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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 retrospective review was conducted of 34 women who underwent emergency peripartum hysterectomy at Hutzel Hospital--Wayne State University, Detroit from January 1986 to December 1991. Indications for hysterectomy were placenta accreta, uterine rupture, uterine atony and unspecified uterine bleeding. The median age of the patients was 33 years (20-40 years). The median hospital stay was 6 days (4-26 days) and median blood loss was 2000 ml (1000-6000 ml), with a median blood replacement of 4 units of packed cells (0-16 RPC). Postoperative complications included urinary tract infection (2), vaginal cuff cellulitis (3), wound infections (2), septic thrombophlebitis (2), acute tubular necrosis (1) and wound hematoma (1). No patient died.
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PMID:[Emergency postpartum hysterectomy. A study over 5 years]. 799 96

After transplantation the kidney is subjected to rejection and other deleterious factors including ischemic damage, acute tubular necrosis, rejection and the use of cyclosporine A (CsA) or FK506. As a result, kidney damage may be generalized with azotemia as its hallmark. These tubular syndromes may cause profound changes in the acid base balance and in the level of certain blood electrolytes and minerals. As a general rule, the renal tubular acidosis (RTA) that appears early following transplantation disappears spontaneously and is predominantly a sequela to acute renal failure. On the other hand, defects occurring in the late posttransplant period are often due to chronic rejection or CsA-induced nephrotoxicity. Secondary hyperparathyroidism, urinary tract infection and obstructive uropathy may also play a contributory urinary role in the pathogenesis of RTA. Chronic RTA following transplantation may interfere with bone metabolism and at times lead to nephrocalcinosis and nephrolithiasis. Therefore, if the condition is prolonged, a supplement of bicarbonate should be given if for no other reason that to protect the skeleton. As these patients may develop either hyperkalemia or hypokalemia, treatment with potassium supplements or potassium-sparing diuretics should be carried out with caution and under constant surveillance. Furthermore, magnesium replacement may be advisable if hypomagnesemia by decreased proximal reabsorption becomes clinically evident. Tubular dysfunction may occur following renal transplantation even in patients with maintained glomerular filtration rate and may induce a number of clinical problems including deterioration of renal graft function.
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PMID:Tubular dysfunction following kidney transplantation. 893 72

Recommendations for the work-up of asymptomatic microscopic hematuria (AMH) often derive from studies including both men and women. This study was undertaken to determine whether that work-up is appropriate for a female patient population. We studied 49 women referred to a urogynecologist for AMH. Patients underwent formal urinalysis, urine culture and cytology, cystoscopy, and either renal ultrasound or intravenous urography (IVU). Highly significant lesions diagnosed were one renal cell carcinoma and one acute tubular necrosis (ATN). Moderately significant lesions included one candidal urinary tract infection. Insignificant lesions included bladder inflammation in 46 patients and renal cysts in 5. Our findings confirm the importance of the work-up of AMH in women. Ultrasound was effective in diagnosing upper tract lesions, with less cost and morbidity than IVU. Larger studies are needed to determine who should be screened, whether the work-up should differ for younger women, possible treatments for benign findings, and appropriate follow-up.
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PMID:Asymptomatic microscopic hematuria in women: case series and brief review. 1061 70

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

Since December 1995, pediatric renal transplant recipients in our unit have received a DMSA scan as soon as possible post-transplant in order to provide a baseline for comparison in the event of subsequent complications. We retrospectively reviewed the case notes and DMSA scans of the 45 patients who underwent a scan within 9 wk of their transplant to see if pre or peri-transplant factors or post-transplant complications were associated with defects on scanning. Forty percentage of scans had defects. The presence of defects was not associated with potential predisposing factors such as patient or donor age, cadaveric or live donation, cold ischemia time, multiple donor vessels, the use of non-heart beating donors, the mean time to scan, the serum creatinine, or the presence of structural renal tract anomalies predisposing to UTI. However, 87% of patients had complications before the scan, including UTI, rejection, acute tubular necrosis, transplant biopsy and drug toxicity. Children with no clinical complications had a significantly reduced risk of a defect (p = 0.035), while biopsy was associated with the presence of defects (p = 0.0034). Twenty patients had one or more follow up DMSA scans: one patient developed a new focal defect. In conclusion, renal transplant defects are frequently found on DMSA scanning even early after transplantation and are non-specifically associated with many different complications.
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PMID:The significance of a defect on DMSA scan in children with renal transplants. 1487 Aug 90

