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)

During a 4-year period, acute renal failure was observed in 27 patients (mean age 65 years) treated by various angiotensin-converting-enzyme (ACE) inhibitors for hypertension, heart failure, or a combination of both. None had significant renal artery stenosis on angiography. Overt volume depletion was present in 21 and hypotension in 12 cases. All patients received diuretic therapy and/or a low-salt diet. Other facilitating factors included cardiac failure, pre-existing chronic renal insufficiency, combined therapy with non-steroidal anti-inflammatory drugs, and diabetes mellitus. Twenty-two patients had two or more of these factors at presentation. A renal biopsy performed in 10 cases showed severe arteriosclerosis of small renal arteries in eight and acute tubular necrosis in five instances. Therapy comprised volume expansion, and withdrawal of diuretics and, except in two patients, of ACE inhibitors. Twenty-one patients recovered normal renal function, two died, and permanent renal damage remained in four. These results suggest that sodium depletion has a critical role in inducing acute renal failure, whose outcome is not always benign. A combination of diuretics and ACE inhibitors should be prescribed with caution, especially in older patients with small as well as with large renal vessel disease.
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PMID:Acute renal failure after the use of angiotensin-converting-enzyme inhibitors in patients without renal artery stenosis. 131 66

Nifedipine caused acute, reversible deterioration in renal function in four patients with chronic renal insufficiency. The absence of hypotension, clinical course, benign urinary sediments, and normal results of renal ultrasound examinations excluded acute tubular necrosis, pyelonephritis, interstitial nephritis, obstructive uropathy, and acute glomerulonephritis. It is postulated that this slow calcium channel blocker produced deleterious intrarenal hemodynamic alterations in the setting of moderate to severe renal functional impairment. Nifedipine may alter renal function by blocking calcium entry into renal vascular smooth muscle, thereby reducing the efficacy of vasoconstrictor hormones in regulation of renal blood flow and glomerular filtration rate. An alternative explanation is that nifedipine may inhibit the compensatory synthesis of vasodilatory prostaglandin E2 analogous to the clinical observation of acute deterioration in renal function by nonsteroidal anti-inflammatory drugs in patients with pre-existing renal insufficiency. These observations suggest that clinicians should monitor renal function closely and exercise caution when administering nifedipine to patients with underlying renal insufficiency.
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PMID:Nifedipine-induced renal dysfunction. Alterations in renal hemodynamics. 649 46

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

Nonsteroidal anti-inflammatory drugs predispose to acute renal failure in conditions associated with decreased RBF. Such conditions include advanced age, hypertension, chronic renal insufficiency, diuretic use, and any condition decreasing effective circulating volume. Strenuous exercise also causes marked reductions in RBF. The patient discussed developed severe acute renal failure after strenuous exercise and therapeutic doses of ibuprofen and hydrochlorothiazide-triamterene. Urinalysis showed a nephritic sediment with red blood cell casts. Renal biopsy showed acute tubular necrosis and arteriolar nephrosclerosis. Although exercise-associated acute renal failure is uncommon, susceptible patients with exercise-induced renal ischemia and prostaglandin inhibition may develop this complication.
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PMID:Exercise-induced acute renal failure associated with ibuprofen, hydrochlorothiazide, and triamterene. 757 49

There are conflicting reports on the ability of aspirin as a single agent to cause acute or chronic renal failure in experimental animals. Chronic administration of aspirin alone over 18 to 68 weeks in doses of 120 to 500 mg/kg/d has been reported to cause renal papillary necrosis in rats. However, some investigators have been unable to produce renal papillary necrosis in other species or in rats given lower divided doses comparable to therapeutic doses used in humans. In a variety of rat strains, aspirin administered as a single high dose intravenously or by oral gavage produces acute tubular necrosis of proximal tubules, rarely accompanied by renal papillary necrosis in susceptible strains. Several human studies have addressed the chronic nephrotoxicity of aspirin alone or relative risk of end-stage renal disease in association with aspirin use after correction for other analgesics. With the exception of one case control study demonstrating a low, but statistically significant risk of end-stage renal disease in association with aspirin use, all other case control studies and several prospective studies have been unable to identify a significant risk of chronic renal failure in patients using aspirin alone in therapeutic doses. In healthy adults, short-term aspirin administration in therapeutic doses has no effect on creatinine clearance, urine volume, osmolar clearance, or sodium and potassium excretion. However, in predisposed individuals with glomerulonephritis, cirrhosis, and chronic renal insufficiency, and in children with congestive heart failure, short-term aspirin use in therapeutic doses may precipitate reversible acute renal failure. Acute aspirin intoxication (>300 mg/kg) frequently causes acute renal failure and doses of 500 mg/kg may be lethal. Chronic salicylate intoxication has been reported to cause reversible or irreversible acute renal failure in association with a pseudosepsis syndrome.
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PMID:Does aspirin cause acute or chronic renal failure in experimental animals and in humans? 866 25

