Clinical features of acute kidney injury in patients with Kawasaki disease

Although acute kidney injury (AKI) is a common complication in hospitalized children, AKI has rarely been reported in patients with Kawasaki disease (KD). Herein, we review the clinical trajectories of AKI in patients with KD. A total of 39 patients with KD who developed AKI have been reported in 28 publications as case reports. The causes of AKI include prerenal AKI associated with acute heart failure (AHF), intrinsic AKI caused by tubulointerstitial nephritis (TIN), acute nephritic syndrome (ANS), hemolytic uremic syndrome (HUS), immune complex-mediated nephropathy, rhabdomyolysis, and KD shock syndrome (KDSS). Six of the 39 patients (15.4%) underwent renal replacement therapy. While AHF and multiple organ dysfunction syndrome developed in 41% and 68% of KD patients with AKI, respectively, all patients recovered without any renal sequelae. Although the precise pathogenic mechanism underlying the development of AKI in patients with KD is unknown, several possible mechanisms have been proposed, including T-cell-mediated immunologic abnormalities for TIN, renal and glomerular endothelial injury resulting from vasculitis for HUS, immune complex-mediated kidney injury for immune complex-mediated nephropathy and ASN, and capillary leak and an increased release of cytokines with myocardial dysfunction for KDSS.     

Management of Acute Kidney Injury

Acute kidney injury is common in hospitalized children and is associated with siginficant morbidity and mortality especially in critically ill children. A complete evaluation is necessary for all children with AKI as early recognition and treatment is paramount. Apart from clinical evaluation, urinalysis, biochemical investigations and imaging studies helps in the diagnosis of the specific cause of AKI and assessing its severity. Attention should be given to assessment of volume status and fluid administration because volume depletion is a common and modifiable risk factor for AKI. Prevention or prompt management of complications like fliud overload, hyperkalemia and metabolic acidosis improves outcomes. Immediate initiation of renal replacement therapy (RRT) is indicated in the presence of life threatening changes in fluid, electrolyte and acid-base balance. Other measures like treating the underlying cause of AKI, adapting dosage of drugs to renal function, treatment of infections and providing adequate nutrition is important. Children with AKI should be followed up as they are at risk for development of chronic kidney disease.     

Epidemiology and outcomes of children with renal failure in the pediatric ward of a tertiary hospital in Cameroon

Background

Pediatric nephrology is challenging in developing countries and data on the burden of kidney disease in children is difficult to estimate due to absence of renal registries. We aimed to describe the epidemiology and outcomes of children with renal failure in Cameroon.

Methods

We retrospectively reviewed 103 medical records of children from 0 to 17 years with renal failure admitted in the Pediatric ward of the Douala General Hospital from 2004 to 2013. Renal failure referred to either acute kidney injury (AKI) or Stage 3–5 chronic kidney disease (CKD). AKI was defined and graded using either the modified RIFLE criteria or the Pediatrics RIFLE criteria, while CKD was graded using the KDIGO criteria. Outcomes of interest were need and access to dialysis and in-hospital mortality. For patients with AKI renal recovery was evaluated at 3 months.

Results

Median age was 84 months (1QR:15–144) with 62.1% males. Frequent clinical symptoms were asthenia, anorexia, 68.8% of participants had anuria. AKI accounted for 84.5% (n?=?87) and CKD for 15.5% (n?=?16). Chronic glomerulonephritis (9/16) and urologic malformations (7/16) were the causes of CKD and 81.3% were at stage 5. In the AKI subgroup, 86.2% were in stage F, with acute tubular necrosis (n?=?50) and pre-renal AKI (n?=?31) being the most frequent mechanisms. Sepsis, severe malaria, hypovolemia and herbal concoction were the main etiologies. Eight of 14 (57%) patients with CKD, and 27 of 40 (67.5%) with AKI who required dialysis, accessed it. In-hospital mortality was 50.7% for AKI and 50% for CKD. Of the 25 patients in the AKI group with available data at 3 months, renal recovery was complete in 22, partial in one and 2 were dialysis dependent. Factors associated to mortality were young age (p?=?0.001), presence of a coma (p?=?0.021), use of herbal concoction (p?=?0.024) and acute pulmonary edema (p?=?0.011).

Conclusion

Renal failure is severe and carries a high mortality in hospitalized children in Cameroon. Limited access to dialysis and lack of specialized paediatric nephrology services may explain this dismal picture.

