Background: Acute renal failure is a common emergency and esspecial dangerous in the neonatal disease group, account for from 8% to 24% of among total patients to be treated at Intensive Care Unit with the high rate of mortality and complication. The mortality rate due to acute renal failure in neonatal group account for from 24.4% to 66,7%. Objectives: This study aims to learn about the clinical and laboratory characteristics as well as some risks factors of neonatal acute renal failure. Subjects and method:A descriptive, retrospective study was conduct on 64 patients without diagnosed of acute renal failure in control group and other 32 cases of acute renal failure whom treated at Neonatal Department of National Hospital for Pediatric from 1st January 2005 to 31st March 2006. Results:The diagnosis was often done in the 1st week of life and the incidence occurred in boy more than in girl.The average reatininernie\r\n', u'was 251.7\xb112.96 \xb5ol/l, the electrical disorder (in which hyperkaliernie: 78.1%, hyponatrernie: 46.9%), anernie was 18.7%, acidosis netabolique was 71.9%. Risk factors of neonatal acute renal failure: the pre-puerperal eclampsia (p = 0.023, OR=1.23), infection (p <0.001, OR = 9.53), suffocation (p <0.05, OR = 2.489), respiratory failure (p <0.001, OR = 2.489). Conclusion: The clinical signs were hyponurie and anuria, oederne and arterial hypertension.\r\n', u'\r\n', u'
Acute Kidney Injury/ diagnosis ; pathology ; Infant

Acute renal cortical necrosis in which there is destruction of the renal cortex and sparing of the renalmedulla, is a relatively rare cause of acute renal failure. A definitive diagnosis of acute renal corticalnecrosis is based on renal biopsy, but on CT(computed tomography) the rather specific contrast-enhanced appearance of acute renal cortical necrosis has been described. As renal biopsy is not available, contrast-enhanced CT is auseful, noninvasive investigate modality for the early diagnosis of acute renal cortical necrosis. We report the characteristic CT findings of acute renal cortical necrosis in a patient with acute renal failure following anoperation for abdominal trauma.
Acute Kidney Injury ; Biopsy ; Diagnosis ; Early Diagnosis ; Humans ; Kidney Cortex Necrosis* ; Tomography, X-Ray Computed*

Acute kidney injury (AKI) has various triggers, such as ischemia, nephrotoxins, radiocontrast, and bacterial endotoxins. It occurs in about one-third of patients treated in the intensive care unit. There is a higher mortality in patients with AKI compared with their non-AKI counterparts. The diagnosis of AKI usually depends on serum creatinine (SCr) measurements. However, SCr is a delayed and unreliable indicator of AKI. The lack of early biomarkers has limited the ability to manage AKI. Fortunately, understanding the early stress response of the kidney to injury has resulted in the identification and validation of several potential novel urine and blood biomarkers. Recently, new biomarkers of AKI with more favorable characteristics than SCr have been identified and studied in various experimental and clinical settings. This article reviews the most well-established biomarkers of AKI.
Acute Kidney Injury* ; Biomarkers* ; Creatinine ; Diagnosis ; Endotoxins ; Humans ; Intensive Care Units ; Ischemia ; Kidney ; Mortality

Idiopathic renal hypouricemia is a disorder characterized by impaired urate handling in the renal tubules. Most patients with hypouricemia are asymptomatic and are found incidentally, but the condition is known to be at high risk for exercise-induced acute renal failure or urolithiasis. URAT1 protein encoded by SLC22A12 gene has been identified recently as a urate/anion exchanger in the human kidney. Inactivation mutations in SLC22A12 gene have been shown to cause renal idiopathic hypouricemia. We experienced a 3-year-old boy who presented with persistent orange-colored urine since infancy. His urine contained many uric acid crystals, while the serum showed hypouricemia(0.7 mg/dL). The fractional excretion of uric acid was increased to 41.7%. SLC22a12 gene analysis revealed W258X homozygote alleles. Renal hypouricemia must be included in the differential diagnosis of red-urine and SLC22A12 gene analysis is recommended in idiopathic renal hypouricemia.
Acute Kidney Injury ; Alleles ; Child, Preschool ; Diagnosis, Differential ; Homozygote ; Humans ; Kidney ; Male ; Uric Acid ; Urolithiasis

