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Query: UMLS:C0022672 (acute tubular necrosis)
 2,175 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In most severe cases of strychnine poisoning, the patient dies before reaching the hospital. This report describes the treatment and successful outcome of a patient who had taken a dose of strychnine that would normally be fatal. A 28-y-old man was admitted 2 h after ingestion of 1 to 1.5 g of strychnine. He had a Glasgow Coma Score of 14/15 and was severely agitated and in mild respiratory distress; blood pressure was 90/60 mmHg, pulse 110/min, and peripheral pulses weak. He had generalized hyperactive reflexes and had several generalized tonic-clonic convulsions in the emergency department. Treatment consisted of gastric lavage with water, oral administration of activated charcoal and sorbitol solution, continuous intravenous administration of midazolam and then sodium thiopental, furosemide, sodium bicarbonate and hemodialysis for acute renal failure. His clinical course included respiratory distress, agitation, generalized tonic-clonic convulsions, hyperactivity, oliguria and acute tubular necrosis prior to recovery in 23 days. This patient ingested what would normally be a fatal amount of strychnine, had signs and symptoms of severe toxicity and recovered, suggesting that with aggressive supportive care patients may have favorable outcomes.
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PMID:A case of acute strychnine poisoning. 1508 Feb 7

Although previous reports have attributed acute renal failure (ARF) following cardiovascular surgery to acute tubular necrosis (ATN), little emphasis has been placed on renal failure due to congestive heart failure (CARF). Of 100 cases of ARF studied prospectively over an 18-month period, 36 occurred after open-heart surgery. Nineteen of these cases were associated with heart failure. The remaining 17 had ATN as manifested by high urinary sodium, low urine/plasma creatinine, and abnormal urinary sediment. At the onset of CARF, intravascular volume expansion was universally present, and oliguria with pulmonary edema was common. Urinary chemistries were (mean +/- SD): sodium (mEq/L) 8 +/- 7, U/P creatinine 72 +/- 45, and FENa (%) 0.1 +/- 0.1. Therapy consisted of digoxin, furosemide (F), vasopressors (V), and, when indicated, intraaortic balloon counterpulsation. Survivors of CARF responded more frequently to F and required less V. Ultimately, survival depended upon improvement in cardiac performance. All oliguric ATN patients failed to respond to F. Mortality for the CARF group was 52%. In contrast, 82% of the oliguric ATN group expired, whereas overall ATN mortality was 60%. Cardiogenic acute renal failure is a frequent cause of ARF after open-heart surgery in our institution. It is characterized by prerenal urinary chemistries, has a high mortality, and may be reversible.
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PMID:CARDIOGENIC ACUTE RENAL FAILURE (CARF) FOLLOWING OPEN-HEART SURGERY. 1521 6

A retrospective study was conducted in nine patients with rabies admitted to a hospital of Fortaleza, Brazil. Autopsy was performed in all cases. The ages ranged from three to 81 years and six were males. They all were bitten by dogs. The time between the accident and the hospital admission ranged from 20 to 120 days (mean 45 +/- 34 days). The time until death ranged from one to nine days (mean 3.3 +/- 5.5 days). The signs and symptoms presented were fever, hydrophobia, aerophobia, agitation, disorientation, dyspnea, sialorrhea, vomiting, oliguria, sore throat, pain and hypoesthesia in the site of the bite, headache, syncope, cough, hematemesis, mydriasis, hematuria, constipation, cervical pain and priapism. In three out of six patients, there was evidence of acute renal failure, defined as serum creatinine > or = 1.4 mg/dL. The post-mortem findings in the kidneys were mild to moderate glomerular congestion and mild to intense peritubular capillary congestion. Acute tubular necrosis was seen in only two cases. This study shows some evidence of renal involvement in rabies. Histopathologic findings are nonspecific, so hemodynamic instability, caused by autonomic dysfunction, hydrophobia and dehydration must be responsible for acute renal failure in rabies.
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PMID:Renal involvement in human rabies: clinical manifestations and autopsy findings of nine cases from northeast of Brazil. 1655 20

