests consisting of proliferative trophoblastic tissue and abundant trophoblast stem cells (TSCs) in the labyrinth. Lethality of Ggnbp2 null embryos was caused by insufficient placental perfusion as a result of remarkable decreases in both fetal and maternal blood vessels in the labyrinth. These defects were accompanied by a significant elevation of c-Met expression and phosphorylation and its downstream effector Stat3 activation. Knockdown of Ggnbp2 in wild-type TSCs in vitro provoked the proliferation but delayed the differentiation with an upregulation of c-Met expression and an enhanced phosphorylation of c-Met and Stat3. In contrast, overexpression of Ggnbp2 in wild-type TSCs exhibited completely opposite effects compared to knockdown TSCs. These results suggest that loss of GGNBP2 in the placenta aberrantly overactivates c-Met-Stat3 signaling, alters TSC proliferation and differentiation, and ultimately compromises the structure of placental vascular labyrinth. Our studies for the first time demonstrate that GGNBP2 is an essential factor for pregnancy success acting through the maintenance of a balance of TSC proliferation and differentiation during placental development.

HMGB1 Turns Renal Tubular Epithelial Cells into Inflammatory Promoters by Interacting with TLR4 During Sepsis.

Our study was undertaken to investigate whether the inflammatory mediator high-mobility group box 1 (HMGB1) can enter the renal tissue and urine and what is the functional change of renal tubular epithelial cells (TECs) interacting with HMGB1 during sepsis. We found that the transcription levels of interleukin 1 (IL-1) and interleukin 6 (IL-6) mRNA in TECs increased significantly during sepsis and these processes can be blocked by splenectomy. We also found out HMGB1 accumulated in the renal tissue and entered urine during sepsis and toll-like receptor 4 (TLR4) was expressed by TECs. In vitro, we demonstrated that HMGB1 induced MAPK and NF-κB activation and G1 cell cycle arrest in TECs. We also found that the mRNA transcription levels of IL-1, IL-6, and tissue inhibitor of metalloproteinases 2 (TIMP2) increased significantly and the IL-1, IL-6, and TIMP2 can be secreted by TECs stimulated by HMGB1. In contrast, LPS RS can block all of the processes above in vitro. In vivo, the increase of the mRNA transcription level of TIMP2 was also observed. These data indicate that HMGB1 accumulates in renal tissue and enters the urine and the interaction between HMGB1 and TLR4 turns TECs into inflammatory promoters during sepsis.

IQGAP1 regulates actin cytoskeleton organization in podocytes through interaction with nephrin.

Increasing data has shown that the cytoskeletal reorganization of podocytes is involved in the onset of proteinuria and the progression of glomerular disease. Nephrin behaves as a signal sensor of the slit diaphragm to transmit cytoskeletal signals to maintain the unique structure of podocytes. However, the nephrin signaling cascade deserves further study. IQGAP1 is a scaffolding protein with the ability to regulate cytoskeletal organization. It is hypothesized that IQGAP1 contributes to actin reorganization in podocytes through interaction with nephrin. IQGAP1 expression and IQGAP1-nephrin colocalization in glomeruli were progressively decreased and then gradually recovered in line with the development of foot process fusion and proteinuria in puromycin aminonucleoside-injected rats. In cultured human podocytes, puromycin aminonucleoside-induced disruption of F-actin and disorders of migration and spreading were aggravated by IQGAP1 siRNA, and these effects were partially restored by a wild-type IQGAP1 plasmid. Furthermore, the cytoskeletal disorganization stimulated by cytochalasin D in COS7 cells was recovered by cotransfection with wild-type IQGAP1 and nephrin plasmids but was not recovered either by single transfection of the wild-type IQGAP1 plasmid or by cotransfection of mutant IQGAP1 [△1443(S→A)] and wild-type nephrin plasmids. Co-immunoprecipitation analysis using lysates of COS7 cells overexpressing nephrin and each derivative-domain molecule of IQGAP1 demonstrated that the poly-proline binding domain and RasGAP domain in the carboxyl terminus of IQGAP1 are the target modules that interact with nephrin. Collectively, these findings showed that activated IQGAP1, as an intracellular partner of nephrin, is involved in actin cytoskeleton organization and functional regulation of podocytes.

sPLA2 IB induces human podocyte apoptosis via the M-type phospholipase A2 receptor.

