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)

Twenty-three women of ages 13 to 44 years were hospitalized with illnesses fulfilling the criteria of the case definition for the toxic-shock syndrome (TSS) associated with coagulase-positive staphylococci. Disease onset occurred during menses in 22, and all were oliguric when admitted. Prolonged hypotension and a reduced central venous pressure were common features. Measurements of urine volume and creatinine clearance in eight patients identified two types of acute renal failure, oliguric and nonoliguric, and prerenal azotemia related to intravascular volume depletion. Urinary sodium excretion and measurement of the renal index (UNa divided by U/PCr) provided further support for the presence of both prerenal and intrinsic renal failure. Hemodialysis was required in one patient in whom findings on renal nuclide scan were consistent with acute tubular necrosis. Pyuria was frequent, but proteinuria and more than five erythrocytes per high-power field were infrequent. Other features included initial hyponatremia and the combination of hypoproteinemia, hypoalbuminemia, hypocalcemia and hypophosphatemia of several days' duration. The hypoalbuminemia was believed to be due to exudation of protein from the intra- to the extravascular space. The hypoalbuminemia was believed to be due to exudation of protein from the intra- to the extravascular space. The hypocalcemia was probably related to the hypoalbuminemia. The pathogenesis of hypophosphatemia in the presence of acute renal failure is unclear. Following the intravenous administration of colloids, fluids and, in seven patients, dopamine, all recovered from the acute illness.
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PMID:Renal manifestations of the staphylococcal toxic-shock syndrome. 728 46

A 42-year-old female was admitted to a hospital, because of acute hepatitis A. Laboratory data were GOT 8210mU/ml. GPT 4650mU/ml, LDH 11860mU/ml, total bilirubin 4.7mg/dl, BUN 19.5mg/dl and creatinine 1.9mg/dl. Urinalysis showed proteinuria 3+ and occult blood 1+. Soon after admission, she suffered from anuric acute renal failure and was transferred to our hospital for hemodialysis. Her urine-volume was under 20 ml per day. Urinalysis showed proteinuria 4+, occult blood 1+ and casts. Laboratory data showed BUN 58.2mg/dl and creatinine 8.5mg/dl. She was treated by hemodialysis for 35 days, before recovering from renal failure. However, her renal function did not recover perfectly and her 24-hour creatinine clearance remained at 50ml/min after 6 months. Renal biopsy was performed on the 17th day after admission. Examination by light microscopy revealed the findings of acute tubular necrosis and examination by immunofluorescence antibody method was negative. Urinalysis of 8 patients with acute hepatitis A showed that all patients had proteinuria at the onset. Patients with acute hepatitis A have symptoms of appetite-loss, nausea, vomiting and/or diarrhea. These symptoms cause hypovolemia, and hepatic dysfunction causes discontrol of vasoactive hormones, which gives rise to disturbance of renal circulation. Subsequently, acute tubular necrosis and acute renal failure occur.
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PMID:[A case of acute hepatitis A associated with acute renal failure from the onset]. 823 Aug 22

Acute renal insufficiency developed in four idiopathic nephrotic patients with minimal change or mild proliferative glomerulonephritis. The reduction in glomerular filtration rate (CInulin) was not in proportion to the renal plasma flow (CPAH) as evidenced by a low filtration fraction. Diuretic therapy failed to reverse renal insufficiency, and renal biopsy showed no evidence of interstitial nephritis, acute tubular necrosis or interstitial edema. Corticosteroid therapy induced a recovery of renal function with a decrease in proteinuria. These observations suggest that acute renal insufficiency in the idiopathic nephrotic syndrome might be caused by impaired glomerular permeability.
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PMID:Reversible acute renal failure in idiopathic nephrotic syndrome. 849 41

Nonfulminant hepatitis A viral infection has rarely been associated with renal abnormalities, most commonly microscopic hematuria and minimal proteinuria. An unusual case is presented of a 37-yr-old female with serologically proven acute hepatitis A infection complicated by acute oliguric renal failure. The patient recovered, and laboratory tests returned to normal 1 month after initial hospitalization. Renal biopsy revealed acute tubular necrosis; dialysis was not necessary. The relevant world literature is reviewed.
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PMID:Acute renal failure associated with nonfulminant hepatitis A viral infection. 885 78

Although the therapeutic administration of lithium in the psychiatric setting has been associated with various renal side effects, only a few reported cases have suggested a possible link to glomerular disease. We report two patients who, while taking lithium, developed heavy proteinuria caused by minimal change disease and acute renal insufficiency attributable to acute tubular necrosis. These clinical findings resolved on discontinuation of the drug, suggesting a role for lithium in their development. We also postulate that lithium, with its unique properties as a modulator of the phosphoinositol pathway, may play a key role in the pathogenesis of minimal change disease.
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PMID:Nephrotic syndrome and renal insufficiency associated with lithium therapy. 862 33