Acute renal failure (ARF) incidence varies depending on whether the intensive care unit only or also general and specialist medicine departments are considered. In some cases, however, such as after major cardiosurgical operations, ARF can occur in up to 30% of patients. Most of ARFs in intensive care units are secondary to acute tubular necrosis occurring because of a multi-organ dysfunction syndrome. Factors most often associated with acute renal damage are: advanced age, volume depletion, arterial hypotension, massive bleeding, and sepsis. ARF often leads to complications for the following pathologies: serious liver disease, pancreatitis, pre-existing renal dysfunction, great burns, and cardiosurgical and vascular operations on large vessels. Among the so-called 'iatrogenic factors', contrast media and aminoglycosides are definitely the main cause of a rapid deterioration of renal function. Mortality is low for the isolated forms of ARF,whereas it peaks to 0-80% in multi-organ failures where co-existing pathologies often dominate. The mortality rate over the past 20 years has not changed, although pharmacological supports and especially dialysis instruments have improved. Patients are now older and older, affected by multiple pathologies and with poor recovery capacity. Mortality is higher among elderly patients, while toxic forms (from contrast media or from myoglobinuria) result generally in better outcomes. Patients with acute renal damage and oliguria have a worse prognosis than non-oliguric patients. Finally, some unfavorable prognostic factors include the prolonged use of high dose inotropic drugs, mechanical ventilation, cardiac failure and a septic state.
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PMID:[Epidemiology of acute renal failure]. 1706 24

A young man presented to the emergency department with mental status changes, severe metabolic acidosis, and oliguria. Acute ethylene glycol intoxication was diagnosed. The patient suffered clinical brain death three days after admission despite intensive care and continuous hemodiafiltration. The patient died one month after admission. Autopsy revealed acute tubular necrosis of the kidneys with significant calcium oxalate depositions. The brain was markedly softening and with chronic meningoencephalitis and dural sinus thrombosis. We considered that the amount and the persistence of the calcium oxalate deposition in the kidney may afford a best clue to the postmortem diagnosis of ethylene glycol poisoning even in the chronic stage.
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PMID:Brain death with calcium oxalate deposition in the kidney: clue to the diagnosis of ethylene glycol poisoning. 1769 92

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

Escherichia coli strains producing Shiga toxins (Stxs) colonize the lower gastrointestinal tract and cause watery diarrhea, hemorrhagic colitis, and hemolytic-uremic syndrome (HUS). HUS is characterized by hemolytic anemia, thrombocytopenia, and acute renal failure. Oliguria associated with acute tubular necrosis and microangiopathic thrombosis has been reported as the most common cause of renal failure in Argentinean children. Our study was undertaken to obtain a model of HUS in rats that was similar to the clinical and renal histopathology findings described in humans. Rats were intraperitoneally inoculated with culture supernatant from recombinant E. coli expressing Stx2. Glomerular filtrate volume evaluated from clearance of creatinine resulted in a progressive reduction (from 53% at 24 h to 90% at 48 h). Urine volume increased significantly at 24 h but returned to normal levels at 48 h. Evidence of thrombocytopenia, anemia and leukocytosis was documented. Macroscopic analysis revealed a hyperemic peritoneal face with intestinal water accumulation. The kidneys were friable and congestive. Histopathological analysis showed glomerular and tubular necrosis as well as microangiopathic thrombosis. Our findings indicated vascular damage and kidney lesions similar to those described in humans with HUS.
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PMID:Development of an experimental hemolytic uremic syndrome in rats. 1825 62

