BACKGROUND/AIMS: A diagnosis of hepatorenal syndrome (HRS) is based on a differential evaluation of acute kidney injury (AKI), which may aggravate the clinical course. This study assessed the clinical significance of the urinary neutrophil gelatinase-associated lipocalin (u-NGAL) levels in a differential diagnosis of AKI in patients with liver cirrhosis (LC).METHODS: Patients with LC who developed AKI were enrolled prospectively. Clinically, patients with AKI were classified into prerenal azotemia (PRA), HRS, and acute tubular necrosis (ATN) groups.RESULTS: Fifty-five patients (male, 74.5%) with LC who exhibited AKI upon admission were enrolled; 28, 9, and 18 patients were included in the PRA, HRS, and ATN groups, respectively. The baseline model for end-stage liver disease (MELD) scores was similar in the subgroups. The median event creatinine level, measured at the time of the AKI diagnosis, was similar in the HRS and ATN subgroups. On the other hand, the median event u-NGAL level differed significantly between the three subgroups (PRA, HRS, and ATN: 37 vs. 134 vs. 2,625 ng/mL, p=0.003). In particular, the median u-NGAL level of the HRS group was clearly different from those of the PRA (p<0.001) and ATN (p<0.001) groups. Multivariable analysis revealed the natural logarithm of the u-NGAL level (hazard ratio [HR] 1.77, p=0.031) and the MELD score (HR 1.17, p=0.027) to be independent prognostic factors for in-hospital mortality in patients with LC and AKI.CONCLUSIONS: The median u-NGAL level differentiated HRS from ATN and served as a clinical indicator of in-hospital mortality for patients with LC and AKI.
Acute Kidney Injury ; Azotemia ; Creatinine ; Diagnosis ; Diagnosis, Differential ; Hand ; Hepatorenal Syndrome ; Hospital Mortality ; Humans ; Kidney Tubular Necrosis, Acute ; Lipocalins ; Liver Cirrhosis ; Liver Diseases ; Liver ; Necrosis ; Neutrophils ; Prospective Studies

BACKGROUND/AIMS: A diagnosis of hepatorenal syndrome (HRS) is based on a differential evaluation of acute kidney injury (AKI), which may aggravate the clinical course. This study assessed the clinical significance of the urinary neutrophil gelatinase-associated lipocalin (u-NGAL) levels in a differential diagnosis of AKI in patients with liver cirrhosis (LC). METHODS: Patients with LC who developed AKI were enrolled prospectively. Clinically, patients with AKI were classified into prerenal azotemia (PRA), HRS, and acute tubular necrosis (ATN) groups. RESULTS: Fifty-five patients (male, 74.5%) with LC who exhibited AKI upon admission were enrolled; 28, 9, and 18 patients were included in the PRA, HRS, and ATN groups, respectively. The baseline model for end-stage liver disease (MELD) scores was similar in the subgroups. The median event creatinine level, measured at the time of the AKI diagnosis, was similar in the HRS and ATN subgroups. On the other hand, the median event u-NGAL level differed significantly between the three subgroups (PRA, HRS, and ATN: 37 vs. 134 vs. 2,625 ng/mL, p=0.003). In particular, the median u-NGAL level of the HRS group was clearly different from those of the PRA (p<0.001) and ATN (p<0.001) groups. Multivariable analysis revealed the natural logarithm of the u-NGAL level (hazard ratio [HR] 1.77, p=0.031) and the MELD score (HR 1.17, p=0.027) to be independent prognostic factors for in-hospital mortality in patients with LC and AKI. CONCLUSIONS: The median u-NGAL level differentiated HRS from ATN and served as a clinical indicator of in-hospital mortality for patients with LC and AKI.
Acute Kidney Injury ; Azotemia ; Creatinine ; Diagnosis ; Diagnosis, Differential ; Hand ; Hepatorenal Syndrome ; Hospital Mortality ; Humans ; Kidney Tubular Necrosis, Acute ; Lipocalins ; Liver Cirrhosis ; Liver Diseases ; Liver ; Necrosis ; Neutrophils ; Prospective Studies

Drug rash with eosinophilia and systemic symptoms (DRESS) syndrome is a rare and potentially fatal condition characterized by skin rash, fever, eosinophilia, and multiorgan involvement. Various drugs may be associated with this syndrome including carbamazepine, allopurinol, and sulfasalazine. Renal involvement in DRESS syndrome most commonly presents as acute kidney injury due to interstitial nephritis. An 11-year-old boy was referred to the Children's Hospital of Pusan National University because of persistent fever, rash, abdominal distension, generalized edema, lymphadenopathy, and eosinophilia. He previously received vancomycin and ceftriaxone for 10 days at another hospital. He developed acute kidney injury with nephrotic range proteinuria and hypocomplementemia. A subsequent renal biopsy indicated the presence of acute tubular necrosis (ATN) and late exudative phase of postinfectious glomerulonephritis (PIGN). Systemic symptoms and renal function improved with corticosteroid therapy after the discontinuation of vancomycin. Here, we describe a biopsy-proven case of severe ATN that manifested as a part of vancomycin-induced DRESS syndrome with coincident PIGN. It is important for clinicians to be aware of this syndrome due to its severity and potentially fatal nature.
Acute Kidney Injury ; Allopurinol ; Biopsy ; Busan ; Carbamazepine ; Ceftriaxone ; Child ; Drug Hypersensitivity Syndrome ; Edema ; Eosinophilia* ; Exanthema* ; Fever ; Glomerulonephritis* ; Humans ; Kidney Tubular Necrosis, Acute ; Lymphatic Diseases ; Male ; Necrosis* ; Nephritis, Interstitial ; Proteinuria ; Sulfasalazine ; Vancomycin*

