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)

Renal biopsy is a fundamental tool in the diagnosis and prognostic of multiple nephrological and systemic pathologies. At our institution the first patient submitted to this technique, at 1994, showed Berger disease. Until 2002 we have performed 91 renal biopsies (57 men and 34 women) with the following annual distribution: 1994 (n=3), 1995 (n=3), 1996 (n=3), 1997 (n=15), 1998 (n=5), 1999 (n=23), 2000 (n=13) and 2001 (n=26). Ultrasound guidance was always used and in most of cases the technique was performed with Vim-Silverman (14G) needle. BARD automatic system was employed in only five patients. The clinical diagnosis that lead to renal biopsy were: nephrotic syndrome (n=27), asyntomatic urinary abnormalities (n=25), acute or rapidly progressive renal failure (n=18), chronic renal failure (n=15), hypertension (n=4) and acute nephritis (n=2). The efficacy for optic histological diagnosis was 92.3% (84/91). However, if we include seven cases of presumed IgA nephropathy that don't included fragment for immunofluorescence (IF) analysis the efficacy declined to 84.6% (77/91). The mean number of glomeruli per fragment was 18.3 -/+ 14.2 [0-80]. Histological diagnosis were the following: Berger disease (n=24), idiopathic nephrotic syndrome (n=18), lupus nephritis (n=8), mesangial proliferative glomerulonephritis without glomeruli in the IF fragment (n=6), without glomeruli (n=6), secondary nephrotic syndrome (n=4), tubulointerstitial nephritis or acute tubular necrosis (n=4), diabetic nephropathy (n=3), myeloma kidney (n=3), pauci-imune and crescentic glomerulonephritis (n=3), hypertensive nephropathy (n=2), IgM mesangial proliferative glomerulonephritis (n=2) and various (n=8). Gross hematuria appeared in 9 patients (9.9%). Only in three of these patients it was showed, by ecography, the existence of kidney haematoma. Bleeding throughout the mandrill in four cases, leaded to transfusion in only three patients. We have registered one accidental spleen puncture. Nephrectomy for incontrollable bleeding was never needed. Higher glomerulosclerosis (30% vs 8%; p<0.01) and also a greater extent of tubulointersticial lesions (100% vs 63%; p<0.01), were predictors of progression into end-stage or advanced renal failure. Concluding, renal biopsy with ultrasound guidance was valuable for diagnosis in 84.6% of our proceedings. Our serie is similar to others concerning serious complications. Nephrologists and radiologists improved progressively their coordination performing this technique, improving the results during this period of 8 years.
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PMID:[Percutaneous kidney biopsy: eight years-experience]. 1563 24

NSAIDs are commonly used drugs. Even with the advent of selective COX-2 inhibitors, nephrotoxicity still remains a concern. The adverse effects of NSAIDs are mediated via inhibition of prostaglandin synthesis from arachidonic acid by non-specific blocking of the enzyme cyclooxygenase leading to vasoconstriction and reversible mild renal impairment in volume contracted states. When unopposed, this may lead to acute tubular necrosis and acute renal failure. NSAIDs also produce interstitial nephritis with or without nephrotic syndrome secondary to minimal change disease. Although this presents as acute renal failure, it can progress in some cases to chronic renal failure. Papillary necrosis has been incriminated in the development of chronic renal failure secondary to NSAIDs. In patients on long term NSAIDs without acute or chronic renal failure, subclinical renal dysfunction such as reduced creatinine clearance and impaired urine concentrating ability has been shown to be present. Although this sub-clinical dysfunction is reversible on withdrawal of NSAIDs, some reports have suggested a persistent residual dysfunction. Even with a wide range of NSAIDs at our disposal, a renal safe NSAID is yet to be discovered.
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PMID:NSAIDs and kidney. 1584 59

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

From July 1998 to July 1999, 45 cases of acute renal failure were treated at Bir Hospital, Kathmandu. Out of which 24 were male and 21 were female. Age ranged from 11 months to 84 years with mean age being 35 years and 9 cases were below 10 years. Four cases with pre-renal azotaemia and twenty five cases of acute tubular necrosis (ATN) accounted for 64% of all cases. These were due to gastroenteritis 10, sepsis 6, post surgical 1, trauma 1 and obstretical complications 5. Multiple hornet stings were responsible for acute renal failure in 3 cases, acute urate nephropathy in 1 case and miscellaneous causes in 2 cases. Glomerulonephritis / vasculitis accounted for 17.7%, acute interstitial nephritis 4.4%, haemotytic uraemic syndrome (HUS) 6.6%, and post renal azotaemia in 6.6% of all cases. Mean serum creatinine was 8 mg/dl, mean blood urea 190 mg/dl. Eight cases were treated only conservatively, eighteen received haemodialysis, fourteen received peritoneal dialysis, three received both and two refused for dialysis. Average duration of hospital stay was 13.6 days. Out of the forty-five cases twenty-nine recovered normal renal function, ten expired, two recovered partially, two progressed to chronic renal failure and two left against medical advice. Overall mortality was 22.2%. Common causes of acute renal failure in our setting were gastroenteritis (22%) and sepsis (20%). HUS was exclusively seen in children following bacillary dysentery. Multiple hornet stings is an important cause of acute renal failure in our country.
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PMID:Acute renal failure in a tertiary care center in Nepal. 1655 67