Diagnosis and classification of acute pathology in the kidney are major clinical problems. Azotemia and oliguria represent not only disease but normal responses of the kidney to extracellular volume depletion or decreased renal blood flow. Changes in urine output and glomerular filtration rate are therefore neither necessary nor sufficient for the diagnosis of renal pathology. However, no simple alternative for the diagnosis currently exists. By examining both glomerular and tubular function, clinicians routinely make inferences not only on the presence of renal dysfunction but also on its cause. However, pure prerenal physiology is unusual in hospitalized patients, and its effects are not necessary benign. Sepsis, the most common condition associated with acute renal failure in the intensive care unit, may alter renal function without any characteristic changes in urine indices, and classification of these abnormalities as prerenal will undoubtedly lead to incorrect management decisions. The clinical syndrome known as acute tubular necrosis does not actually manifest the morphologic changes that the name implies. A precise biochemical definition of acute renal failure has never been proposed, and until recently, there has been no consensus on the diagnostic criteria or clinical definition. Depending on the definition used, acute renal failure has been reported to affect from 1% to 25% of intensive care unit patients and has led to mortality rates ranging from 15% to 60%. From this chaos, two principles emerged: first, the need for a standard definition and, second, the need to classify the severity of the syndrome rather than only consider its most severe form. The RIFLE criteria were developed to achieve these goals, and the term acute kidney injury has been proposed to encompass the entire spectrum of the syndrome, from minor changes in renal function to requirement for renal replacement therapy. Thus, acute kidney injury is not acute tubular necrosis, nor is it renal failure. Small changes in kidney function in hospitalized patients are important and are associated with significant changes in short-term and possibly long-term outcomes. The RIFLE criteria provide a uniform definition of acute kidney injury and have now been validated in numerous studies.
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PMID:Acute kidney injury. 1838 85

Leptospirosis is a worldwide zoonosis. Typically, patients are young men, although children can be affected. In children, this disease causes mainly alterations of sensorium. Acute renal failure and jaundice (Weil's syndrome) are less common in children than in adults. The main renal histological findings are acute interstitial nephritis and acute tubular necrosis. Acute renal failure is characterized by hypokalemia and nonoliguria. Many factors are involved in its physiopathology: hypotension, hypovolemia, rhabdomyolysis, hyperbilirubinemia, and, primarily, the direct action of leptospiral proteins. Antibiotic administration (especially early administration) reduces length of hospitalization and leptospiruria. For children, even late antibiotic treatment has been shown to reduce the extent of acute renal failure and thrombocytopenia. Although the best method of dialysis is not yet established, early and intensive dialysis can decrease mortality. Mortality in patients with acute renal failure is approximately 15-20% in association with the presence of oliguria, higher levels of creatinine, and older age. Functional recovery is fast and complete; however, abnormal urinary concentration can persist.
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PMID:The kidney in leptospirosis. 1844 81

There are few studies on the relationship between the morphology of acute tubular necrosis (ATN) in native kidneys and late functional recovery. Eighteen patients with acute renal failure (ARF) who had undergone renal biopsy were studied. All had the histological diagnosis of ATN and were followed for at least six months. Clinical characteristics of ARF were analyzed, and histological features were semi-quantitatively evaluated (tubular atrophy, interstitial inflammatory infiltrate, interstitial fibrosis, and ATN). According to the maximal GFR achieved during the follow-up, patients were divided into two groups: complete recovery (GFR >or= 90 mL/min/1.73 m(2)) and partial recovery (GFR < 90 mL/min/1.73 m(2)). Only 39% of the patients achieved complete recovery. Patients with partial recovery achieved their maximal GFR (63 +/- 9 mL/min/1.73 m(2)) 37 +/- 14 months after ARF, a period of time similar to those patients with complete recovery (i.e., 54 +/- 22 months). Patients with partial recovery had more severe ARF: oliguria was more frequent (90 versus 17%, p < 0.01), and they had higher peak creatinine (13.85 +/- 1.12 versus 8.95 +/- 1.30 mg/dL, p = 0.01), and longer hospitalization (45 +/- 7 versus 20 +/- 4 days, p = 0.03). No single histological parameter was associated with partial recovery, but the sum of all was when expressed as an injury index [4.00 (2.73-5.45) versus 2.00 (1.25-3.31), p < 0.05]. In conclusion, among patients with atypical ATN course, those with more severe ARF and tubule-interstitial lesions are more prone to partial recovery.
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PMID:Histological features of acute tubular necrosis in native kidneys and long-term renal function. 1870 14


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