     

Acute kidney injury

The definition and classification of acute kidney injury (AKI) in children has become clearer over the last decade. The paediatric RIFLE criteria stratify AKI in children into five groups (R = risk, I = injury, F = failure, L = loss of kidney function, E = end stage renal disease) enabling earlier recognition and intervention. This article reviews the definition, classification, causes and management of AKI as relevant to the general paediatrician.Common causes of AKI in neonates and children are reviewed including E. Coli associated haemolytic uraemic syndrome, hypoxic ischaemic insults and medication related kidney injury. Initial management of acute kidney injury and its complications is outlined in the context of the role of the general paediatrician and factors which should prompt discussion with a tertiary paediatric nephrologist. The outcome and complications of kidney injury are discussed and future directions in the field considered.     

An uncommon cause of acute kidney injury in young children: Cystinuria

Bilateral obstructive nephrolithiasis is a rare cause of acute kidney injury (AKI) in early childhood. As soon as the identification of AKI secondary to ureteral stone is made, it will necessitate an emergency treatment.PatientsWe report three infants with AKI caused by bilateral obstructive ureteral cystine stones. They were diagnosed with acute post-renal injury due to obstructive bilateral ureteral stones based on ultrasound scan findings. Immediately, bilateral ureteral stents were inserted for urinary drainage. Once renal function recovered to normal, each patient underwent ureteroscopy and percutaneous nephrolithotomy at the same session. Cystinuria was diagnosed by stone analysis and increased urinary excretion of cystine. Patients were advised to maintain a high fluid intake and were treated with potassium citrate in addition to tiopronin.ConclusionsWith these three cases we would like to emphasize the importance of urolithiasis in the differential diagnosis of acute renal failure in young children, since urolithiasis may only cause nonspecific symptoms in this population. An early diagnosis with prompt treatment and a close follow-up are the key for achieving the best long-term outcome in cystinuria.     

Causes, prognostic factors and treatment results of acute renal failure in children treated in a tertiary hospital in South Africa

The aim of this study was to determine the causes, prognostic factors and treatment results of acute renal failure (ARF) in children admitted to the Pretoria Academic Hospital from 1986 to 2002. A retrospective chart review of 102 children (mean age 37 months) was done. Various factors were analysed including age, sex, causes of ARF, morbidity, mortality, dialysis requirement and outcome. Peritoneal dialysis was the only form of dialysis available. Patients were categorized as those who survived without dialysis or in whom renal function recovered without the need for continuing dialysis (Group I, termed 'survivors'), and those who died or remained dialysis dependent (Group II, termed 'non-survivors'). The most common causes of ARF were haemolytic uraemic syndrome (35.3%), acute tubular necrosis (31.4%) and acute glomerulonephritis (15.7%). There were 77 patients in Group I of whom 38 required dialysis, and 25 in Group II of whom 16 were dialysed. Fifteen patients in Group II died and 10 remained dialysis dependent ('renal deaths'). Only four patients with 'renal death' received long-term dialysis. Coma (P < 0.001), liver dysfunction (P < 0.009), a clotting deficiency (P < 0.001), respiratory failure (P < 0.001) and multi-organ failure (P < 0.001) were significantly associated with poor outcome. These factors should be taken into account before initiating dialysis in children in countries where available resources for long-term dialysis are limited.     

Clinical practice

The haemolytic uraemic syndrome (HUS) includes the triad of haemolytic anaemia, thrombocytopenia, and acute renal failure. The classical form [D(+) HUS] is caused by infectious agents, and it is a common cause of acute renal failure in children. The enterohaemorrhagic Escherichia coli-producing Shiga toxin (Stx) is the most common infectious agent causing HUS. Other infectious agents are Shigella and Streptococcus pneumoniae. Infections by S. pneumoniae can be particularly severe and has a higher acute mortality and a higher long-term morbidity compared to HUS by Stx. Atypical HUS [D(−)Stx(−)HUS] are often used by paediatricians to indicate a presentation of HUS without preceding diarrhoea. Almost all patients with D(−)Stx(−)HUS have a defect in the alternative pathway, for example, mutations in the genes for complement factor H, factor I, and membrane co-factor protein. Mutations in the factor H gene are described more often. The majority of children with D(+) HUS develop some degree of renal insufficiency, and approximately two thirds of children with HUS will require dialysis therapy, while about one third will have milder renal involvement without the need for dialysis therapy. General management of acute renal failure includes appropriate fluid and electrolyte management, antihypertensive therapy, and the initiation of renal replacement therapy when appropriate. Specific management issues in HUS include management of the haematological complications of HUS, monitoring for extra-renal involvement, avoiding antidiarrhoeal drugs, and possibly avoiding of antibiotic therapy. In addition to the obligatory supportive treatment and tight control of hypertension, there is anecdotal evidence that plasma therapy may induce remission and, in some cases, maintain it. Fresh frozen plasma contains factor H at physiological concentrations. A new therapy for D(−)Stx(−)HUS is a humanised monoclonal antibody (Eculizumab) that blocks complement activity by cleavage of the complement protein C5. It prevents the generation of the inflammatory peptide C5a and the cytotoxic membrane–attack complex C5b-9. We have first positive results, but it is still not approved for HUS.     

