Megakaryocytes are traditionally recognized as cells responsible for platelet production. However, beyond their role in thrombopoiesis, megakaryocytes also participate in inflammatory responses and regulate immune system functions. Sepsis, characterized by life-threatening organ dysfunction due to a dysregulated response to infection, prominently features coagulopathy, severe inflammation, and immune dysfunction as key pathophysiological aspects. Given the diverse functions of megakaryocytes, we explore their roles in coagulation in the context of sepsis, and also in inflammatory and immune regulation. We try to infer future research directions and potential strategies for sepsis prevention and treatment based on the properties of megakaryocytes. The purpose of this review is to both highlight and provide an update on the functions of megakaryocytes and pathophysiological changes in sepsis. Specific emphasis is given to the role of megakaryocytes in sepsis, which suggests value of future research and clinical application.

The mechanisms of traumatic injury-induced acute kidney injury (AKI) are very complicated. Among these mechanisms, sepsis-related AKI is the most harmful and the most difficult to treat. The medical community gave a high priority on this disease, dedicated to raise the level of awareness and treatment through its pathogenesis, early diagnosis ideas and biomarkers, and standardization of treatment. There has been some consensus on the classification of sepsis, AKI, and treatments of antiinfection, fluid resuscitation, renal replacement therapy. A series articles and guidelines have also been published and the survival status of patients have been improved, but many basic and clinical issues are still controversial and need to be answered by further trails. This article focuses on the progress of pathogenesis, diagnosis and treatment about sepsis-related AKI, and tries to raise the understanding level of early diagnosis and standardized treatment of it. DOI: 10.11855/j.issn.0577-7402.2019.07.05

To investigate the role of toll like receptors (TLRs) 2 and 4 in rhabdomyolysis (RM)-related acute kidney injury (AKI). Wild-type (WT) mice and TLR2 knockout (TLR2-/-) or TLR4 knockout (TLR4-/-) mice were injected with either saline (sham) or glycerin (to induce RM-related AKI). Samples were collected for detection of 0 h 24 h (Cr) creatinine, urea nitrogen (BUN), creatine kinase (CK), and PAS staining of renal tissues. Serum Cr and BUN level was significantly increased in TLR2-/- and TLR4-/-AKI groups more than those in the control group and the WT mice in AKI group. TLR4-/-AKI group Cr, BUN level, and the pathological damage was lightest. The expression levels of signal transduction proteins in TLR2-/- and TLR4-/-AKI group were higher than in the control group, but was lower than that in the wild AKI group, with the TLR4-/-AKI group having the lowest levels. The expression level of inflammatory factor mRNA in TLR2-/- and TLR4-/-AKI groups was higher than that in control group, but was lower than that in wild AKI group, with TLR4-/-AKI group displaying lowest levels. Knockout of TLRs 2 and 4 decreased kidney inflammation and improved RM-related AKI.

Interleukins (IL-35) is a novel anti-inflammatory cytokine found in the clinic. It belongs to the family of IL-12, which is considered to be of potential therapeutic value. The current study found that IL-35 may be involved in the immune response, which can regulate the internal inflammatory reaction and cell infection process. It has a significant correlation with occurrence and development of tumors, autoimmune diseases and other diseases. So it's a hot spot in the study of cellular factors for these diseases, and it may provides a new research method.

BACKGROUNDPatients with chronic kidney disease (CKD) have abnormal calcification in vascular tissue that is a risk factor for cardiovascular disease. However, the specific molecular mechanisms for vascular calcification remain largely unknown. The present study aimed to determine the differentially expressed miRs and the underlying molecular mechanisms of miR-153-3p in vascular calcification induced by adenine.METHODSDifferentially expressed miRs were screened using a microarray chip in the thoracic aorta. miRs and mRNA expression were measured by RT-qPCR. Protein expression was performed by western blotting analysis. Aortic calcification was confirmed by Von Kossa staining. The targeted genes were predicted by a bioinformatics algorithm and confirmed by a dual luciferase reporter assay.RESULTSOur results revealed that the expression of miR-153-3p was significantly down-regulated in the thoracic aorta from adenine-fed rats compared with that of the control group. Transfection of miR-153-3p into the thoracic aorta markedly suppressed adenine-induced aortic calcification and significantly decreased the mRNA expression of ALP, OC, OSX, SOST and Runx2. Further studies indicated that Runx2 was a direct target gene of miR-153-3p, which was verified by dual luciferase reporter assay.CONCLUSIONThese results suggest that increased vascular miR-153-3p expression attenuates adenine-induced aortic calcification via inhibiting osteogenic trans-differentiation in the thoracic aorta.