Studies in animals suggest that hepatocyte growth factor (HGF) is an important mediator of kidney development, compensatory growth and tubule repair following acute injury, however, evidence for HGF action in human renal disease is scant. To determine whether increased renal production of HGF occurs in man, urine HGF excretion rate was measured in normals and in patients with a variety of acute and chronic renal diseases. Urine samples were collected from 9 healthy individuals, 25 individuals with acute tubular necrosis (ATN), 20 individuals with chronic glomerular disease, 9 patients with polycystic kidney disease and 10 individuals with severe chronic renal failure not yet receiving renal replacement therapy. Samples were initially frozen and then HGF content measured by ELISA and factored for creatinine concentration measured by autoanalyzer. Detectable but low levels of HGF were found in the urine of normals and in patients with chronic glomerular or polycystic disease. Levels were also not increased in patients with advanced, chronic renal insufficiency. In contrast, a marked increase in urine HGF was observed in patients with acute renal failure. In addition, HGF excretion tended to correlate with disease severity as higher levels were observed in patients with oliguric ATN. Urine HGF levels declined to control values in patients recovering from ATN, generally within one week. These findings are consistent with a role for HGF in promoting tubule cell proliferation, differentiation and recovery from acute tubular injury in man.
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PMID:Increase urinary hepatocyte growth factor excretion in human acute renal failure. 935 59

A retrospective study was done of thirty-patients with severe preeclampsia and HELLP syndrome whose developed acute renal failure, 25 patients also had acute tubular necrosis and five cases bilateral cortical necrosis with chronic renal insufficiency. Severe hypertension was present in all cases and anti-hypertensive therapy was needed. Six patients died, three due to intracranial hemorrhage, other two secondary to hypovolemic shock, and in one case multiple organ dysfunction.
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PMID:[Severe pre-eclampsia, HELLP syndrome and renal failure]. 958 85

The present report addresses the status of the renal dopaminergic system activity in patients afflicted with different renal disorders and in the remnant kidney of uninephrectomized (UNX) rats, based on the urinary excretion of L-DOPA, dopamine and amine metabolites. In renal transplant recipients with good recovery of graft function (group 1, n=11), the daily urinary excretion of DOPAC, but not that of HVA, was found to increase progressively throughout the first 12 days post-transplantation from 698+/-57 nmol in the first day to 3498+/-414 nmol on day 9, and then remained constant until day 12. This resulted in a 6-fold increase in the urinary DOPAC/dopamine ratios. In renal transplant recipients with acute tubular necrosis (group 2, n=8), the urinary levels of dopamine, DOPAC and HVA were approximately 30% of those in group 1. In a group of 28 patients with chronic renal parenchymal disorders, the daily urinary excretion of L-DOPA, free dopamine and dopamine metabolites (DOPAC and HVA) correlated positively with the degree of deterioration of renal function (P<0.01). However, the U(Dopamine/(L)-DOPA) and U(DOPAC/Dopamine) ratios in patients with chronic renal insufficiency were found to be similar to those observed in patients with normal renal function. In 14 IgA nephropathy (IgA-N) patients with near normal renal function, the changes in 24 h mean blood pressure when going from 20 to 350 mmol/day sodium intake correlated negatively with the daily urinary excretion of dopamine (r(2)=0.597, P<0.01). The urinary excretion of L-DOPA and dopamine in IgA-N patients with salt-sensitive (SS) blood pressure was lower than in salt-resistant (SR) patients (P<0.05), irrespective of their daily sodium intake. However, the rise in urinary dopamine output during salt loading (from 20 to 350 mmol/day) was greater (P<0.05) in IgA-N SS patients (21.2+/-2.5% increase) than in SR patients (6.3+/-1.4% increase). Fifteen days after the surgery, uninephrectomy (UNX) in the rat was accompanied by an enhanced (P<0.05) urinary excretion of dopamine (36+/-3 vs 26+/-2), DOPAC (124+/-11 vs 69+/-6) and HVA (611+/-42 vs 354+/-7) (nmol/g kidney/kg body weight). This was accompanied by an increase in V(max) values for renal aromatic L-amino acid decarboxylase in the remnant kidney of UNX rats (P<0.05). Sch 23390, a D1 dopamine receptor antagonist, produced a marked reduction in the urinary excretion of sodium in UNX rats, whereas in sham-operated rats the decrease in urinary sodium did not attain a significant difference. It is concluded that the study of the renal dopaminergic system in patients afflicted with renal parenchymal disorders should address parameters other than free urinary dopamine, namely the urinary excretion of L-DOPA and dopamine metabolites (DOPAC and HVA). It is also suggested that in SS hypertension of chronic renal parenchymal diseases, renal dopamine produced in the residual tubular units may be enhanced during a sodium challenge, thus behaving appropriately as a compensatory natriuretic hormone.
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PMID:Renal dopaminergic mechanisms in renal parenchymal diseases and hypertension. 1136 22

