Oral penicillin‐associated acute kidney injury in an infant with acute pyelonephritis

Beta‐lactam‐associated acute tubulointerstitial nephritis (ATIN) is a rare condition in childhood. We report the case of an infant with penicillin‐associated ATIN and concomitant acute pyelonephritis resulting in the development of severe acute kidney injury (AKI). The treatment consisted of penicillin suspension and appropriate AKI management, which required a short period of dialysis. Finally, full recovery and normalization of laboratory parameters occurred. We present here the first case of oral penicillin‐associated ATIN in childhood.     

Posterior reversible encephalopathy syndrome with exercise-induced acute kidney injury in renal hypouricemia type 1

Renal hypouricemia type 1 is caused by mutations in the SLC22A12 gene, whereas type 2 is caused by defects in the SLC2A9 gene. Although both subtypes predispose to exercise-induced acute kidney injury (EIAKI), posterior reversible encephalopathy syndrome (PRES) occurring with this disorder is an uncommon phenomenon that has only been reported to date in a patient with renal hypouricemia type 2. We describe a 13-year-old boy with renal hypouricemia type 1 (serum uric acid, 0.9 mg/dL) with a homozygous W258X mutation in the SLC22A12 gene, presenting with EIAKI and PRES. On admission, his body weight was 61 kg (11 kg above the dry weight), and blood pressure was 153/88 mmHg. Cranial magnetic resonance imaging revealed high-intensity areas in the cortical and subcortical white matter of the occipital lobe. After admission, the patient responded well to a combination of hemodialysis and intravenous nicardipine. This is the first case of concurrent PRES and EIAKI in a patient with renal hypouricemia type 1. We suggest that PRES is not due to severe hypouricemia caused by SLC2A9 mutation but is a manifestation of severe EIAKI associated with renal hypouricemia.     

Acute renal failure after exercise in a child with renal hypouricemia

We describe a 15 year old boy with renal hypouricemia who developed acute renal failure after a school athletics meeting, accompanied by appendicitis. During acute renal failure, the highest level of uric acid was 5.0 mg/dL, creatinine 7.9 mg/dL and urea nitrogen 58.6 mg/dL. After recovery, the serum uric acid fell to 0.9 mg/dL and the fractional excretion of uric acid (FEu_A) exceeded the normal range. The probenecid and pyrazinamide tests showed that the patient had a total defect of uric acid reabsorption. This case suggested that strenuous exercise could be responsible for acute renal failure in patients with renal hypouricemia.     

Evaluation of infant feeding in acute gastroenteritis

Sixty-eight bottle-fed babies under 9 months of age with mild acute gastroenteritis were observed to evaluate current feeding regimens following acute gastroenteritis in infancy. All babies were fed for 24 h with a glucose-electrolyte mixture (GEM) and then randomly assigned to either a gradual reintroduction to their normal milk, i.e., slow regrade; immediate return to full-strength formula; or a rapid regrade to a hypoallergenic whey hydrolysate formula. All groups were well matched for age, sex, ethnic origin, nutritional state, and degree of hydration. There was no significance difference in stool frequency or reducing substances, vomiting, and duration of hospital stay between the three groups. Many infants (6/24) refused to take the whey hydrolysate formula, presumably because of unpalatability. Weight gain was more rapid when full-strength milk was given. Clinical relapse developed in 12 (17%) of patients. An enteric pathogen was detected in eight of this group and cow's milk protein intolerance in three (one from each feeding group). No infant had clinically significant lactose intolerance, in marked contrast to previous experience at Queen Elizabeth Hospital. In this group of previously healthy, well-nourished babies with mild acute gastroenteritis, there was no advantage in regrading slowly to milk or a hypoallergenic formula. An immediate return to normal formula 24 h after GEM feeding was well tolerated and simpler for parents.     

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.     

