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 kidney injury (AKI) secondary to near-drowning is rarely described and poorly understood. Only few cases of severe isolated AKI resulting from near-drowning exist in the literature. We report a case of near-drowning who developed to isolated AKI due to acute tubular necrosis (ATN) requiring dialysis. A 21-yr-old man who recovered from near-drowning in freshwater 3 days earlier was admitted to our hospital with anuria and elevated level of serum creatinine. He needed five sessions of hemodialysis and then renal function recovered spontaneously. Renal biopsy confirmed ATN. We review the existing literature on near-drowning-induced AKI and discuss the possible pathogenesis.
Acute Kidney Injury/*diagnosis/*etiology ; Anuria/etiology ; Creatinine/blood ; Humans ; Kidney Tubular Necrosis, Acute/etiology/pathology ; Male ; Near Drowning/*complications ; Renal Dialysis ; Young Adult

Acute kidney injury (AKI), associated with significant morbidity and mortality, is widely known to involve epithelial apoptosis, excessive inflammation, and fibrosis in response to ischemia or reperfusion injury, which results in either chronic pathological changes or death. Therefore, it is imperative that investigations are conducted in order to find effective, early diagnoses, and therapeutic targets needed to help prevent and treat AKI. However, the mechanisms modulating the pathogenesis of AKI still remain largely undetermined. MicroRNAs (miRNAs), small non-coding RNA molecules, play an important role in several fundamental biological and pathological processes by a post transcriptional regulatory function of gene expression. MicroRNA-21 (miR-21) is a recently identified, typical miRNA that is functional as a regulator known to be involved in apoptosis as well as inflammatory and fibrotic signaling pathways in AKI. As a result, miR-21 is now considered a novel biomarker when diagnosing and treating AKI. This article reviews the correlative literature and research progress regarding the roles of miR-21 in AKI.
Acute Kidney Injury ; diagnosis ; drug therapy ; genetics ; pathology ; Animals ; Apoptosis ; Biomarkers ; metabolism ; Humans ; MicroRNAs ; genetics ; metabolism ; Molecular Targeted Therapy

BACKGROUNDInfants in some areas of China developed urinary lithiasis after being fed with powdered milk that was tainted with melamine in 2008 and very small proportion of the infants developed acute renal failure caused by urinary tract calculus obstruction. The aim of this article was to summarize clinical characteristics, diagnosis and treatment of infants with urinary calculus and acute renal failure developed after being fed with melamine tainted formula milk.

METHODSData of infant patients with urinary calculus and acute renal failure due to melamine tainted formula milk admitted to the Beijing Children's Hospital Affiliated to the Capital Medical University and the Xuzhou Children's Hospital in 2008 were used to analyze the epidemiological characteristics, clinical manifestations, imaging features as well as effects of 4 types of therapies.

RESULTSAll the 34 infants with urinary calculus were complicated with acute renal failure, their blood urea nitrogen (BUN) was (24.1+/-8.2) mmol/L and creatinine (Cr) was (384.2+/-201.2) micromol/L. The chemical analysis on the urinary calculus sampled from 15 of the infants showed that the calculus contained melamine and acidum uricum. The time needed for the four types of therapies for returning Cr to normal was (3.5+/-1.9) days for cystoscopy group, (2.7+/-1.1) days for lithotomy group, (3.8+/-2.3) days for dialysis group, and (2.7+/-1.6) days for medical treatment group, which had no statistically significant difference (P=0.508). Renal failure of all the 34 infants was relieved within 1 to 7 days, averaging (3.00+/-1.78) days.

CONCLUSIONSMelamine tainted formula milk may cause urinary calculus and obstructive acute renal failure. It is suggested that firstly the patients with urinary calculus complicated with acute renal failure should be treated with dialysis or medication to correct electrolyte disturbance, in particular hyperkalemia, and then relieve the obstruction with available medical and surgical methods as soon as possible. It was observed that the short-term prognosis was satisfactory.

Acute Kidney Injury ; diagnosis ; etiology ; pathology ; therapy ; Child, Preschool ; Cystoscopy ; Female ; Humans ; Infant ; Male ; Peritoneal Dialysis ; Retrospective Studies ; Treatment Outcome ; Triazines ; poisoning ; Urinary Calculi ; complications ; diagnosis ; pathology ; therapy

We have recently identified a new clinical syndrome in patients receiving warfarin for anticoagulation therapy. This syndrome has been named warfarin-related nephropathy (WRN), and patients with chronic kidney disease (CKD) appear to be particularly susceptible. WRN is defined as an acute increase in international normalized ratio (INR) to > 3.0, followed by evidence of acute kidney injury (AKI) within 1 week of the INR increase. AKI was defined as a sustained increase in serum creatinine of greater than or equal to 0.3 mg/dL. The AKI cannot be explained by any other factors, and the kidney biopsy demonstrates extensive glomerular hemorrhage with tubular obstruction by red blood cells (RBCs). Beyond AKI, WRN is a significant risk factor for mortality within the first 2 months of diagnosis and it accelerates the progression of CKD. We demonstrated that 5/6 nephrectomy in rats is a suitable experimental model to study WRN. Animals treated with warfarin showed an increase in serum creatinine and morphologic findings in the kidney similar to those in humans with WRN. Our recent evidence suggests that novel oral anticoagulants may induce AKI. Diagnosis of WRN may be challenging for a renal pathologist. A few cases with suspected WRN and pathologic considerations are described.
Acute Kidney Injury* ; Animals ; Anticoagulants* ; Biopsy ; Creatinine ; Diagnosis ; Erythrocytes ; Hemorrhage ; Humans ; International Normalized Ratio ; Kidney ; Models, Theoretical ; Mortality ; Nephrectomy ; Pathology* ; Rats ; Renal Insufficiency, Chronic ; Risk Factors ; Warfarin