Renal transplantation is at present a standard therapeutic method in chronic renal insufficiency. For a favourable development of the graft some investigated criteria are of basic importance: basic diagnosis which led to renal failure, period of dialyzation treatment, high standard collection and perfusion and early diagnosis of the rejection episode. Non-invasive diagnostic methods of the rejection episode are always indirect and correlate with histologically confirmed rejection, depending on the period of transplantation in 10-90% patients. Indirect diagnosis is based in particular on a rise of the creatinemia, decline of glomerular filtration, fluid retention variations of blood pressure and increase of the Doppler assessed index of resistance (IR) in the peripheral veins of the graft [1]. For many years the role of nuclear diagnostics are tested. The disadvantage of direct diagnosis--biopsy--is increased haemorrhage and loss of the graft [1, 2, 3, 4]. The greatest problem is the differentiation of acute (cellular) rejection as compared with acute tubular necrosis during the initial days after transplantation. The authors describe their experience with 81 biopsies in the course of 3 years in patients during the first 10 days after transplantation, comparison with dynamic scintigraphy of the graft. Their attention is focused on the technique and risks of renal biopsy.
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PMID:[Comparison of 2 methods of diagnosis of changes in transplanted kidneys in the early postoperative period: biopsy vs dynamic scintigraphy of the graft]. 1150 90

Acute Renal Failure (ARF) is characterized by a rapid decline of the glomerular filtration rate, due to hypotension (prerenal ARF), obstruction of the urinary tract (post-renal ARF) or renal parenchymal disease (renal ARF). The differential diagnosis among different causes of ARF is based on anamnesis, clinical symptoms and laboratory data. Usually ultrasound (US) is the only imaging examination performed in these patients, because it is safe and readily available. In patients with ARF gray scale US is usually performed to rule out obstruction since it is highly sensitive to recognize hydronephrosis. Patients with renal ARF have no specific changes in renal morphology. The size of the kidneys is usually normal or increased, with smooth margins. Detection of small kidneys suggests underlying chronic renal pathology and worse prognosis. Echogenicity and parenchymal thickness are usually normal, but in some cases there are hyperechogenic kidneys, increased parenchymal thickness and increased cortico-medullary differentiation. Evaluation of renal vasculature with pulsed Doppler US is useful in the differential diagnosis between prerenal ARF and acute tubular necrosis (ATN), and in the diagnosis of renal obstruction. Latest generation US apparatus allow color Doppler and power Doppler evaluation of renal vasculature up to the interlobular vessels. A significant, but non specific, reduction in renal perfusion is usually appreciable in the patients with ARF. There are renal pathologic conditions presenting with ARF in which color Doppler US provides more specific morphologic and functional information. In particular, color Doppler US often provides direct or indirect signs which can lead to the right diagnosis in old patients with chronic renal insufficiency complicated with ARF, in patients with acute pyelonephritis, hepatic disease, vasculitis, thrombotic microangiopathies, and in patients with acute thrombosis of the renal artery and vein. Contrast enhanced US is another useful diagnostic tool in patients with ARF which has been recently introduced in clinical practice. Microbubble administration may reduce technical failure in the evaluation of the renal artery. Moreover, perfusion defects due to stenosis or thrombosis of the renal segmentary vessels are better recognized. New diagnostic possibilities of enhanced US include evaluation of both cortical and medullar vessels, and functional evaluation of renal perfusion. Measuring the transit time of the microbubbles is useful for the diagnosis of renal artery stenosis and, in transplanted kidneys, for differential diagnosis between ATN and acute rejection.
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PMID:[Current role of color Doppler ultrasound in acute renal failure]. 1177 81


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