Renal dysfunction and injury secondary to medications are common, and can present as subtle injury and/or overt renal failure. Some drugs perturb renal perfusion and induce loss of filtration capacity. Others directly injure vascular, tubular, glomerular and interstitial cells, such that specific loss of renal function leads to clinical findings, including microangiopathy, Fanconi syndrome, acute tubular necrosis, acute interstitial nephritis, nephrotic syndrome, obstruction, nephrogenic diabetes insipidus, electrolyte abnormalities and chronic renal failure. Understanding the mechanisms involved, and recognizing the clinical presentations of renal dysfunction arising from use of commonly prescribed medications, are important if injury is to be detected early and prevented. This article reviews the clinical features and basic processes underlying renal injury related to the use of common drugs.
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PMID:Drug-associated renal dysfunction and injury. 1693 99

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

Insulinlike growth factor I (IGF-I), IGF-I receptors, and IGF-binding proteins are expressed in different segments of the nephron in a relationship that suggests autocrine, paracrine, and endocrine modes of action. IGF-I contributes to compensatory nephron growth in a variety of experimental renal diseases with loss in functioning nephron number, and to tissue repair after ischemic acute tubular necrosis. IGF-I causes arteriolar dilatation in the kidney and increases the glomerular filtration rate in experimental animals, in normal subjects, as well as in patients with chronic renal failure, and this effect of the peptide is probably mediated by nitric oxide. IGF-I raises proximal tubular phosphate reabsorption and may increase sodium absorption in distal tubules. In the nephrotic syndrome, IGF-I- and IGF-binding protein complexes are excreted in urine and IGFBP-3 protease activity is increased, causing complex abnormalities in the IGF-system.
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PMID:Insulinlike growth factor I and the kidney. 1840 31

Renal transplantation has emerged as the most cost-effective and patient-supportive way to treat chronic renal failure, with excellent graft survival rates thanks to improved surgical techniques and rejection management. Its success has placed a heavy burden on imaging, especially ultrasound, which is used in the selection of live donors and in monitoring each stage of the postoperative care of the recipient. Ultrasound is particularly useful for detecting vascular complications such as early occlusions and arterial stenosis. It can detect and monitor perinephric complications and transplant hydronephrosis, all clinically significant complications that affect management. Ultrasound can detect many of the late acquired diseases, especially intercurrent tumors that require surgery. It is the best method to guide interventions such as aspiration of collections and insertion of nephrostomy drains. It can also detect postbiopsy arteriovenous shunts and the end-stage kidney of chronic rejection. These, however, are of no great clinical significance, and the findings rarely affect clinical decisions. Ultrasound fails to discriminate between the important causes of early graft dysfunction, especially acute tubular necrosis, rejection, and drug toxicity: these important distinctions still rely on biopsy. There is hope that some of the newer ultrasound methods, especially the functional data from microbubble contrast agent dynamics, might supply useful information for their detection and differentiation.
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PMID:Renal transplants: what ultrasound can and cannot do. 1852 43

A simultaneous pancreas-kidney transplantation (SPKT) is the best treatment option for type I diabetic patients with advanced chronic renal failure. Infectious complications affect 7-50% of the patients receiving this procedure. We conducted a nested case-control study to assess the risk factors for surgical site infection (SSI) in patients receiving SPKT at our centre between 2000 and 2006. Of the 119 evaluated transplant recipients, 55 (46.2%) developed SSIs and the 30 day mortality was 11.8%. Gram-negative organisms were the predominant organisms isolated from SSIs. After multivariate logistic regression, the variables independently associated with SSI were: acute tubular necrosis, post-transplant fistula and graft rejection. This study demonstrated a high incidence of SSI in this patient cohort and variables related to the surgical procedure were closely associated with the development of SSI.
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PMID:Incidence and risk factors for surgical site infection after simultaneous pancreas-kidney transplantation. 1959 36

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


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