To assess the impact of long-lasting acute renal failure after renal transplantation on late graft prognosis, we compared the risk factors and outcome in renal allografts with delayed function for >3 weeks after renal transplantation (long-lasting delayed graft function [LLDGF]) (group A, n=64), and in four control groups: group B, initially functioning grafts (n=322); group C, grafts with delayed function for <2 weeks after transplantation (n=110); group D, grafts with delayed function for 14 to 20 days after transplantation (n=57); and group E, never-functioning grafts (n=88). Donor asystolia or instability, stroke as a cause of donor's death, and prolonged cold ischemia and vascular surgical times were some predictors of LLDGF. Overlap was important, but 43% of patients of group A, 15% of group B, 25% of group C, 31% of group D, and 40% of group E (P<0.01) presented two or more risk factors for severe acute tubular necrosis after transplantation. Acute rejection and early complications were very frequent in group A. Also, patient survival was significantly decreased in group A, due to a higher incidence of infectious mortality. Graft survival was moderately (NS) decreased in group A. Serum creatinine was initially higher in patients of group A, but differences disappeared after the second year. However, late proteinuria was more frequent in group A, and there was also a trend for a higher prevalence of hypertension in this group. LLDGF cannot be reliably predicted at the time of renal transplantation. The main consequence of LLDGF is an excess mortality, while the impact on late graft function is less significant. Short-lasting delayed graft function does not seem to have a negative impact on the outcome of renal transplantation.
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PMID:Outcome of grafts with long-lasting delayed function after renal transplantation. 869 42

Renal changes that occur with aging mainly consist of impairment in the ability to concentrate urine and to conserve sodium and water. These physiological changes increase the risk of volume depletion and the prerenal type of acute renal failure (ARF) in elderly people. Bladder outlet obstruction caused by benign prostatic hypertrophy is a common cause of ARF in elderly men. Another frequent cause of ARF in the elderly is drug-induced nephropathy. Nonsteroidal anti-inflammatory drugs (NSAIDs) and antibiotics are most often implicated in the development of ARF in the elderly. However, considering the high usage of these drugs, the incidence of drug-induced nephropathy is relatively small. NSAIDs are more likely to cause ARF in patients with congestive heart failure, chronic renal disease (including diabetic nephropathy) or chronic liver disease than in otherwise healthy individuals. NSAID-induced ARF is often of the prerenal type, but may be caused by acute interstitial nephritis (AIN). The presence of heavy proteinuria or nephrotic syndrome differentiates NSAID-induced AIN from AIN caused by other drugs. Antibiotics, especially semisynthetic penicillins, more commonly give rise to AIN associated with peripheral blood eosinophilia and eosinophiluria than NSAIDs. Ciprofloxacin is increasingly reported to cause AIN. Fever commonly accompanies AIN, especially when induced by antibiotics. Aminoglycosides produce ARF by inducing acute tubular necrosis (ATN), which results from the excessive accumulation of myeloid bodies in the tubules. In all cases of ARF it is essential to obtain a good history, to perform a through physical examination, with particular attention to skin turgor, and to measure blood pressure, pulse rate (supine and upright), urinary electrolyte and creatinine levels. Fractional excretion of sodium and the urine:plasma creatinine ratio are reliable indices that distinguish prerenal ARF from ATN. A prompt response to fluid challenge, with an increase in urine output and urinary sodium excretion, and a rapid decrease in blood urea nitrogen, constitutes strong evidence for prerenal ARF. However, these indices are unreliable when prerenal ARF has progressed to ATN or when ARF has an obstructive pattern to begin with. In all cases of ARF, especially in elderly men, urinary tract obstruction should be suspected unless the history is otherwise clear cut. Ultrasound of the kidneys and bladder is a simple, non-invasive and meaningful test that can be used to rule out obstructive causes of ARF. If obstruction is the cause of ARF, ultrasound will be positive; in contrast, urinary obstruction is very unlikely if ultrasound findings are normal in a patient who has been oliguric or anuric for 48 hours or more. Similarly, acute glomerulonephritis, including rapidly progressive glomerulonephritis, should be suspected when ARF is associated with heavy proteinuria. In such instances, percutaneous renal biopsy is essential to document the diagnosis. It is of utmost importance to establish whether ARF is of prerenal or postrenal type, both of which are potentially fully reversible. In contrast, patients with ATN or rapidly progressive glomerulonephritis may not recover, or may only partially recover, their renal function. Haemodialysis and nutritional support are common measures for patients with severe ATN and a highly catabolic state. Corticosteroids and immunosuppressive therapy should be instituted for rapidly progressive glomerulonephritis, in addition to haemodialysis. haemodiafiltration instead of haemodialysis is recommended for patients who are haemodynamically unstable [i.e., with a persistently low blood pressure (systolic < or = 100 mm Hg)]. Haemodiafiltration has been shown to improve acid-base balance and uraemia better than standard haemodialysis. However, despite dialysis, mortality in patients with ARF associated with ischaemic ATN remains high.
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PMID:Management of acute renal failure in the elderly. Treatment options. 889 22

