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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 has been a rare, uniformly fatal complication of infection with Francisella tularensis. The literature suggests that either acute tubular necrosis, interstitial nephritis, or glomerulonephritis may be responsible for this syndrome. We have described a patient with tularemia who had nonoliguric acute renal failure probably due to interstitial nephritis and who recovered slowly but spontaneously during antimicrobial therapy with doxycycline.
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PMID:Tularemia complicated by acute renal failure. 682 14

Urinalysis is a simple, efficient, and accurate guide in the diagnosis of renal disease. By determining a patient's history and obtaining a physical examination, the physician is very often able to diagnose a patient's renal lesion. Heavy proteinuria and a microscopic sediment containing red cells and red cell casts strongly suggest acute glomerulonephritis. The causes of this nephropathy are legion. On the other hand, mild proteinuria and a lack of microscopic findings suggest nephrosclerosis, interstitial nephritis, or acute tubular necrosis in the proper clinical setting. When glomerular disease produces nephrotic syndrome, the various types of glomerular disease can be diagnosed accurately without biopsy in a high percentage of cases.
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PMID:Urinalysis and clinical renal disease. 721 37

The diagnostic work-up of the urologic patient must be tailored to the presenting symptom complex, carefully selecting from the many modilities available, those most likely to establish the diagnosis and extent of the suspected lesions. Intravenous urography is the most rewarding initial procedure for many presenting symptoms, including suspected masses, pyuria, hematuria, and flank pain. Nuclear imaging is particularly effective in differentiating renal lobulations from true masses, in demonstrating parenchymal scarring in chronic pyelonephritis when the IVP is equivocal, and in assessing the decrease in perfusion and function in obstructive nephropathy when the IVP is indeterminate. It is the preferred procedure for acute renal infarction and acute tubular necrosis and has a greater sensitivity of detection for renal trauma than the IVP. Gallium-67 renal imaging appear helpful in the detection of occult pyelonephritis or interstitial nephritis. However, it cannot differentiate focal acute pyelonephritis from abscess or abscess from neoplasm. Ultrasoneography is the initial procedure of choice in the differentiation of cystic from solid renal masses and in anuria or oliguria. When a kidney fails to visualize by IVP or nuclear imaging, it can confirm or rule out obstruction. In upper tract infections, it may demonstrate renal or perirenal abscess. Although retrograde pyelography is performed less frequently in recent years, it remains extremely useful in confirming and relieving obstructive uropathy and in delineating tumors of the collecting system. Computed tomography effectively demonstrates hydronephrosis, renal abscess, tumors, and cysts and retroperitoneal involvement. More experience is needed to judge the efficiency of "dynamic" CT for the quantification of renal function. Renal angiography remains invaluable as a secondary procedure (as opposed to initial screening) in renal trauma, vascular anomalies, and in renal tumors to delineate the anatomy of the arterial supply and possible renal vein involvement.
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PMID:Medical imaging of renal diseases-suggested indication for different modalities. 724 59

We report on 4 cases of reversible acute renal failure (ARF), appearing within the first days after institution of a sulfinpyrazone treatment (600 mg p. day) early after a myocardial infarction. Urinary data were consistent with an acute tubular necrosis. A renal biopsy, performed in 3 patients, revealed only very discrete tubular and interstitial lesions, not helpful in the understanding of the ARF. Three pathogenetic mechanisms could be evoked. Data in favour of an acute tubular precipitation of uric acid or an immunologically induced acute interstitial nephritis are lacking. More probably this ARF is due to an inhibitory effect of sulfinpyrazone on the renal prostaglandin synthesis. Early after a myocardial infarction, renal prostaglandins could play an important protective role in maintaining the renal circulation. Renal function should be monitored closely when sulfinpyrazone is prescribed, especially early after a myocardial infarction.
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PMID:[Acute renal failure induced by sulfinpyrazone (author's transl)]. 730 Oct 34

Tubulo-interstitial nephropathy or nephritis is suggested if renal function is deteriorated and urinary findings are slight. In most cases, the daily urinary protein excretion is less than 1 g and macrohematuria is not present. Urinary excretion of N- acetyl-beta-glucosaminidase and beta 2-microglobulin is a good indicator for tubulo-interstitial damage. Acute renal failure is caused either by acute tubulo-interstitial nephritis or acute tubular necrosis. In either case, renal biopsy is essential for diagnosis and to characterize the renal damage. In the interstitium, edema and fibrosis are seen and lymphocytes, plasma cells, polymorpholeukocytes, and/or eosinophils infiltrate. Tubular basement membrane is sometimes disrupted and lymphocytes have infiltrated inside (tubulitis).
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PMID:[Renal biopsy for diagnosis of interstitial nephritis]. 756 31

The incidence of in-hospital acute renal failure (ARF) due to drugs is estimated at 20% of all patients hospitalized for ARF. According to recent surveys, analgesic and non-steroidal anti-inflammatory drugs are now more frequently involved than antibiotics. The incidence of ARF in patients taking angiotensin-converting enzyme inhibitors is increasing. More than half of the patients have a non-oliguric course. Acute tubular necrosis and acute interstitial nephritis are found in most biopsied cases. The mortality rate ranges between 6% and 12%. Most patients recover but 15% to 20% have some degree of residual renal impairment, particularly older and oliguric patients, those with previous chronic renal insufficiency and whose ARF period is prolonged. The long-term renal effects of NSAIDs is a concern. ARF due to drugs is a preventable disease since two-thirds of patients received inappropriately high or prolonged doses of the offending drug and or were patients at risk to develop ARF.
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PMID:[Acute kidney failure induced by drugs or contrast media]. 756 90