Interleukin-35 (IL-35) is a novel immunosuppressive and anti-inflammatory cytokine. IL-35 is mainly secreted by regulatory T cells (Tregs), and exerts its effects through inducing proliferation of Tregs and reducing activity of helper T cells Th17. However, the effect of IL-35 on sepsis-associated acute kidney injury (SA-AKI) remains unclear. This study is aimed to examine the expression and role of IL-35 in an animal model of SA-AKI induced by cecal ligation and puncture (CLP). Eleven C57 male mice with SA-AKI and eight controls were used, and blood and kidney tissues were collected. Blood creatinine (Cr), urea nitrogen (BUN), alanine transaminase (ALT) and aspartate transaminase (AST) were measured to assess kidney and liver injury. The renal morphology and cell apoptosis were examined. The mRNA and protein expression levels of IL-35 in kidney tissues were tested by qRT-PCR, IHC-P, IF, and ELISA. Biochemical and histological examinations indicated CLP induced SA-AKI in mice. TUNEL assay showed apoptosis of renal tubular epithelial cells in SA-AKI mice. The mRNA and protein expression of IL-12α and EBI3 in kidney tissues decreased significantly in SA-AKI mice compared with those in sham controls. IL-35 levels in kidney tissues displayed a significantly negative correlation with the levels of Cr (r = -0.584, P = 0.009), ALT (r = -0.549, P = 0.015), AST (r = -0.475, P = 0.04), but not with BUN (r = -0.437, P = 0.061). These results demonstrated that IL-35 is associated with the pathological process of SA-AKI, and might represent a potential therapeutic agent for SA-AKI treatment.

Xuebijing (XBJ) injection, a concoction of several Chinese herbs, has been widely used as an immunomodulator for the treatment of severe sepsis in China. However, the precise mechanisms responsible for its efficacy have not been fully elucidated. In our study, we determined the flow cytometry markers (F4/80, CD11c, and CD206), the levels of secreted cytokines (TNF-α, IL-6, and IL-10), and the expression of specific proteins of M2 (Ym1, Fizz1, and Arg1) to assess macrophage polarization. Treatment with XBJ lowered M1 associated cytokine levels and increased the level of M2 associated cytokine level. The percentage of M2 phenotype cells of XBJ group was much higher than that of the control group. Expressions of phosphorylated Janus kinase 1 (JAK1) and signal transducer and activator of transcription 6 (STAT6) were markedly enhanced after the administration of XBJ; on the other hand, the M2 associated cytokines and proteins were decreased following treatment with JAK1 or STAT6 inhibitor. In addition, the treatment of XBJ significantly improved the survival rate of septic mice. These studies demonstrate that XBJ can markedly promote M2 polarization and improve the survival rate of septic mice, thereby contributing to therapeutic effect in the treatment of septic complications.

Objective To investigate the changes in levels of serum soluble transferrin receptor ( sTfR) after switc-hing from maintenance hemodialysis to high-flux hemodialysis ( HFD) in patients with uremia, and to analyze its related factors.Methods Forty patients undergoing low-flux maintenance hemodialysis were treated by high-flux maintenance he-modialysis for 12 months.The levels of sTfR, iron metabolism indices, anemia index and inflammatory index were meas-ured before HFD treatment ( T0 ) and after HFD treatment for 2 months ( T1 ) , 6 months ( T2 ) and 12 months ( T3 ) .Pear-son correlation and multiple regression method were used to analyze the relationship between serum sTfR and other indexes. At the same time, we observed the changing trend of erythropoietin and the amount of iron therapy.Results Serum sTfR level was significantly decreased at T1 , T2 and T3 as compared with that at T0 , and significant difference was found ( all P<0.01).Pearson correlation analysis showed that sTfR was positively correlated with Ret%, SF (r=0.154, 0.152;all P<0.05) and was negatively correlated with Hb, HCT, β2-MG and TBC ( r =-0.251, -0.299, -0.384 and-0.166;P<0.01 or P<0.05).Multiple regression showed that HCT, TSAT andβ2-MG levels were closed related with serum sTfR level in HFD patients (all P<0.01).The erythropoietin and iron dosage in this group reduced with prolonged HFD treatment.Conclusions HFD can effectively improve renal anemia in patients with maintenance hemodialysis.The detection of sTfR level reflects the effects of iron reserves and erythropoietic stimulation on patients.