Renal replacement therapies in pediatric intensive care patients: Experiences of one center in Turkey

BACKGROUND: Despite constant improvements in caring for critically ill neonates and infants with congenital cardiac disease, sepsis, bone marrow and solid organ transplantation, acute renal failure (ARF) is an important problem in these children. ARF, severe fluid overload and inborn errors of metabolism are some of the indications for acute dialysis in infants and children. METHODS: The authors had retrospectively evaluated the medical records of Pediatric Intensive Care Unit, Ankara University School of Medicine, Ankara, Turkey patients who had required acute renal replacement therapy between the dates of January 2002 to February 2005. RESULTS: Medical records of 332 patients were reviewed. Acute renal replacement therapy was performed in 21 patients (6.3%; mean age, 9.6 +/- 7.4 years). Dialysis modalities were peritoneal dialysis in 15 patients (71.4%; mean age, 3.9 +/- 5.6 years) and hemodialysis in six patients (28.6%; mean age, 12.1 +/- 3.2 years). A total of 90% of patients had severe systemic disease leading to ARF. A total of 95% of patients had multiple organ dysfunction syndrome. The most common cause of ARF was refractory shock. At the beginning of renal replacement therapy, 10 patients were anuric, nine patients had volume overload, seven patients had decompensated metabolic acidosis and nine patients had hypotension. The average dialysis period was 4.7 +/- 6.4 days. Mortality rate was 66.7%. Eight patients recovered from ARF and chronic renal failure had developed in one patient. CONCLUSION: In the Pediatric Intensive Care Unit, ARF is frequently seen together with multiple organ dysfunction syndrome and the mortality rate is high. Both peritoneal dialysis and hemodialysis are important renal replacement treatment modalities in patients with ARF. The age and hemodynamic status of the patients are important when choosing treatment modality; generally peritoneal dialysis is preferred in infants and toddler, while hemodialysis is preferred in older children.     

Antibiotic resistant <Emphasis Type="Italic"> Streptococcus pneumoniae </Emphasis>and hemolytic uremic syndrome

The hemolytic uremic syndrome (HUS) is the most common cause of acute renal failure in young children and most often follows an episode of gastroenteritis caused by an enterohemorrhagic strain of Escherichia coli (O157:H7). HUS induced by Streptococcus pneumoniae (SP) is rare. We report an 18-month-old patient who presented with HUS associated with SP resistant to penicillin and cephalosporins. Conclusion:Despite a protracted course including renal failure requiring 15 days of peritoneal dialysis, her kidney function completely recovered.     

Epidemiology and outcome of acute kidney injury in New Zealand children

Objectives: To determine the aetiology, incidence and short‐term outcomes of New Zealand children with acute kidney injury (AKI) requiring renal replacement therapy (RRT) over a 6‐year period. Methods: A retrospective chart review of all children requiring RRT for AKI from January 2001 to December 2006 at Starship Children's Hospital, Auckland, New Zealand was conducted. The primary outcome was survival to discharge. Results: A total of 226 children required RRT for AKI over the 6‐year study period. The annual incidence was 4.0 per 100 000 total population under 15 years of age. The commonest causes of AKI were post cardiac surgery (58%), haemolytic uraemic syndrome (17%), sepsis (13%) and glomerulonephritis (4%). The survival rate to hospital discharge was 89%. A total of 40% of all surviving children had one or more abnormalities at the time of discharge suggestive of ongoing renal dysfunction (hypertension, continuing need for antihypertensive medication, reduced estimated glomerular filtration rate or abnormal urinalysis). More Maori and Pacific Island children were treated for AKI than would be expected from population data (P < 0.0001). Sepsis and glomerulonephritis were seen more commonly as causes of AKI in Maori and Pacific Island children compared with New Zealand European children. Conclusion: In our study, 40% of surviving children had evidence of short‐term renal dysfunction at discharge following AKI. This suggests that all children should undergo a period of follow‐up after any episode of AKI to look for resolution or further development of signs of renal injury.     