The mortality rate of acute renal failure is still high, about 50%. About 10% of the survivors have chronic renal failure, sometimes requiring dialysis. The course of some of these cases can be improved by appropriate therapeutic measures, if they are undertaken early. Early identification of these lesions is therefore mandatory. The clinical diagnosis is often difficult: 1. rare atypical forms of acute tubular necrosis, with renal or extrarenal signs, may lead to renal biopsy; 2. vascular and glomerular disease are most often recognized clinically (sometimes misdiagnosed), but the histological type (and therefore the appropriate treatment) cannot be determined; 3. acute interstitial nephritis is rarely diagnosed clinically and the nature of the infiltrate remains unknown. In certain cases of acute renal failure, the contribution of early renal biopsy to the etiological diagnosis and to prognosis and therapy is obvious. In acute renal failure, renal biopsy should be considered early in a rather limited number of patients (about 20%), everytime the diagnosis of tubular necrosis is doubtful, especially in acute renal failure associated with persistent infection, in order to guide the therapy.
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PMID:[Contribution of renal biopsy to the diagnosis and treatment of acute kidney failure]. 756 93

The class of nephrotoxins which are directly tubulotoxic in animal studies (cis-platinum, gentamicin, and cephaloridine) produce minimal histological changes in the human kidney. Such alterations do not correlate with the degree of organ dysfunction and fall into the broad category of what has been called 'acute tubular necrosis'. Some nephrotoxins (cyclosporine and amphotericin), acutely and chronically diminish renal perfusion, causing injury to renal parenchymal zones known to have limited oxygen a availability (medullary ray and inner stripe). In cyclosporine toxicity, the human and animal models appear equivalent. This is less clear with amphotericin where there appears to be a tubulotoxic component. Other nephrotoxic substances (contrast, nonsteroidal anti-inflammatory drugs) acutely alter renal perfusion, particularly affecting the medulla. In animal models of renal failure induced by these substances, there is an excellent correlation between medullary thick ascending limb injury and renal failure. Documentation of this phenomenon in human biopsies/autopsies is lacking, probably because of the lack of biopsy material and problems in defining medullary injury. Finally, in toxicological screening programs for nephrotoxic substances, there are groups of reactions which cannot be predicted and are thought to be mediated by immune mechanisms, i.e., immune complex glomerular disease, nil disease and interstitial nephritis.
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PMID:The pathology of nephrotoxic injury: a reappraisal. 784 19

Familiarity with renal issues that can challenge the care of patients with human immunodeficiency virus (HIV) should expedite diagnosis and therapeutic interventions. Among the most common problems are electrolyte and acid-base imbalances from many opportunistic infections or their treatments, including hyponatremia, hyperkalemia, hypokalemia, and hypo- and hypercalcemia. Acid-base disturbances, simple or mixed, can be due to underlying sepsis, opportunistic infections, or the therapy thereof. A recent report of seven patients with HIV with type B lactic acidosis failed to identify a satisfactory etiology. Elevations in creatinine or diminishing urine output should alert the physician to the possibilities of prerenal azotemia or acute tubular necrosis, which can result from progression of prerenal azotemia or can occur secondary to administered nephrotoxins, such as certain antibiotics and radiocontrast agents. Agents associated with nephrotoxicity include aminoglycosides, antifungal, antiviral, and radiocontrast agents, and nonsteroidal anti-inflammatory pain medications. Although prerenal azotemia and acute tubular necrosis are the most frequent causes of acute renal failure, the differential diagnosis should include acute interstitial nephritis, obstructive nephropathy, and glomerulopathies such as hemolytic uremic syndrome, thrombotic thrombocytopenia purpura, the newly described IgA nephropathy, and, in certain populations, HIV nephropathy.
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PMID:The spectrum of kidney diseases in patients with human immunodeficiency virus infection. 792 95

Of 2457 patients in the North American Pediatric Renal Transplant Cooperative Study registry who were followed for 5481 patient-years after the index transplantation, we observed 136 deaths, for an average annual rate of 24.8 deaths per 1000 patient-years. Death resulted primarily from infection (n = 55, 40%), cardiovascular causes (n = 28, 21%), hemorrhage (n = 16, 12%), and malignancies (n = 9, 7%). Cadaver-donor source was associated with greater mortality (6.7%) than a living-donor source (4.0%) (P < 0.005). Recipients aged 0-1, 2-5, 6-12, and 13-17 years old had mortality rates of 17.5, 8.0, 3.6, and 4.5%, respectively (P < .001). Mortality rates increased substantially when examined by recipient and cadaver donor ages (mortality rates of up to 45%), the greater the concordance between young donor and recipient ages. Interestingly, acute tubular necrosis and graft failure less than 30 days after transplantation (GH30) were each associated with markedly elevated mortality rates. (The risk ratio for ATN was 3.1 [P < 0.001] and for GF30 it was 6.4 [P < 0.001].) Mortality after transplantation was also affected by the underlying renal disease, with high mortality rates observed for oxalosis (n = 21, 33.3%), congenital nephrotic syndrome (n = 79, 15.2%), pyelo/interstitial nephritis (n = 54, 11.1%), and Drash syndrome (n = 14, 21.4%). When the joint effect of these risk factors was examined in a Cox proportional hazards model, young recipient age (0-1 years old) and GF30 were significant (P < .001) risk factors of mortality for recipients of living-donor organs. For recipients of cadaver kidneys, young recipient age--0-1 years old (P < .001) and 2-5 years old (P = .002)--ATN (P = .029), and GF30 (P < .001) were all significant risk factors. Recipient age is the major determinant of increased mortality after renal transplantation. Avoidance of acute tubular necrosis by reducing cold time and preventing early graft failure by better matching techniques in this vulnerable population may improve the mortality rate.
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PMID:Posttransplant deaths and factors that influence the mortality rate in North American children. 811 40


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