The present study was designed to elucidate the expression levels and the proliferative effect of flotillin-1, an integral membrane protein encoded by the FLOT1 gene, in human clear-cell renal cell carcinoma (RCC). Flotillin has been implicated in other types of cancer, but the role of flotillin in RCC has not been established. Immunohistochemistry and western blotting were used to determine FLOT1 protein expression levels in RCC samples from 182 patients who underwent nephrectomy. FLOT1 mRNA expression levels were analyzed using reverse-transcription (RT) and RT-quantitative polymerase chain reaction (PCR). The association between FLOT1 expression levels in the tumor samples and patient survival time was examined using Kaplan‑Meier analysis. To demonstrate the proliferative effect of FLOT1 on RCC cells, a FLOT1 vector was transfected into four RCC cell lines and FLOT1 expression was inhibited using small interfering RNA. The proliferative ability of the RCC cells was investigated using a WST-1 assay and xenograft experiments with BALB/C nude mice. The results demonstrated that FLOT1 expression levels were significantly higher in RCC cell samples from patients than in healthy renal tissue, and the expression levels were associated with tumor stage, size and histological grade. In addition, FLOT1 significantly enhanced the proliferation of RCC cell lines in vitro and in vivo. These findings suggest that FLOT1, which is upregulated in RCC, is involved in RCC cell proliferation, tumorigenesis and progression. Therefore, FLOT1 is an independent prognostic marker and therapeutic target for patients with clear-cell RCC.

The apoptotic or necrotic death of renal tubule epithelial cells is the main pathogenesis of renal ischemia-reperfusion-induced acute kidney injury (AKI). Pyroptosis is a programmed cell death pathway that depends on the activation of the caspase cascade and IL-1 cytokine family members. However, the role of pyroptosis in AKI induced by ischemia-reperfusion remains unclear. In this study, we found that the levels of the pyroptosis-related proteins, including caspase-1, caspase-11, and IL-1β, were significantly increased after 6 h of renal ischemia-reperfusion injury (IRI) and peaked at 12 h after IRI. Enhanced pyroptosis was accompanied by elevated renal structural and functional injury. Similarly, hypoxia-reoxygenation injury (HRI) also induced pyroptosis in renal tubule epithelial NRK-52E cells, which was characterized by increased pore formation and elevated lactate dehydrogenase release. In addition, obvious upregulation of the endoplasmic reticulum (ER) stress biomarkers glucose-regulated protein 78 and C/EBP homologous protein (CHOP) preceded the incidence of pyroptosis in cells treated with IRI or HRI. Pretreatment with a low dose of tunicamycin, an inducer of ER stress, relieved IRI-induced pyroptosis and renal tissue injury. Silencing of CHOP by small interfering RNA significantly decreased HRI-induced pyroptosis of NRK-52E cells, as evidenced by reduced caspase-11 activity and IL-1β generation. Therefore, we conclude that pyroptosis of renal tubule epithelial cells is a key event during IRI and that CHOP-caspase-11 triggered by overactivated ER stress may be an essential pathway involved in pyroptosis.

Objective To investigate the potential contributing effects of serum PF4-heparin antibody levels on cardiocerebrovascular events in maintenance hemodialysis(MHD) patients.Methods A total of 112 MHD patients were enrolled in this study.ELISA kit was used to quantify the serum PF4-heparin antibody concentration.All the patients were divided into high-level groups and low-level groups according to the average level of PF4-heparin antibody in all patients.They were followed up for 36 months for cardiocerebrovascular events and death occurrence.Results The prevalence of high-level PF4-heparin antibody was 34.8%.Multiple linear regression analysis showed that PF4-heparin antibody levels were correlated with serum ferritin(r = 0.262,P = 0.035).Cardiocerebrovascular events and mortality rate in high-level group was 50%,while it was 37.5% in low-level group.No significant difference was found in the incidence of all-cause mortality(χ2= 0.480,P = 0.488),cardiocerebrovascular events(χ2= 1.255,P = 0.358),mortality rates(χ2= 1.540,P = 0.265),survival rates(χ2=0.446,P = 0.504) between two groups.Logistic regression analysis showed that age(OR = 1.091,P = 0.000),serum FIB(OR = 10.311,P = 0.002) and serum TG(OR = 1.805,P = 0.040) were the independent risk factors of death.Conclusion Raised serum PF4-heparin antibody may not contribute to cardiocerebrovascular events in MHD patients.