Pulmonary complications of renal disorders

To manage patients with diseases of the lungs and the kidneys, one must first understand the relationship between respiratory and renal function. In treating acute renal failure (ARF), the clinician often must contend with respiratory manifestations of volume overload and metabolic acidosis. Mechanical ventilation in patients with renal failure (RF) can be challenging, particularly with lung protective ventilation and weaning. Patients with chronic renal failure (CRF) experience several respiratory complications. Hypoxaemia during dialysis is now understood to be a predictable effect of the loss of CO(2) into the dialysate. Critical illness of any primary cause predisposes patients not only to acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) but also to the development of ARF. Meanwhile, the potential for ventilator-induced renal injury has increasingly become the subject of active investigation.     

Renal complications of seasonal and pandemic influenza A virus infections

Renal complications of influenza A virus infections are uncommon but can contribute to a deterioration in the patient’s condition, which include acute kidney injury (AKI) in critically ill patients, rhabdomyolysis, hemolytic uremic syndrome (HUS), acute glomerulonephritis (AGN), disseminated intravascular coagulation (DIC), Goodpasture’s syndrome, and acute tubulointerstitial nephritis (TIN). The clinical characteristics of AKI in critically ill patients with pandemic influenza A(H1N1) 2009 virus (A(H1N1)pdm09) infection are similar to uninfected patients. Underlying conditions associated with AKI include older age, diabetes mellitus, obesity, pregnancy, history of asthma, and chronic kidney disease. Histologic examination of the kidneys from patients with A(H1N1)pdm09 infection who died include acute tubular necrosis (ATN), myoglobin pigment, and DIC. A(H1N1)pdm09 is present in the kidneys of some patients. The clinical characteristics of patients with rhabdomyolysis associated with influenza A include younger age and the frequent occurrence of muscle symptoms. AKI occurs in approximately one third of patients with rhabdomyolysis due to influenza A. HUS is associated with A(H1N1)pdm09 as follows: Streptococcus pneumoniae-associated HUS following A(H1N1)pdm09 infection, HUS triggered by A(H1N1)pdm09 in patients with genetic complement dysregulation, and HUS associated with A(H1N1)pdm09 without known underlying disorder. AGN, Goodpasture’s syndrome, and acute TIN are extremely rare complications of influenza A virus infection. Although the pathogenesis underlying renal injuries due to influenza A virus has not been delineated, some hypotheses have been advanced, including ATN due to renal hypoperfusion or rhabdomyolysis, glomerular microthrombosis due to DIC, direct viral injury to the kidney, and an altered immune system with systemic mononuclear cell activation following influenza A virus infections.     

Prospective evaluation of acute and chronic renal function in children following matched related donor hematopoietic stem cell transplantation

Ileri T, Ertem M, Ozcakar ZB, Ince Unal E, Biyikli Z, Uysal Z, Ekim M, Yalcinkaya F. Prospective evaluation of acute and chronic renal function in children following matched related donor hematopoietic stem cell transplantation.
Pediatr Transplantation 2010: 14: 138–144. © 2009 John Wiley & Sons A/S.
Abstract:  Acute and chronic renal impairment are important complications after HSCT. A prospective study was conducted to investigate the glomerular renal function in children who received allogeneic HSCT from matched related donors. Non-radiation conditioning regimens were used in all but one patient. CrCl and serial measurements of serum creatinine were evaluated prior to HSCT, within the first 100 days and one yr after. AKI was defined as at least a 1.5-fold rise in pre-HSCT serum creatinine within the first 100 days and classified as grade 1 to 3 according to the new definition criteria proposed by "AKI Network." Fifty-seven patients were enrolled in the study and 24 patients (42%) had AKI. CsA, amphotericin B, and SOS were found as risk factors for AKI. One yr after HSCT five patients (10%) had CKD and none of them required dialysis. None of the parameters were found as a predictor for CKD. We conclude that AKI is an important complication of HSCT. Careful monitoring of renal function, minimizing the use of nephrotoxic medication, prophylaxis, and effective treatment of SOS might be effective preventive measures to decrease the incidence of AKI.     