The M-type phospholipase A2 receptor (PLA2R) is expressed in podocytes in human glomeruli. Group IB secretory phospholipase A2 (sPLA2 IB), which is one of the ligands of the PLA2R, is more highly expressed in chronic renal failure patients than in controls. However, the roles of the PLA2R and sPLA2 IB in the pathogenesis of glomerular diseases are unknown. In the present study, we found that more podocyte apoptosis occurs in the kidneys of patients with higher PLA2R and serum sPLA2 IB levels. In vitro, we demonstrated that human podocyte cells expressed the PLA2R in the cell membrane. After binding with the PLA2R, sPLA2 IB induced podocyte apoptosis in a time- and concentration-dependent manner. sPLA2 IB-induced podocyte PLA2R upregulation was not only associated with increased ERK1/2 and cPLA2α phosphorylation but also displayed enhanced apoptosis. In contrast, PLA2R-silenced human podocytes displayed attenuated apoptosis. sPLA2 IB enhanced podocyte arachidonic acid (AA) content in a dose-dependent manner. These data indicate that sPLA2 IB has the potential to induce human podocyte apoptosis via binding to the PLA2R. The sPLA2 IB-PLA2R interaction stimulated podocyte apoptosis through activating ERK1/2 and cPLA2α and through increasing the podocyte AA content.

Selection of single chain variable fragments specific for the human-inducible costimulator using ribosome display.

We applied a ribosome display technique to a mouse single chain variable fragment (scFv) library to select scFvs specific for the inducible costimulator (ICOS). mRNA was isolated from the spleens of BALB/c mice immunized with ICOS protein. Heavy and κ chain genes (VH and κ) were amplified separately by reverse transcriptase polymerase chain reaction, and the anti-ICOS VH/κ chain ribosome display library was constructed with a special flexible linker by overlap extension PCR. The VH/κ chain library was transcribed and translated in vitro using a rabbit reticulocyte lysate system. Then, antibody-ribosome-mRNA complexes were produced and panned against ICOS protein under appropriate conditions. However, in order to isolate specific scFvs for ICOS, negative selection using CD28 was carried out before three rounds of positive selection on ICOS. After three rounds of panning, the selected scFv DNAs were cloned into pET43.1a and detected by SDS-PAGE. Then, enzyme-linked immunosorbent assay showed that we successfully constructed a native ribosome display library, and among seven clones, clone 5 had the highest affinity for the ICOS and low for the CD28. Anti-ICOS scFvs are assessed for binding specificity and affinity and may provide the potential for development of the humanized and acute and chronic allograft rejection.

Bone marrow-derived mesenchymal stem cells differentiation into tubular epithelial-like cells in vitro.

The possibility of differentiating bone marrow-derived mesenchymal stem cells (BMSCs) into tubular epithelial-like cells is explored in vitro. Purified BMSCs from Sprague-Dawley rats were obtained by density gradient centrifugation. Third generation BMSCs were divided into six groups and were cultured under different conditions. The expression of alkaline phosphatase and cytokeratin (CK)-18 protein was detected through staining and immunocytochemistry, respectively, and the expression of E-cadherin proteins was recorded through immunofluorescence. Some cells in ischemia/reperfusion (I/R), all-trans retinoic acid (ATRA), epidermal growth factor (EGF) and bone morphogenetic protein-7 (BMP-7) groups turned positive, whereas the positive cells in the combined group significantly increased compared with the other groups. Compared with the control group, the positive expression rates of CK-18 in the I/R, ATRA, EGF, BMP-7 and the combined group were 11·50% ± 3·84%, 27·40% ± 2·70%, 29·60% ± 4·51%, 26·80% ± 5·00% and 44·00% ± 3·16%, respectively, and CK-18 mRNA expression in the combined group was obviously higher than that in the other groups (P < 0·01). Immunofluorescence detection showed that E-cadherin expression was not detectable in the control group, whereas the positive expression rates of E-cadherin in the I/R, ATRA, EGF, BMP-7 and the combined group were 6·75% ± 2·13%, 16·40% ± 2·69%, 18·25% ± 3·50%, 16·06% ± 2·00% and 30·26% ± 5·16%, respectively. The addition of ATRA, EGF and BMP-7 induces BMSCs differentiation into tubular epithelial-like cells in stimulated acute renal failure microenvironment in vitro.

