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)

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

Marginal donors (advanced age, comorbidities, and so on) provide an increasing contribution to the kidneys used to alleviate the relative organ shortage. We describe the evaluation process and clinical outcome of two kidneys with hemosiderosis used as a double graft. The donor was a 59-year-old hypertensive man, known to have a mechanical mitral valve, who died from a cerebral hemorrhage, with a normal serum creatinine (SCr) and kidneys with normal appearances at sonography. A protocol donor biopsy showed a Karpinsky score of 5 for both kidneys. A double graft was therefore scheduled. The recipient was a 59-year-old man, on dialysis because of chronic glomerulonephritis. HLA match was incompatibility 4/6; immunosuppression was based on steroids, cyclosporine, and mycophenolate mofetil with basiliximab as induction therapy. The grafts showed delayed function with dialysis treatments performed from postoperative day (POD) 1. On POD 2, a magnetic resonance imaging (MRI) study showed the typical appearance of siderosis. Pearl's staining performed on a protocol biopsy confirmed the presence of widespread iron deposits. On POD 5, a recipient renal biopsy showed a superimposed severe acute tubular necrosis. Renal function recovered slowly; SCr at discharge on POD 22 was still 4.2 mg/dL. Two months later, the SCr was 2.2 mg/dL. A second MRI performed at 3 years and 6 months after transplantation confirmed a progressive removal of iron overload while the patient had stable renal function (glomerular filtration rate) of 33 mL/min and SCr: 2.3 mg/dL. We concluded that donors with hemosiderosis should be treated as marginal donors and may be grafted based on a pretransplant biopsy.
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PMID:Donor affected by hemosiderosis: is kidney transplantation possible? A case report. 1867 62