目的 X盒结合蛋白1(XBP-1)是内质网应激(ERS)的关键调节分子,本研究探讨XBP-1活化在高迁移率族蛋白BI(HMGB1)诱导树突状细胞(DC)成熟分化中的作用.方法 分离正常BALB/c小鼠脾脏DC进行体外培养,给予HMGB1刺激后检测细胞XBP-1活化情况;应用RNAi技术诱导XBP-1基因沉默后检测DC功能状态.结果 HMGB1刺激后,XBP-1表达特别是活化水平明显升高(P<0.05);XBP-1基因沉默DC给予HMGB1刺激不能有效诱导其成熟分化,表面标志物CD80、CD86及主要组织相容性复合体Ⅱ分子表达上调受抑,分泌白细胞介素-12、肿瘤坏死因子-α功能增强不明显.结论 XBP-1活化对HMGB1诱导DC成熟分化至关重要.

High mobility group box-1 protein (HMGB1) had been proved to induce maturation and activation of dendritic cell (DC), however, the endogenous changes and mechanisms underlying are unknown. Since endoplasmic reticulum stress (ERS) activates an adaptive unfolded protein response (UPR) that facilitates cellular survival and repair, we hypothesized that HMGB1 may regulate the function of DC by modulating ERS. In our study, HMGB1 stimulation induced significant ERS responses in DCs in a time- and dose-dependent manner, demonstrated by the up-regulation of a number of ERS markers. Gene silence of XBP-1 in splenic DCs decreased the levels of CD80, CD86 as well as major histocompatibility complex (MHC)-II expression and cytokine secretion after HMGB1 treatment, when compared with untransfected or nontargeting-transfected DCs (all P < 0.05). Moreover, XBP-1 silenced DCs after treatment with HMGB1 failed to stimulate notable proliferation and differentiation of T cells, unlike normal DCs or nontargeting-transfected DCs (all P < 0.05). Gene silence of XBP-1 resulted in down-regulation of the receptor for advanced glycation end products (RAGE) expression on the surface of splenic DCs induced by HMGB1 stimulation (P < 0.05). These findings demonstrate an important role for ERS and its regulator XBP-1 in HMGB1-induced maturation and activation of DCs.

High mobility group box-1 protein (HMGB1), which is a nuclear protein, participates in chromatin architecture and transcriptional regulation. When released from cells, HMGB1 also plays a well-established role as a pro-inflammatory mediator during innate immune responses to injury. In the initial stage of injury, there is a release of large quantities of early pro-inflammatory mediators to initiate or perpetuate immune responses against pathogens, but this pro-inflammatory period is transient, and it is followed by a prolonged period of immune suppression. At present, several lines of evidences have suggested that HMGB1 is a late cytokine provoking delayed endotoxin morbidity, which may enhance the production of early proinflammatory mediators, and it can contribute potently to the activation of different immune cells and play a role in the development of host cell-mediated immunity. The biology of HMGB1 has been extensively studied as a pro-inflammatory cytokine of systemic inflammation, however, this review will attempt to provide a summary of the effects of HMGB1 on different immune cells and its regulatory mechanism in acute insults.

Objective To explore the effects of high mobility group box-1(HMGB1) protein expression on the phenotype of regulatory T cells(Treg) and the functional polarization of splenic T cells in severe burn rats after delayed resuscitation.Methods One hundred and four Wistar rats were involved in present study and randomly divided into normal control group(n=8),sham burn group(n=32),burn group(n=32) and ethyl pyruvate(EP) treatment group(n=32).Thirty percent TBSA full-thickness burn models were established with the animals in both burn and EP treatment group,and Ringer’s solution or EP solution was respectively injected intraperitoneally for delayed resuscitation.Animals in each of the later three groups were further divided into four subgroups(8 each),sacrificed and simultaneously harvesting the spleen samples on day 1,3,5 and 7 after burn,respectively.Spleen CD4+CD25+ Treg were isolated by magnetic-activated cell sorting(MACS) system.The levels of HMGB1 in splenic tissue and IL-4,IFN-γ in T cells supernatant were determined by ELISA,and the expression of forkhead/winged helix transcription factor 3(Foxp3) as a surface marker of Treg was analyzed by flow cytometry.Results Compared with those in sham burn group,the HMGB1 level elevated significantly at day 1 to 7(P < 0.01),reached the peak value(46.73±8.27ng/mg) on day 1,and declined obviously(P < 0.01) by EP treatment in burn group;The expression of Foxp3 on splenic Treg increased from day 1 and reached the peak(72.46%±11.02%) on day 3 in burn group,while after EP treatment,it decreased obviously on day 1 to 7(P < 0.01 or 0.05).The IL-4 level increased(P < 0.01 or 0.05) and IFN-γ level decreased(P < 0.01) markedly in burn group compared with those in sham burn group.The IL-4 level was significantly lower(P < 0.05) on day 1 to 5,while the IFN-γ level was markedly higher on day 1 to 7(P < 0.05),in EP group than in burn group.Conclusion The excessive release of HMGB1 after severe burn might stimulate the maturation of splenic CD4+CD25+ Treg,thereby mediate the transformation of T cell subsets from Th1 to Th2 and induce the inhibition of cellular immunity.