Drug rash with eosinophilia and systemic symptoms (DRESS) syndrome is a rare and potentially fatal condition characterized by skin rash, fever, eosinophilia, and multiorgan involvement. Various drugs may be associated with this syndrome including carbamazepine, allopurinol, and sulfasalazine. Renal involvement in DRESS syndrome most commonly presents as acute kidney injury due to interstitial nephritis. An 11-year-old boy was referred to the Children's Hospital of Pusan National University because of persistent fever, rash, abdominal distension, generalized edema, lymphadenopathy, and eosinophilia. He previously received vancomycin and ceftriaxone for 10 days at another hospital. He developed acute kidney injury with nephrotic range proteinuria and hypocomplementemia. A subsequent renal biopsy indicated the presence of acute tubular necrosis (ATN) and late exudative phase of postinfectious glomerulonephritis (PIGN). Systemic symptoms and renal function improved with corticosteroid therapy after the discontinuation of vancomycin. Here, we describe a biopsy-proven case of severe ATN that manifested as a part of vancomycin-induced DRESS syndrome with coincident PIGN. It is important for clinicians to be aware of this syndrome due to its severity and potentially fatal nature.
Acute Kidney Injury ; Allopurinol ; Biopsy ; Busan ; Carbamazepine ; Ceftriaxone ; Child ; Drug Hypersensitivity Syndrome ; Edema ; Eosinophilia* ; Exanthema* ; Fever ; Glomerulonephritis* ; Humans ; Kidney Tubular Necrosis, Acute ; Lymphatic Diseases ; Male ; Necrosis* ; Nephritis, Interstitial ; Proteinuria ; Sulfasalazine ; Vancomycin*

BACKGROUND/AIMS: The potential physiologic roles of Klotho in acute kidney injury (AKI) have recently been demonstrated in animal models. However, to date, there have been no human studies investigating the expression of renal Klotho in AKI. METHODS: We retrospectively collected biopsy specimens and clinical data of AKI patients between January 2001 and December 2012. Klotho expression was determined by immunohistochemical staining, and the clinical-pathological correlation was examined. RESULTS: Among the 34 patients diagnosed with acute tubular necrosis or acute tubulointerstitial nephritis, 21 patients without chronic histological lesions were included. The mean age was 37.3 +/- 18.5 years and the mean peak creatinine level was 8.2 +/- 5.5 mg/dL. In total, 10 patients (47.6%) received temporary renal replacement therapy (RRT); however, 17 patients (81%) showed functional recovery with creatinine levels of < 1.3 mg/dL after 1 month. The intensity of Klotho expression was scored as a percentage of Klotho-positive area. The renal Klotho score showed a significant negative correlation with the initial or peak creatinine level. When the patients were divided into three groups according to the Klotho score (low, middle, high), the low group had a significantly higher peak creatinine level and a more frequent requirement for RRT. However, the Klotho score was not a significant predictor of renal recovery. CONCLUSIONS: The results demonstrated that renal Klotho expression in humans decreased significantly according to the severity of AKI, regardless of the etiology, and that low expression was associated with a poor short-term outcome.
Acute Kidney Injury/diagnosis/etiology/*metabolism/physiopathology/therapy ; Adolescent ; Adult ; Biomarkers/analysis ; Biopsy ; Down-Regulation ; Female ; Glucuronidase/*analysis ; Humans ; Immunohistochemistry ; Kidney/*chemistry/pathology/physiopathology ; Kidney Tubular Necrosis, Acute/diagnosis/etiology/*metabolism/physiopathology/therapy ; Male ; Middle Aged ; Necrosis ; Predictive Value of Tests ; Recovery of Function ; Renal Replacement Therapy ; Retrospective Studies ; Risk Factors ; Severity of Illness Index ; Time Factors ; Treatment Outcome ; Young Adult