Acute Kidney Injury ; classification ; diagnosis ; Humans ; Kidney ; injuries ; Practice Patterns, Physicians'

Acute Kidney Injury ; diagnosis ; etiology ; Biomarkers ; Early Diagnosis ; Humans ; Liver Cirrhosis ; complications ; diagnosis

A 24-year-old male visited our hospital because of pain in both flanks. His biochemistry profile showed an elevated serum creatinine level and low serum uric acid level. History taking revealed that he had undertaken exercise prior to the acute kidney injury (AKI) event, and he stated that family members had a history of urolithiasis. His renal profile improved after hydration and supportive care during hospitalization. Although the patient was subsequently admitted again due to AKI, his status recovered with similar treatment. Since the diagnosis of the patient was familial renal hypouricemia with exercise-induced AKI, we performed genotyping of SLC22A12, which encodes human urate transporter 1. The diagnosis was confirmed by the detection of a homozygous mutation of W258X. We herein, report a case of familial renal hypouricemia confirmed by genotyping of SLC22A12, and review the relevant literature.
Acute Kidney Injury ; Biochemistry ; Creatinine ; Diagnosis ; Hospitalization ; Humans ; Male ; Uric Acid ; Urolithiasis ; Young Adult

Idiopathic renal hypouricemia is a disorder characterized by impaired urate handling in the renal tubules. This disease usually produces no symptoms, but hematuria, uric acid nephrolithiasis or acute renal failure may develop. A defect in the SLC22A12 gene, which encodes the human urate transporter, is the known major cause of this disorder. We describe a 10-month-old boy with idiopathic renal hypouricemia. He was diagnosed with transient pseudohypoaldosteronism at admission, but hypouricemia was accidentally found through follow-up study. By gene analysis, his diagnosis was confirmed to idiopathic renal hypouricemia. In addition, we report a mutation in the human urate transporter 1 (hURAT1) gene identified in his family.
Acute Kidney Injury ; Diagnosis ; Follow-Up Studies ; Hematuria ; Humans ; Infant ; Male ; Nephrolithiasis ; Pseudohypoaldosteronism ; Uric Acid

Acute renal failure secondary to acute pyelonephritis is developed rarely. But acute pyelonephritis is considered in differential diagnosis of acute renal failure, particularly in elderly patient. Elderly patient showed subtle symptoms or signs of infections and can be missed easily. We experienced two cases of acute renal failure secondary to acute pyelonephritis. In first case, one patient complained fever, chilling and right flank pain for 10 days. Three repeated blood and urine cultures showed E. coli, respectively. At admission serum creatinine showed 2.4 mg/dL and thereafter increased to 4.5 mg/dL, and then decreased to 1.7 mg/dL with antibiotic therapy and hydration at 14 days of admission. In second case, patient complained right flank pain, costovertebral tenderness and urinary difficulty at admission. Two repeated blood culture showed no growth, two repeated urine culture showed > 105 ml/dL of E. coli. At admission serum creatinine level was 2.69 mg/dL and then decreased to 1.7 mg/dL with antibiotic therapy and hydration at 14 days of admission.Acute pyelonephritis should be considered in differential diagnosis of acute renal failure in the elder ages, although this developed rarely. Early recognition and appropriate antibiotic treatment helps recover acute renal failure secondary to acute pyelonephritis.
Acute Kidney Injury* ; Aged ; Creatinine ; Diagnosis, Differential ; Fever ; Flank Pain ; Humans ; Pyelonephritis*

Splenic artery pseudoaneurysm is a rare, but potentially lethal, vascular lesion. The mortality rate may be 75-90%, if the aneurysm ruptures. The risk for rupture of an untreated splenic artery pseudoaneurysm is about 37%. Hence, early diagnosis and prompt surgical intervention are vital to improve survival. However, vague symptoms make early diagnosis difficult. We report here a case of a giant splenic artery pseudoaneurysm presenting with acute kidney injury. The patient had been treated previously for infective endocarditis, and after 4 months, acute kidney injury developed. Imaging studies revealed a giant splenic artery pseudoaneurysm. Splenectomy and distal pancreatectomy were performed. After surgery, renal function was improved.
Acute Kidney Injury ; Aneurysm ; Aneurysm, False ; Early Diagnosis ; Endocarditis ; Humans ; Pancreatectomy ; Rupture ; Splenectomy ; Splenic Artery