We report a 46-year-old woman who has been suffered from myasthenia gravis and underwent thymomectomy in December 1988. Her myasthenic symptoms improved by treatment with corticosteroid and azathioprine; the latter drug was administrated for more than one year. She noticed weight gain of 10 kg and edema in both legs and feet, which developed acutely in August 1994. Laboratory data showed that she suffered from nephrotic syndrome with a large amount of proteinuria (15 g/day). Renal biopsy revealed that biopsied glomeruli showed early stage of membranous nephropathy associated with acute tubular necrosis. Although therapeutic trials of steroid pulses could not eliminate proteinuria, substitution of cyclophosphamide for azathioprine brought marked improvement of the nephrotic syndrome with disappearance of the urinary protein excretion within 10 days. From reports of similar cases with myasthenia gravis in Japan and in Europe, therapeutic usage of azathioprine in patients with myasthenia gravis associated with thymoma should be cautious for appearance of nephrotic syndrome when azathioprine is continued for more than one year.
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PMID:[A post-thymomectomy case of myasthenia gravis which developed nephrotic syndrome with membranous nephropathy during azathioprine administration]. 895 54

Twenty-six cases (4.8%) from a total of 540 patients with acute renal failure (ARF) of diverse aetiology had ARF in association with falciparum malaria. Their ages ranged from 15 to 85 years (mean 31.2). Urinary sediment abnormalities and proteinuria (less than 1 g/24 h) were observed in 15 (57.7%) cases. The probable underlying factors leading to ARF were: volume depletion 17 (65.3%), intravascular haemolysis 8 (30.8%), hyperparasitaemia 8 (30.8%), cholestatic jaundice 6 (23%), and hypotension 5 (19.2%). Dialysis therapy was required in 15 patients (57.7%) as they had severe renal failure, and the remaining 11 patients improved with supportive measures. All patients received antimalarial therapy. The clinical course of ARF was consistent with acute tubular necrosis in 20 patients. Six cases were subjected to percutaneous renal biopsy. One patient showed histological features of necrotizing glomerulonephritis along with acute tubulointerstitial nephritis. The biopsies in the other five patients showed features of acute tubular necrosis in three, and acute interstitial oedema with patchy tubular necrosis in two. The mortality rate was 30.8%. Thus falciparum malaria, which has been an important cause of ARF in certain highly endemic zones of India, is showing an increasing prevalence in other parts such as Eastern Uttar Pradesh due to an imbalance between the increasing population and inadequate sanitary facilities, which further worsen during floods.
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PMID:Acute renal failure in falciparum malaria--increasing prevalence in some areas of India--a need for awareness. 930 75

The clearance ratios of endogenous plasma proteins with the same size but a different charge, such as the amylase isoenzymes and the immunoglobulin (Ig) G subclasses, have been used to assess glomerular charge selectivity in man. These proteins are, however, subject to tubular reabsorption. In this study we measured the IgG subclass/IgG clearance ratios for IgG1 (pI 8.0-9.5), IgG2 (pI 7.0-7.5) and IgG4 (pI < 6) in 6 healthy volunteers. Our results suggested a selective influence of tubular reabsorption: the IgG1/IgG clearance ratio was 0.68 +/- 0.14 (mean +/- SD) and lower than IgG2/IgG (2.02 +/- 1.06, p < or = 0.01). IgG4/IgG was 0.89 +/- 0.39. In addition, we studied the clearance ratios of pancreatic (PA, pI 7.0) and salivary amylase (SA, pI 5.9-6.4) and of IgG1 and IgG2 in 8 patients with minimal change nephrotic syndrome (MCNS), 11 patients recovering from acute tubular necrosis (ATN) and 9 healthy volunteers (controls). In MCNS glomerular charge selectivity is lost, while in recovering ATN tubular function is severely disturbed. The PA/SA clearance ratio was 3.25 +/- 0.89 in controls, reflecting intact glomerular charge selectivity. In MCNS patients the PA/SA clearance ratio had decreased to 1.21 +/- 0.23 (p < or = 0.001). In ATN patients the PA/SA clearance ratio was reduced as well: 1.55 +/- 0.41 (p < or = 0.001), although the aselective nature of the proteinuria and the modest albuminuria indicated intact glomerular charge selectivity. The IgG1/ IgG2 clearance ratio was 0.54 +/- 0.15 in controls, again suggesting preferential tubular reabsorption of IgG1. In MCNS patients the IgG1/IgG2 clearance ratio was 0.16 +/- 0.10 (p < or = 0.001); this probably reflects the relatively increased glomerular sieving of IgG2 when glomerular charge selectivity is lost. In ATN patients the IgG1/IgG2 clearance ratio was 1.07 +/- 0.47 (p < or = 0.001), which suggests a partial loss of preferential reabsorption of IgG1. It was concluded that the PA/SA clearance ratio is influenced by loss of tubular function and therefore does not reflect glomerular charge selectivity specifically. The IgG1/IgG2 ratio cannot be used to assess glomerular charge selectivity either because of the interference of selective tubular reabsorption of the subclasses. These findings put the assessment of glomerular charge using endogenous proteins in a new light and bring forward the necessity to interpret these ratios with the utmost cautiousness.
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PMID:Clearance ratios of amylase isoenzymes and IgG subclasses: do they reflect glomerular charge selectivity? 912 32


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