OBJECTIVE:To observe the influence of high mobility group box-1 protein (HMGB1) derived from spleen on the phenotype of regulatory T lymphocytes (Treg) and HMGB1-mediated immune function in severely scalded rats after delayed resuscitation.METHODS:One hundred and four Wistar rats were divided into normal control group (NC, n = 8), sham scald group (SS, n = 32), scald group (S, n = 32), and ethyl pyruvate (EP) treatment group (EPT, n = 32) according to the random comparison table. Rats in the latter 2 groups were subjected to 30%TBSA full-thickness scald, which were intraperitoneally injected with Ringer solution or EP solution at post scald hour (PSH) 6 (delayed antishock treatment) and administered with 4 mL Ringer solution or EP solution per 12 hours after PSH 12 till PSH 48. Rats in SS group were treated the same as that of S group except for sham scald with 37 degrees C water. Injured rats were sacrificed at post scald day (PSD) 1, 3, 5, 7 (rats in NC group were also sacrificed), and CD4(+)CD25(+)Treg were isolated from spleen with magnetic-activated cell sorting method. The content of HMGB1 in spleen and IL-2 level in supernatant were determined with ELISA. The expression of cytotoxic T lymphocyte-associated antigen 4 (CTLA-4) on Treg was determined with flow cytometry, and the proliferation activity of T lymphocytes was also detected (recorded as absorbance value). Data were processed with analysis of variance among groups and independent samples t test.RESULTS:(1) Compared with that of rats in SS group and EPT group, the expression of splenic HMGB1 in S group increased significantly on PSD 1 through PSD 7 [peaked on PSD 1: (46.7 +/- 8.3) ng/mg protein]. (2) Compared with that in SS group, the expression of CTLA-4 in S group was enhanced significantly on PSD 1 through PSD 5 (with t value respectively 10.459, 12.051, 4.029, P < 0.05 or P < 0.01); while that in EPT group decreased significantly on PSD 1 through PSD 7 as compared with that from S group (with t value respectively 2.796, 9.913, 9.581, 10.022, P < 0.05 or P < 0.01). (3) Compared with that of rats in SS group, the proliferation activity of T lymphocytes in S group was markedly suppressed on PSD 1 through PSD 7 (nadir on PSD1: 0.167 +/- 0.059), and release of IL-2 was decreased significantly [nadir on PSD 5: (44 +/- 24) pg/mL]. T lymphocytes proliferation activity was restored and excretion of IL-2 increased in EPT group as compared respectively with that of S group at each time point.CONCLUSIONS:The release of HMGB1 may stimulate splenic Treg to mature, thereby induce suppression of proliferation activity of T lymphocytes and immune function. EP can ameliorate immune dysfunction in animals with delayed resuscitation through inhibiting the synthesis and release of HMGB1.

A 60-year-old woman with systemic lupus erythematosus initially received oral methylprednisolone 40 mg/d.After 45 days of methylprednisolone therapy,mycophenolate mofetil 0.75 g was added to her regimen.A further 38 day's later,the patient developed fever,tight chest,and hypoxemia.A chest X-ray showed that the lines in her lungs was increased and blurred,and her lung field was ground-glass pattern.Laboratory tests revealed that her CD4+ T-lymphocyte count was 103/mm3,and pneumocystis jirovecii was detected in her brochovesicular lavage solution.The patient was diagnosed with pneumocystis pneumonia.The dosage of mycophenolate mofetil was reduced to 0.5 g twice daily.In addition,caspofungin 50 mg/d and 2 sulfamethoxazole,sulfadiazine and trimethoprim tablets four times daily were given.Five days after drug administration,her tight chest and dyspnea improved.