低白蛋白血症对心脏手术后患儿急性肾损伤发生的影响

目的 探讨小儿心脏病体外循环（CPB）手术后的低白蛋白血症对术后急性肾损伤（AKI）发生的影响。方法 回顾性分析2012~2016年行心脏病CPB手术患儿1 110例临床资料,按术后48 h内最低白蛋白浓度分为低白蛋白组（≤35 g/L）和正常白蛋白组（> 35 g/L）,比较两组患儿的围手术期资料和AKI发生率。对不均衡的围手术期各因素进行倾向评分匹配后再次比较AKI发生率。采用logistic回归分析术后AKI发生的围手术期危险因素。结果 术后AKI发生率为13.78%（153/1 110）,病死率为2.52%（28/1 110）,AKI患儿病死率为13.1%（20/153）,术后白蛋白≤35 g/L 的患儿占44.50%（494/1 110）。匹配前后低白蛋白组AKI发生率均比正常白蛋白组要高（P < 0.05）;匹配前后AKI患儿术后白蛋白浓度均低于非AKI患儿（P < 0.05）;Logistic多因素回归分析结果显示术后白蛋白≤35 g/L是术后AKI发生的独立危险因素之一。结论 术后48 h内白蛋白≤35 g/L是心脏CPB术后患儿AKI发生的独立危险因素,术后加强对白蛋白的检测和补充对控制术后AKI的发生有积极作用。     

Acute kidney injury in children

Acute kidney injury (AKI) affects 5% of critically ill hospitalized children and is a risk factor for increased morbidity and mortality. The current review focuses on new definitions of acute kidney injury, standardized to reflect the entire spectrum of the disease, as well as on ongoing research to identify early biomarkers of kidney injury. Its also provides an overview of current practice and available therapies, with emphasis on new strategies for the prevention and pharmacological treatment of diarrhea-associated hemolytic uremic syndrome. Furthermore, a decision-making algorithm is presented for the use of renal replacement therapies in critically ill children with AKI.     

儿童急性肾损伤

急性肾衰竭(acute renal failure,ARF)是由多种原因导致肾小球滤过率突然和持续性下降,尿素和其他代谢产物在血液中蓄积而出现的临床综合征,ARF是发生在各种临床情况之下的一种复杂的肾功能紊乱.     

Eosinophilic cystitis and coexistent eosinophilic gastroenteritis in an infant

This report describes the first documented case of eosinophilic cystitis and eosinophilic gastroenteritis occurring in a child.     

急性肾损伤患儿的营养支持

急性肾损伤是危重患儿常见的多器官功能障碍之一,常发生在危重疾病的严重分解代谢期,代谢紊乱又使肾损伤进一步加重。营养支持对于改善预后至关重要。伴有急性肾损伤的危重患儿存在特殊的营养需求,需要提供肠内或肠外营养支持。应反复评估此类患儿营养需求的变化,以寻求个体化营养支持以及与肾脏替代治疗的精细整合。     

新生儿急性肾损伤与慢性肾脏病

由于新生儿处于从宫内环境向宫外环境的过渡期,内环境变化大,且肾脏的结构、功能发育不成熟,与成人相比,肾脏储备能力低下。在正常情况下,新生儿肾脏的成熟能与生长发育相适应,维持内环境于一个相对平衡状态,但在各病理因素影响下,却极易出现急性肾损伤,不仅会造成水电解质紊乱和酸碱失衡,增加短期的不良预后,还会影响生后肾脏结构功能的进一步成熟,甚而增加远期慢性肾脏病的风险。     

Eosinophilic gastroenteritis in a patient with Albright's hereditary osteodystrophy

Eosinophilic gastroenteritis is an uncommon chronic disease, of unknown cause, characterized by eosinophilic infiltration of the gastrointestinal tract, which is usually associated with peripheral blood eosinophilia. The symptoms of this complex disorder are variable, and frequently include abdominal pain, nausea, diarrhea, protein losing enteropathy and malabsorption. In general, patients can be successfully treated with corticosteroids, but relapses are common. We present the first case of a 6-year-old boy with Albright's hereditary osteodystrophy (Pseudohypoparathyroidism Ia) associated with eosinophilic gastroenteritis. Alternatives to traditional treatment with corticosteroids are discussed.