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

Vancomycin has been associated with acute kidney injury, particularly in the concomitant treatment with aminoglycoside or in the presence of other risk factor such as preexisting renal disease, sepsis, or hemodynamic instability. Vancomycin-related nephrotoxicity typically manifests as acute tubulointerstitial nephritis. Biopsy-proven acute tubular necrosis associated with vancomycin intoxication in the absence of aminoglycoside has been reported only in very few cases. We report a case of biopsy-proven acute tubular necrosis associated with vancomycin intoxication that was treated by continuous venovenous hemodiafiltration. A 28-year-old male without preexisting renal disease received a massive overdose of vancomycin. The plasma vancomycin level was 440.3 microg/mL. Renal biopsy revealed acute tubular necrosis that there is marked thinning of the tubular epithelium with dilatation of the tubular lumens and severe foamy epithelial cell changes in tubules. Continuous venovenous hemodiafiltration resulted in efficient reduction of serum vancomycin levels, which was followed clinically by recovered of renal function.
Acute Kidney Injury ; Adult ; Biopsy ; Dilatation ; Epithelial Cells ; Epithelium ; Hemodiafiltration ; Hemodynamics ; Humans ; Kidney Tubular Necrosis, Acute ; Male ; Necrosis ; Nephritis, Interstitial ; Plasma ; Risk Factors ; Sepsis ; Vancomycin

Aristolochic Acids ; adverse effects ; Drugs, Chinese Herbal ; adverse effects ; Female ; Follow-Up Studies ; Glomerular Filtration Rate ; Humans ; Infant, Newborn ; Kidney Diseases ; chemically induced ; Kidney Tubular Necrosis, Acute ; chemically induced ; Magnoliopsida ; adverse effects ; Male ; Retrospective Studies

OBJECTIVETo summarize the clinical characteristics and prognosis of newborn aristolochic acid nephropathy induced by akebia.

METHODRetrospective analysis of clinical manifestations, therapy and prognosis was made upon data of 3 newborn infants with renal function lesion induced by akebia.

RESULTThree infants who were fed with Chinese herbal medicines containing akebia trifoliate suffered from acute renal failure, renal glomerular and tubular injury, with symptoms of vomiting, diarrhea, and oliguria. Laboratory tests manifested hyperpotassemia, hyponatremia, elevation of serum creatinine and urea nitrogen, and metabolic acidosis. Renal glomerular lesion was mild, presented with proteinuria and increased serum β(2) microglobin. Renal dysfunction was manifested with alkaline urine, glucosuria, positiveness of urine glucose, ketone and aminoaciduria, and increased urine β(2) microglobin excretion. After symptomatic treatment for 3 to 4 weeks, the renal function of these infants recovered. Proteinuria, aminoaciduria and glucosuria turned negative within 5 to 8 months, 3 months to 1 year, and 9 months to 3 years, respectively. Urine pH decreased to 7.0 after 5.0 - 5.5 years. All cases took citric acid mixtures for 5.5 to 6 years. A 12-years follow-up demonstrated that serum creatinine of 3 cases were within normal range during the first 11 years of life, however recent follow-up showed increased serum creatinine of case 1 and case 2, except for serum creatinine of case 3 remained normal. The estimated glomerular filtration rate (eGFR) of all the 3 cases decreased. Among which, eGFR of case 1 and case 2 were lower than 90 [ml/(min·1.73 m(2))], and decreased 1.1 [ml/(min·1.73 m(2))] and 0.6 [ml/(min·1.73 m(2))] per year during recent six years, respectively. No obvious decrease of eGFR was observed in case 3. Blood gas analysis and urine routine were normal, yet blood and urine β(2) microglobin excretion were still high. Urinary N-acetyl-β-D-glucosaminidase increased again after having returned to normal.

CONCLUSIONNewborn aristolochic acid nephropathy induced by akebia might induce acute renal failure and renal tubules injury. Renal function could recover after symptomatic treatment in short-term. Nevertheless, glomerular filtration rate presents a slow descending tendency and renal tubules lesion lasted for many years, which requires a long-term follow-up.

Aristolochic Acids ; adverse effects ; Drugs, Chinese Herbal ; adverse effects ; Female ; Follow-Up Studies ; Glomerular Filtration Rate ; Humans ; Infant, Newborn ; Kidney Diseases ; chemically induced ; Kidney Tubular Necrosis, Acute ; chemically induced ; Magnoliopsida ; adverse effects ; Male ; Retrospective Studies

Drug-induced nephrotoxicity is very common in both new drug development and clinic practice. Various drugs can induce kidney injuries, including tubulointerstitial, glomerular and renal vascular disease. To investigate the mechanism of drug induced nephrotoxicity is important for risk reduction of new drug development, reasonable drug usage, early discovery and effective prevention/treatment of adverse effects in clinics.
Acute Kidney Injury ; chemically induced ; Animals ; Anti-Infective Agents ; adverse effects ; Anti-Inflammatory Agents, Non-Steroidal ; adverse effects ; Antineoplastic Agents ; adverse effects ; Humans ; Immunosuppressive Agents ; adverse effects ; Kidney Diseases ; chemically induced ; Kidney Tubular Necrosis, Acute ; chemically induced ; Nephritis, Interstitial ; chemically induced ; Renal Insufficiency ; chemically induced