儿童危重症肾替代治疗时机和方法

儿童危重病中的肾替代治疗（renal replacement therapy, RRT）主要作用是替代受损肾功能, 稳定内环境,清除有害代谢产物、 炎症介质和毒素等。RRT绝对适应证为： 急性肾损伤（AKI）患儿出现严重高钾血症（K+＞6.5 mmol/L）,严重酸中毒（pH值＜7.1）,尿毒症相关性脑病和凝血病,以及利尿剂治疗无效的液体超载。连续血液净化（continuous renal replacement therapy,CRRT）适应于脓毒症合并AKI或血流动力学不稳定患儿的液体管理, 合适的时机仍有待循证。CRRT治疗剂量分为肾替代治疗剂量［超滤量20～35 mL/（kg·h）］和脓毒症治疗剂量［超滤量≥35 mL/（kg·h）］。高容量血液滤过［置换液剂量≥50 mL/（kg·h）］可能有助于稳定脓毒性休克患儿的血流动力学指标。     

Pretransplant peritoneal dialysis and graft thrombosis following pediatric kidney transplantation: a NAPRTCS report

Graft thrombosis is a common cause of graft failure in pediatric renal transplantation. Several previous studies, including a North American Pediatric Renal Transplant Cooperative Study (NAPRTCS) review of pretransplant dialysis status and graft outcomes, have described a potential correlation of peritoneal dialysis (PD) and graft thrombosis. This issue is of particular concern for pediatric transplant programs as more than 65% of children with end stage renal disease are treated with PD. We reviewed 7247 pediatric renal transplants performed between 1987 and 2001. Thrombosis was the cause of graft loss in 2.7% (199) of all the transplants performed. Among failed transplants, thrombosis was the third most common cause of graft loss in both index (11.6%) and subsequent transplants (14.5%). Thrombosis becomes the most common cause of graft failure (21%, 61/294) if one looks at transplants in the later cohort, from 1996 to 2001. This change is primarily because of a decrease in the incidence of acute rejection. In the PD group, 3.4% of all grafts were lost as a result of thrombosis. This compares with 1.9% in the hemodialysis group, 2.4% in the pre-emptive transplant group, and 4.1% among patients who received both dialysis modalities. There was a statistically significant difference in thrombosis failure risk in the different dialysis groups (p = 0.005) with those who received only peritoneal dialysis having the highest risk. Additional significant risk factors for graft thrombosis included; cadaver donor source (p < 0.001), cold ischemia time >24 h (p < 0.001), history of prior transplant (p < 0.001), donor age <6 yr (p < 0.001), and >5 pretransplant blood transfusions (p = 0.02). Using stepwise proportional hazards modeling, only pretransplant peritoneal dialysis, >24 h cold ischemia time, prior transplant, and donor age <6 yr were simultaneously associated with an increased risk of thrombosis. We conclude that pretransplant PD is associated with an increased risk of graft thrombosis. Special precautions should be undertaken in pediatric renal transplant patients who have received PD, especially infants and young children.     

Chronic constipation causing obstructive uropathy in an adolescent male

Chronic constipation causing obstructive uropathy is very rare in children and young adults. Nevertheless, it is one of the possible complications of ongoing constipation and can cause severe renal function impairment with the need for emergent disimpaction. We review the case of a young adult who presented to our emergency department with acute renal failure due to fecal impaction.     

Acute renal failure in children: prognostic features after treatment with acute dialysis

A 12-year review (1972–1983) is presented of 76 children who were dialysed because of acute renal failure. The causes of acute renal failure were mainly the haemolyticuraemic syndrome (53%), trauma (16%) and operation (13%).Fifty-eight children (76%) survived, 18 children (24%) died. Fifty-two children, the majority suffering from haemolytic-uraemic syndrome, regained complete or partial renal function after a period of dialysis lasting between 1 and 57 days. One to 7.7 years after dialysis, clearance studies with inulin (C_In), p-aminohippuric acid (C_PAH) and phosphate (T_p/C_In) for staging renal function were carried out. The results of this investigation show a significant inverse correlation between the glomerular function regained and the duration of intermittent dialysis.Abbreviations C_In clearance of inulin - C_PAH clearance of p-aminohippuric acid - FF filtration fraction - T_p/C_In fractional phosphate reabsorption - HUS haemolytic-uraemic syndrome - ARF acute renal failure - SCR serum creatinine - GFR glomerular filtration rate - CRF chronic renal failure - a.t. antihypertensive treatment     