The use of folk remedies is widespread throughout Africa. Acute renal failure (ARF) is one of the most severe, but under-recognized, complications of folk remedy use. This report aims to describe the clinical presentation, outcomes, and nature of renal injury in patients with folk-remedy-associated ARF. Clinical data were evaluated retrospectively in 78 patients with ARF associated with recent folk remedy use. ARF was defined as elevated serum urea and creatinine above the age-appropriate normal ranges, persistent oligoanuria, worsening renal function with time, or need for dialysis. Overall mortality in patients with ARF was 41%. Mortality was higher in adults (45.5%) than in infants (36.6%), in patients with both renal and liver dysfunction (62.5%) than in those with renal dysfunction alone (22.6%), and in HIV-positive (44.4%) versus HIV-negative (34.6%) patients. Vomiting (51.3%) and diarrhea (43.6%) were the most frequent presenting symptoms. Metabolic acidosis (80.8%) and volume depletion (62.8%) were the most frequent clinical findings. The definable causes of ARF were pre-renal (26.9%), acute tubular necrosis (ATN; 26.9%), hepatorenal syndrome (6.4%), urinary tract infection/sepsis (7.7%), and primary renal disorders (7.7%). Twenty-seven patients had concomitant medical conditions unlikely primarily related to folk remedy ingestion. In conclusion, ARF occurring after use of folk remedies in South Africa is associated with significant morbidity and mortality. The most common contributors to ARF in this setting are volume depletion and ATN. Significantly, although a proportion of patients have underlying systemic or renal conditions that may contribute to renal dysfunction, in the majority of patients, folk remedy use appears to be the most likely proximate cause. In view of the large numbers of Africans living abroad, more widespread awareness of this important clinical problem needs to be raised.
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PMID:Acute renal failure associated with the use of traditional folk remedies in South Africa. 1571 33

Glomerular and tubular function of transplanted kidneys were assessed in 46 children aged 15.7 +/- 4.6 yr, 4.2 +/- 2.8 yr after renal transplantation. There were 34 cadaveric, and 12 living-related donors. Twelve patients (26%) had acute episodes (acute tubular necrosis, rejection, or urinary tract infection) during follow-up. All patients were on triple immunosuppression. The mean serum creatinine was 1.5 +/- 0.6 mg/dL. Creatinine clearance (Ccreat) calculated from a 24-h urine collection was 48.0 +/- 19.7 mL/min/1.73 m(2), and that estimated from the Schwartz formula, 61.0 +/- 22.5 mL/min/1.73 m(2). A positive correlation was found between the calculated and estimated clearances. Mean urine concentrating ability was 487 +/- 184 mOsmol/kg, with a value lower than 400 mOsmol/kg in 35% of patients. There was a positive correlation between urine osmolality and estimated Ccreat. Metabolic acidosis (bicarbonate <22 mmol/L) was found in 41% of patients, with relatively alkaline urine and high chloride level. Fractional excretion (FE) of sodium was above 1% in 68% of patients (mean 1.66 +/- 1.06%), and FE(Mg) was above 3% (mean 10.9 +/- 5.2%) in 93% of patients. Tubular reabsorption of phosphate (TP)/glomerular filtration rate (GFR) was 3.2 +/- 0.8 mg/dL glomerular filtrate (GF). FE(K), FE(UA), and Ca/creatinine in urine were normal. There were no functional group differences between the cadaveric and living-related kidneys. Significant group differences were found in those with acute episodes and those with a normal course. Estimated Ccreat was 54 +/- 20 vs. 67 +/- 20 mL/min/1.73 m(2) in the acute episodes and the normal course groups, respectively. Also, the FE(NA), FE(UA), and FE(Mg) were higher in the acute episodes group -2.3 +/- 1.6, 10.6 +/- 4.4, and 14.8 +/- 6.5%, respectively, compared with the normal course group -1.4 +/- 0.6, 8.2 +/- 2.8, and 9.6 +/- 4.0%, respectively. There were no between-group differences in plasma bicarbonate, FE(K), TP/GFR, and urine osmolality. We believe that most, if not all tubular dysfunctions in the transplanted kidney are secondary to renal failure and interstitial damage from acute episodes and nephrotoxic drugs. These dysfunctions are similar to those in chronic renal failure, where interstitial fibrosis plays a role in kidney function deterioration.
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PMID:Tubular and glomerular function in children after renal transplantation. 1604 94

An 84 year-old woman was admitted because of sepsis, thrombocytopenia, anaemia and acute renal failure that required hemodialysis. The diagnostic tests performed during hospitalization showed a severe urinary tract infection due to Enterococcus faecalis, resulting in mild sepsis. This infection was responsible for acute tubular necrosis and thrombotic microangiopathy, in a clinical context of difficult differential diagnosis and hemolytic-uremic syndrome.
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PMID:[Thrombotic microangiopathy during urinary tract infection]. 1686 16

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


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