Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022672 (acute tubular necrosis)
 2,175 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A Chinese patient with paroxysmal nocturnal hemoglobinuria (PNH) developed acute nonoliguric renal failure with intercurrent urinary tract infection and hemolysis. There was no evidence of renal vein thrombosis. Renal biopsy showed features of acute tubular necrosis (ATN) and hemosiderosis. Magnetic resonance imaging (MRI) showed characteristic features of renal hemosiderosis. The patient was stabilized with temporary hemodialysis and intravenous fluid. The renal function fully recovered 3 weeks later. We review the literature and summarize the clinical features of this disease entity. To our knowledge, this case is the first to report such disorder with thorough investigation including concomitant diagnostic MRI imaging and renal biopsy.
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PMID:Reversible renal failure in paroxysmal nocturnal hemoglobinuria. 1115 3

Paroxysmal nocturnal hemoglobinuria (PNH) is an acquired disorder characterized by low-grade, chronic hemolytic anemia accompanied by either thrombocytopenia or leucopenia. Kidney involvement is usually benign and secondary to chronic tubular deposition of hemosiderin. Acute renal failure may occur in association with a hemolytic crisis. We report the case of a 70-year-old Caucasian woman with PNH who developed reversible acute renal failure requiring hemodialysis following a gastointestinal illness. Renal biopsy demonstrated acute tubular necrosis with considerable hemosiderin deposition, but no evidence of vascular thrombosis.
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PMID:Acute renal failure in a patient with paroxysmal nocturnal hemoglobinuria. 1152 96

Hemoglobin and myoglobin heme pigments and iron have acute and chronic nephrotoxic effects, which are often associated with massive hemolysis and rhabdomyolysis. We report a patient with a myelodysplastic syndrome and paroxysmal nocturnal hemoglobinuria phenotype who developed an acute renal failure after a severe haemolytic crisis. There was not evidence of renal vascular pathology, urinary tract obstruction or prerenal factors. Renal biopsy showed features of acute tubular necrosis, with extended iron deposits in tubule cell cytoplasm and tubulo-interstitial fibrosis and atrophy. The patient was oliguric requiring hemodialisys during three weeks, recovering renal function on the fourth week after admission. This case underlines the nephrotoxic role of heme pigment and iron, and possible pathophysiologic mechanisms involved in acute and chronic toxicity of both agents are reviewed.
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PMID:[Acute renal failure in a patient with myelodysplastic syndrome and paroxysmal nocturnal hemoglobinuria phenotype]. 1521 70

A 60-year-old man, who had been diagnosed as having paroxysmal nocturnal hemoglobinuria(PNH) in 1994, was admitted to our hospital with general fatigue, and dark urine after a common-cold in January 2001. In the peripheral blood, the red blood cell count was 136 x 10(4)/microl, hemoglobin 4.0 g/dl and hematocrit 12.4%. The serum creatinine level was 9.9 mg/dl. Kidney biopsy revealed focal and segmental proliferation of mesangial cells, mesangial matrix expansion, acute tubular necrosis, interstitial fibrosis and hemosiderine deposits in the tubular epithelial cells confirmed by Berlin-blue staining. Immunofluorescence microscopy showed IgA and C3 deposition in the mesangium. Electron microscopy revealed electron dense deposits in the mesangial area and heavy electron-dense hemosiderin pigments in proximal tubular epithelial cells. After the transfusion of six units of washed red blood cells and two sessions of hemodialysis, the renal function returned to the levels before admission.
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PMID:[Case of paroxysmal nocturnal hemoglobinuria complicated with IgA nephropathy who developed acute renal failure induced by hemolytic crisis]. 1613 Apr 10

Acute renal failure is a known complication during hemolytic crisis in paroxysmal nocturnal hemoglobinuria (PNH). However, chronic renal failure is rare despite the well-known spectacular hemosiderosis of the kidneys due to chronic hemolysis. Here, we report about a 74-year-old man with PNH who developed acute on chronic renal failure after an episode of intercurrent urinary tract infection and subsequent hemolytic crisis. Mild chronic hemolysis, well-documented over the past decade, had long been considered the cause of a constantly declining glomerular filtration rate. Accordingly, magnetic resonance imaging during admission demonstrated marked siderosis of both kidneys, supporting the hypothesis that chronic renal failure (CRF) was likewise related to PNH. However, a renal biopsy revealed acute tubular necrosis and distinct renal siderosis, as expected. Additionally, tubulointerstitial injury and global glomerular sclerosis, best classified as arterionephrosclerosis, were present. In retrospect, these findings were explained by a 15-year history of hypertension and a 4-year medication with cyclosporine. Careful diagnostic workup including a renal biopsy is mandatory, given a misleadingly suggestive correlation between chronic hemolysis and CRF. Chronic renal failure in PNH is a diagnosis of exclusion, even if radiologic evidence of heavy siderosis draws off the physician's attention.
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PMID:A blue kidney--chronic renal failure as a consequence of siderosis in paroxysmal nocturnal hemoglobinuria? 1699 44