Acute Kidney Injury ; blood ; diagnosis ; etiology ; Child, Preschool ; Humans ; Hyperuricemia ; blood ; complications ; Kidney ; pathology ; Magnetic Resonance Imaging ; Male ; Uric Acid ; blood

Hepatitis A virus (HAV) infection is generally a self-limited disease, but the infection in adults can be serious, to be often complicated by acute kidney injury (AKI) and rarely by virus-associated hemophagocytic syndrome (VAHS). Our patient, a 48-yr-old man, was diagnosed with HAV infection complicated by dialysis-dependent AKI. His kidney biopsy showed acute tubulointerstitial nephritis with massive infiltration of activated macrophages and T cells, and he progressively demonstrated features of VAHS. With hemodialysis and steroid treatment, he was successfully recovered.
Acute Disease ; Acute Kidney Injury/diagnosis/therapy ; Antibodies, Viral/analysis ; Hepatitis A/complications/*diagnosis/immunology ; Humans ; Lymphohistiocytosis, Hemophagocytic/complications/*diagnosis/pathology ; Macrophages/immunology ; Male ; Middle Aged ; Nephritis, Interstitial/complications/*diagnosis ; Renal Dialysis ; T-Lymphocytes/immunology

The traditional diagnostic criteria of renal dysfunction in cirrhosis are a 50% increase in serum creatinine (SCr) with a final value above 1.5 mg/dL. This means that patients with milder degrees of renal dysfunction are not being diagnosed, and therefore not offered timely treatment. The International Ascites Club in 2015 adapted the term acute kidney injury (AKI) to represent acute renal dysfunction in cirrhosis, and defined it by an increase in SCr of 0.3 mg/dL (26.4 µmoL/L) in <48 hours, or a 50% increase in SCr from a baseline within ≤3 months. The severity of AKI is described by stages, with stage 1 represented by these minimal changes, while stages 2 and 3 AKI by 2-fold and 3-fold increases in SCr respectively. Hepatorenal syndrome (HRS), renamed AKI-HRS, is defined by stage 2 or 3 AKI that fulfils all other diagnostic criteria of HRS. Various studies in the past few years have indicated that these new diagnostic criteria are valid in the prediction of prognosis for patients with cirrhosis and AKI. The future in AKI diagnosis may include further refinements such as inclusion of biomarkers that can identify susceptibility for AKI, differentiating the various prototypes of AKI, or track its progression.
Acute Kidney Injury/complications/*diagnosis/drug therapy/pathology ; Biomarkers/blood ; Creatinine/blood ; Humans ; Liver Cirrhosis/*complications ; Prognosis ; Serum Albumin/therapeutic use ; Severity of Illness Index

Hepatitis A is typically a self-limited acute illness that does not progress to chronic hepatitis. In rare cases, acute hepatitis A can be associated with serious complications (such as fulminant hepatitis or acute kidney injury) and may result in death or liver transplantation. Pure red cell aplasia (PRCA) is a rare hematologic disorder characterized by anemia, reticulocytopenia in the blood, and isolated erythroblastopenia with normal granulopoiesis and megakaryopoiesis in the bone marrow. PRCA is a rare hematopoietic complication of acute viral hepatitis, and few cases associated with hepatitis A virus infection have been reported. Recently, we experienced a case of severe hepatitis A complicated by fulminant hepatitis and acute kidney injury followed by PRCA which showed a favorable response to oral corticosteroids.
Acute Disease ; Acute Kidney Injury/etiology ; Adult ; Anti-Inflammatory Agents/therapeutic use ; Bone Marrow/pathology ; Female ; Hepatitis A/complications/*diagnosis ; Humans ; Prednisone/therapeutic use ; Red-Cell Aplasia, Pure/complications/*diagnosis/drug therapy

Paraquat (PQ) has known negative human health effects, but continues to be commonly used worldwide as a herbicide. Our clinical data shows that the main prognostic factor is the time required to achieve a negative urine dithionite test. Patient survival is a 100% when the area affected by ground glass opacity is <20% of the total lung volume on high-resolution computed tomography imaging 7 days post-PQ ingestion. The incidence of acute kidney injury is approximately 50%. The average serum creatinine level reaches its peak around 5 days post-ingestion, and usually normalizes within 3 weeks. We obtain two connecting lines from the highest PQ level for the survivors and the lowest PQ level among the non-survivors at a given time. Patients with a PQ level between these two lines are considered treatable. The following treatment modalities are recommended to preserve kidney function: 1) extracorporeal elimination, 2) intravenous antioxidant administration, 3) diuresis with a fluid, and 4) cytotoxic drugs. In conclusion, this review provides a general overview on the diagnostic procedure and treatment modality of acute PQ intoxication, while focusing on our clinical experience.
Acute Kidney Injury/*diagnosis/pathology/therapy ; Antioxidants/therapeutic use ; Creatinine/blood ; Hemoperfusion ; Herbicides/*poisoning ; Humans ; Iron Chelating Agents/therapeutic use ; Lung Diseases/*diagnosis/pathology/therapy ; Paraquat/blood/*poisoning/urine ; Tomography, X-Ray Computed