溶血性尿毒症综合征急性期后治疗探讨

目的探讨溶血性尿毒症综合征（HUS）患儿渡过急性期后如何促进肾功能的修复、延缓肾损害进程,探讨HUS急性期后的治疗方法。方法分析1993年至2005年我科收治的17例HUS患儿的临床资料。13例接受急性期后治疗患儿除用血管紧张素转化酶抑制剂（ACEI）和限制蛋白质摄入外,参照中华医学会儿科学分会肾脏病学组制定的“小儿肾小球疾病的临床分类、诊断及治疗”（方案）,按临床分型、对泼尼松治疗的反应及病理类型拟定治疗方案。2例临床表现为肾小球肾炎的患儿中1例应用雷公藤多甙。11例表现为肾病综合征的患儿均用泼尼松;其中5例泼尼松治疗不缓解或部分缓解者,加用环磷酰胺冲击（4例）或甲泼尼龙冲击（1例）治疗;3例因肾组织病理改变为膜增殖＋／-局灶节段性肾小球硬化、新月体形成,加用甲泼尼龙冲击。结果随访2个月～8年,轻型4例（1例复发1次）血压、血尿素氮（BUN）、血肌酐（Cr）及尿常规均正常。重型9例中6例血压、BUN、Cr、尿常规正常;3例持续尿检异常,肾功能不全,且没有坚持治疗,分别于病程的第3、9和13个月死亡。4例（均为重型）放弃治疗者分别于病程的第27～48天死亡。结论对渡过急性期的HUS患儿依据其临床分型和肾病理改变参照肾脏病学组制定的方案治疗有望改善预后。除急性期病情轻重、治疗的合理性影响预后外,患儿家长对治疗的依从性也是一个重要因素。     

Rational use of antibiotics in children with diabetic ketoacidosis needs attention

Diabetic ketoacidosis (DKA) in children may lead to acute kidney injury (AKI). Among 45 children with DKA in our center, eight cases had AKI on admission, and in one child, his kidney function did not recover until 3 mo after discharge. This child was treated with antibiotics (cephalosporin), and we cannot rule out delayed AKI recovery due to the combined effects of the drug and the disease. Pediatricians should be concerned about the impact of nephrotoxic drug and disease interactions on children's kidney function, and need to follow up children with DKA and AKI to determine the development of AKI.     

急性肾损伤患儿肾脏促红细胞生成素及其受体的表达

目的 探讨急性肾损伤(AKI)患儿肾脏局部促红细胞生成素(EPO)、EPO受体的表达与肾脏病理损害的关系.方法 2005年1月-2009年12月在本院住院并行肾活检的38例AKI患儿(男29例,女9例).年龄中位数为4.04岁(2个月～11岁9个月),病程中位数为6.89 d(1～30 d).将AKI 1期及AKI 2期患儿归为轻症病例组,AKI 3期患儿归为重症病例组,对照组为同期住院并经肾活检诊断为薄基膜肾病的患儿.采用免疫组织化学方法检测所有患儿肾组织EPO及EPO受体的表达,应用肾脏病理计量评分法对肾小管问质损害进行半定量分析,分析肾小管问质损害程度与肾组织EPO及EPO受体表达之间的关系.结果 1.AKI患儿38例中轻症病例组8例均痊愈,重症病例组28例痊愈,2例预后差.肾脏病理以肾小管间质损害为主.轻症病例组、重症病例组肾小管间质病理损害计分为(10.56±3.40)分、(15.56±4.70)分,组间比较差异有统计学意义(t=-2.832,P<0.01).2.对照组、轻症病例组、重症病例组EPO的阳性表达面积分别为(6.52±2.12)%、(3.02±0.79)%、(1.62±0.18)%,组间比较差异有统计学意义(P<0.01);3组EPO受体的阳性表达面积分别为(40.46±8.42)%、(64.78±16.38)%、(62.36±15.67)%,组间比较差异亦有统计学意义(P<0.01).3.肾小管间质的病理损害与EPO在肾小管间质的阳性表达面积呈负相关(r=-0.872,P<0.01),而与EPO受体在肾小管间质的阳性表达面积呈正相关(r=0.772,P<0.01).结论 AKI患儿肾脏局部EPO的分泌受抑制,而EPO受体表达增高,提示应用外源性EPO可能有助于肾脏修复.