目的 探讨慢性肾脏病者伴肺孢子虫肺炎(PCP)漏诊原因.方法 回顾性分析3例漏诊的慢性肾脏病伴PCP患者的临床症状、影像学及实验室检查资料,并分析漏诊原因.结果 本组3例,IgA肾病2例,肾淀粉样变性病1例.临床表现为发热、咳嗽、胸闷,2例出现Ⅰ型呼吸衰竭,1例出现低氧血症.3例均应用激素治疗,2例同时应用环磷酰胺(CTX).2例诊断为肺部急性细菌性感染,1例诊断为肺部支原体感染.入院时3例X线征象均不典型,2例有典型CT征像.确诊时2例有典型X线征象,3例有典型CT征象.3例常规痰培养均未发现伊氏肺孢子菌,支气管肺泡灌洗液吉姆萨染色涂片发现伊氏肺孢子菌或痰聚合酶链反应(PCR)法检测伊氏肺孢子菌虫体DNA(+).给予卡泊芬净及复方磺胺甲噁唑治疗均治愈.结论 .PCP是接受激素和(或)CTX治疗的慢性肾脏病患者肺部机会感染之一,早期胸部X线和CT征像常不典型,典型的X线或CT征像对PCP的诊断具有重要意义.接受激素和(或)免疫抑制剂治疗的慢性肾脏病患者若出现发热、抗细菌感染治疗效果不佳,应尽早行痰或支气管肺泡灌洗液吉姆萨染色找伊氏肺孢子菌或PCR法检测伊氏肺孢子菌虫体DNA.

The present study was performed to investigate in vivo the effect of high-mobility group box-1 protein (HMGB1) on the maturation of dendritic cell (DC) and the influence on T-cell-mediated immunity after thermal injury. Rats were randomly divided into 3 groups as follows: sham burn group, burn group, and burn with ethyl pyruvate (EP) treatment group, and they were sacrificed on post burn days (PBD) 1, 3, 5, and 7 respectively. MACS microbeads were used to isolate splenic DCs and column of nylon wool to obtain T cells. Phenotypes were analyzed by flow cytometry and cytokines were determined with ELISA kits. The expression levels of splenic HMGB1 were significantly elevated during PBD 1-7. DC expressed similar CD80 levels, strongly enhanced CD86, and slightly elevated MHC class II levels in comparison to DC from sham-injured rats, and protein levels of IL-12 were not increased after thermal injury. Administration of EP to inhibit HMGB1 could significantly enhance expression levels of CD80, MHC class II on DC surface, and IL-12 production after burns. Simultaneously, proliferative activity and expression levels of IL-2 as well as IL-2R alpha of T cell were restored. These results suggested that the excessively released HMGB1 might stimulate splenic DC to mature abnormally and down-regulate the IL-12 production, and further shifting of Th1 to Th2 with suppression of T-lymphocyte immune function following burn injury.

Objective:To improve our understanding toward pneumocystis carinii(PC) pneumonia in patients with chronic kidney disease.Methods:Four patients with chronic kidney disease and pneumocystis carinii (PC) pneumonia were retrospectively analyzed.Results:The clinical manifestations were fever,cough,chest tightness and no resonse to antibiotics.Three patients were confirmed type Ⅰ respiratory failure and 1 hypoxemia.Three patients were detected pneumocystis carinii in bronchoalveolar lavage fluid.One patient was found positive of pneumocystis carinii DNA in bronchoalveolar lavage fluid.Two cases were complicated with IgA nephropathy,one with renal amyloidosis and the other with membranous nephropathy.All patients received hormone therapy and 2 cases combined with cyclophosphamide (CTX).Four patients were treated with Caspofungin+cotrimoxazole (SMZco)+ hormone,and they were all improved and discharged with no occurrence of side effects.Conclusion:PC pneumonia was one of pulmonary opportunistic infections in patients with chronic kidney disease receiving hormone and (or) CTX therapy.Typical chest X-ray or CT sign was important for diagnosis,but the initial sign was non-typical.If patients receiving hormone and (or) immunosuppressive therapy for kidney diseases were having fever and no response to antibiotics,they should be alert to PC pneumonia.Bronchoalveolar lavage fluid giemsa stain and sputum PCR should be done as soon as possible to confirm PC.Treatment of PC pneumonia with Caspofungin and cotrimoxazole (SMZco) was preferred.