Acute renal failure (ARF) is one of the renal expressions in patients with aplastic anemia (AA)-paroxysmal nocturnal hemoglobinuria (PNH) syndrome following hemolytic crisis. We report the case of an AA patient who experienced recurrent episodes of ARF, in association with evidence of PNH. A 46-year-old woman with AA was admitted because of oliguria and dark urine following a urinary tract infection (UTI) caused by Candida. PNH with ARF complication was diagnosed. Hemodialysis treatment was performed nine times and her renal function recovered. However, she suffered from recurrent hemoglobinuria and acute deterioration of renal function 4 months later. The renal biopsy showed features of acute tubular necrosis, deposition of hemosiderin and positive urate stain in the proximal tubular cells, without vascular thrombosis. The patient received management by adequate hydration, diuretics and alkalization. Her renal function recovered completely. This case report shows an AA patient experiencing recurrent episodes of hemoglobinuric ARF within a short period and achieving complete recovery of renal function after hemodialysis and suitable supportive treatment. In conclusion, AA might evolve into PNH and become complicated with presentation of severe ARF. It may occur with precipitating episodes, such as the UTI in this case. Early recognition of hemoglobinuric complications and prompt treatment for precipitating disease and ARF are important to prevent progression to an irreversible adverse renal outcome.
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PMID:Recurrent acute renal failure in a patient with aplastic anemia-paroxysmal nocturnal hemoglobinuria syndrome: a case report. 1805 7

The authors report a 57-year-old male patient who presented with diarrhea, darkened urine, jaundice and increased blood urea nitrogen and creatinine. Initially, his symptoms, which included hemolytic anemia, acute renal failure and low platelet count, seemed to be caused by renal injuries associated with thrombotic microangiopathy, hemolytic-uremic syndrome in particular. However, a renal biopsy indicated acute tubular necrosis and hemosiderin deposition. A CD55 and CD59 assay, Ham test and sugar-water hemolysis test confirmed the diagnosis of paroxysmal nocturnal hemoglobinuria. After fluid infusion, diuresis and urine alkalization, the patient gradually regained nearly normal renal function. This case illustrates that paroxysmal nocturnal hemoglobinuria may present with acute kidney injury when hemolysis, diarrhea and hemosiderin deposits in the renal tubular epithelial cells and renal tubules are present. Early diagnosis and treatment is crucial to prevent disease progression and irreversible chronic renal failure.
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PMID:Reversible acute kidney injury caused by paroxysmal nocturnal hemoglobinuria. 2094 98

Acute renal failure (ARF) is a well-recognized complication of paroxysmal nocturnal hemoglobinuria (PNH). The predominant mechanism is intravascular hemolysis resulting in massive hemoglobinuria ARF. We report a case of acute tubular necrosis (ATN) developed in the absence of overwhelming evidence of intravascular hemolysis in a 21-year-old man with anemia, who was eventually diagnosed to have PNH. The patient presented with rapidly deteriorating renal functions in the background of iron deficiency anemia, which was attributed to reflux esophagitis. There was no clinical or laboratory evidence of intravascular hemolysis. Renal biopsy revealed ATN with deposition of hemosiderin in the proximal tubular epithelial cells. Diagnosis of PNH was confirmed with a positive Ham's test and flow cytometry. Our case emphasizes the need to consider ATN as a possible cause for ARF in patients suspected to have PNH even in the absence of overwhelming evidence of intravascular hemolysis.
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PMID:Acute tubular necrosis in a patient with paroxysmal nocturnal hemoglobinuria. 2335 3

Renal involvement in paroxysmal nocturnal hemoglobinuria (PNH) is not usually apparent but in cases with clinical involvement varies from reversible acute dysfunction to chronic irreversible damage. Early diagnosis and treatment is crucial to prevent disease progression and irreversible chronic kidney disease (CKD). The ultimate outcome of CKD in many patients is the need for renal replacement therapy, which necessitates ever-growing dialysis and transplantation programs, thereby imposing a significant economic burden on the healthcare system. In a third-world country like Pakistan, increased burden due to CKD can be very hard on families. Doctor visits, hospitalization, and dialysis are all out-of-pocket expenses, therefore prevention, early detection, and timely intervention are the only cost-effective strategies. We report a case of acute kidney injury (AKI) due to PNH. This case shows AKI as one of the complications of PNH which may have a clinical course like acute tubular necrosis (ATN). This could be due to ATN or AKI superimposed on CKD due to hemosiderin deposits in the renal tubular epithelial cells. Our patient was dialyzed initially and discharged with a permanent catheter in place with advice to continue dialysis three times a week. He required dialysis for 1 week then started producing urine. His subsequent outpatient visits showed improved renal function. The permanent catheter was removed and maintenance dialysis was stopped. Here, we briefly review the literature on renal involvement in PNH, treatment options for PNH and pigment-induced nephropathy followed by a question-and-answer session at the clinicopathological conference held on March 4, 2011, at Sindh Institute of Urology and Transplantation in Karachi, Pakistan.
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PMID:Renal involvement in paroxysmal nocturnal hemoglobinuria. 2375 25

Kidney failure secondary to renal hemosiderosis has been reported in diseases with intravascular hemolysis, like paroxysmal nocturnal hemoglobinuria, and valvular heart diseases. We present here a case of hemosiderin induced acute tubular necrosis secondary to intravascular hemolysis from Clostridium difficile infection with possible role of supratherapeutic INR. We discuss the pathophysiology, causes, and prognosis of acute tubular injury from hemosiderosis.
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PMID:A Rare Cause of Reversible Renal Hemosiderosis. 2649 80


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