Molecular cloning, expression and functional analysis of interleukin-8 (IL-8) in South African clawed frog (Xenopus laevis).

In this study, an IL-8 homologue has been cloned and identified from South African clawed frog Xenopus laevis (designated XlIL-8). The open reading frame (ORF) of XlIL-8 consists of 312 bases encoding a protein of 103 amino acids. The chemokine CXC domain, which contained Glu-Leu-Arg (ELR) motif and four cysteine residues, was well conserved in South African clawed frog IL-8. By quantitative real-time PCR, mRNA transcript of XlIL-8 was detectable in all the examined tissues with higher level in spleen and kidney. The temporal expression of XlIL-8 mRNA in the monocytes was up-regulated by lipopolysaccharide (LPS) stimulation and reached the maximum level at about 6h post-stimulation. Recombinant soluble XlIL-8 (XlsIL-8) was fused with a small ubiquitin-related modifier gene (SUMO) to enhance the soluble expression level in Escherichia coli BL21 (DE3). The fusing protein SUMO-XlsIL-8 was purified using metal chellate affinity chromatography (Ni-NTA) and cleaved by a SUMO-specific protease, then confirmed by SDS-PAGE and Western blotting analysis. Chemotaxis assays showed that lymphocytes but not monocytes could be recruited toward SUMO-XlsIL-8 or XlsIL-8 protein in a dose-dependent manner in vitro. The present study may be useful for understanding the anti-bacteria immunity in amphibian and gives the potential to use the recombinant proteins to manipulate the immune response.

[Improvement of left ventricular hypertrophy by anemic-correcting erythropoietin therapy in chronic renal insufficiency].

OBJECTIVE: Left ventricular hypertrophy (LVH) is an independent predictor of morbidity and mortality in dialysis patients. It remains unclear whether efforts to correct anemia in patients with mild-to-moderate chronic renal insufficiency (CRI) can reverse LVH. This prospective multi-center Chinese cohort study evaluates left ventricular mass index (LVMI) evolution in anemic CRI patients with or without recombinant human erythropoietin (rHuEPO) therapy. METHODS: Six centers enrolled 158 patients with serum creatinine from 147 to 400 micromol/L, and 86 of whom with hemoglobin (Hb) levels < 110 g/L received rHuEPO (Group A). Forty patients with comparable Hb levels (< 110 g/L) but did not receive rHuEPO (Group B) and those with Hb >/= 110 g/L (Group C, n = 32) were served as controls. Echocardiographic studies were performed to evaluate LVMI at baseline and every 3 months during a two-year period. RESULTS: At baseline, the prevalence of LVH was 72.1% in Group A, 72.5% in Group B and 59.4% in Group C. LVMI was inversely correlated with Hb levels (r = -0.70, P < 0.01). There was no difference in age, gender, aetiology of renal failure, blood pressure (BP) and cardiovascular risk factors between the 3 groups. The administration of rHuEPO in Group A significantly increased Hb levels from (93.8 +/- 14.6) g/L to (111.2 +/- 10.3) g/L and decreased LVMI from (142.6 +/- 25.7) g/m(2) to (132.4 +/- 18.5) g/m(2). The prevalence of LVH decreased 16.3% after a partial correction of anemia at 24 months, whereas Hb levels in controls (Group B and Group C) tended to decrease and LVMI significantly increased compared with baseline. The prevalence of LVH was significantly increased in Group B and C after 24 months. The percentage of patients whose serum creatinine level doubled during the follow-up was 3.4% in Group A, 15.0% in Group B and 9.4% in Group C, the difference between Group A and Group B being significant (P < 0.05). In addition, good BP control was obtained without any adverse effects. CONCLUSION: High prevalence of LVH was present in pre-dialysis CRI patients, which is associated with severity of anemia. Early treatment of anemia with rHuEPO can reverse LVH in CRI patients.