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)

Eleven out of a series of twenty-nine patients (37-9%) with acute copper sulphate poisoning developed acute renal failure. Intravascular haemolysis appeared to be the chief factor responsible for renal lesions in these patients. Histological lesions observed in the kidney varied from those of mild shock to well established acute tubular necrosis. In one case, granulomatous lesions were seen in response to tubulorrhexis. Renal failure was the chief indication for dialysis in ten patients, whereas one patient was dialysed primarily for removal of copper. Notwithstanding the adequate control of uraemia by dialysis, only six of the eleven patients recovered. Septicaemia was responsible for death in three, hepatic failure in one and methaemoglobinaemia in another. It is postulated that release of copper from haemolysed red cells during acute haemolytic episodes may initiate, or contribute to, the development of renal damage.
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PMID:Acute renal failure following copper sulphate intoxication. 87 9

Acute, usually reversible, renal failure has been observed in patients with normal or minimally altered glomeruli on renal biopsy. This review aims to examine the clinical features of acute renal failure in these patients and to evaluate factors that may contribute to the reduction in glomerular filtration rate (GFR). In an analysis of 79 cases affecting 75 patients reported in the English literature since 1966, with acute renal failure associated with minimal change disease or mild histopathological changes in glomeruli, the average age was 58 +/- 2 years (mean +/- 5 SEM), urine protein excretion 11.6 +/- 0.6 g/d, and serum albumin level 19 +/- 1 g/L (1.9 +/- 0.1 g/dL). Acute renal failure was documented an average of 29 +/- 5 days after onset of nephrotic syndrome, and persisted for 7 weeks in 62 episodes in the 58 patients in whom recovery of renal function occurred. Fourteen patients died of uremia or required chronic dialysis, and 3 were lost to follow-up. Although plasma volume depletion was sometimes cited as the cause of renal failure, objective signs of hypovolemia were not documented and most patients did not improve after treatment designed to correct volume deficits. In contrast, histopathological changes consistent with acute tubular necrosis (ATN) were observed in at least 60% of cases. Since the pathogenesis of acute renal failure in minimal change nephrotic syndrome is unknown, we evaluated hemodynamic determinants of GFR in patients with minimal change disease with normal or near-normal renal function, and in relevant animal models, to obtain insights into the effect of nephrotic syndrome on GFR. Although acute renal failure is uncommon, GFR is reduced concurrently with nephrotic syndrome in approximately 30% of children and adults. Absolute and effective blood volume and renal plasma flow are relatively well preserved. However, clinical and experimental observations suggest that the glomerular ultrafiltration coefficient may be reduced by as much as 50%. These findings, together with renal biopsy changes in cases with acute renal failure, suggest that severe reductions in GFR in some patients with minimal change nephrotic syndrome may result from an interaction between acute ischemic tissue injury and preexisting intrinsic renal abnormalities.
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PMID:Reversible renal failure in the nephrotic syndrome. 155 65

Hemorrhagic fever with renal syndrome (HFRS) is an acute viral disease that occurs over wide areas of Europe and Asia. Hantaviruses are the cause of this syndrome. The hallmark of HFRS is the triad of fever, hemorrhage, and renal failure. In its severe form it is associated with significant mortality. The syndrome evolves through five phases: febrile, hypotensive, oliguric, diuretic, and convalescent. The central physiologic derangement in HFRS is vascular dysfunction, manifested by impaired vascular tone and increased vascular permeability. The systemic effects of this dysfunction account for the occurrence of hypotension and shock, while local effects are probably important in the development of renal failure. Shock in HFRS has distributive and oligemic features, while renal failure has features of acute tubular necrosis. Hemorrhage is a consequence of vascular injury and a deficit of functional platelets. Vascular and platelet dysfunction are both compounded by uremia. Disseminated intravascular coagulation contributes to hemorrhage in some patients. Although hantaviruses are infectious for endothelial cells and may cause direct injury, a large body of evidence suggests that immune mechanisms play an important role in the pathogenesis of HFRS.
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PMID:Mechanisms of disease in Hantavirus infection: pathophysiology of hemorrhagic fever with renal syndrome. 167 61

Monitoring of immunoglobulin-secreting cells in peripheral blood was performed in 88 renal transplant recipients using a reverse hemolytic plaque-forming cell assay. Comparison with other in vitro tests for rejection (plasma neopterin, CD4/CD8 ratio) demonstrated that the number of immunoglobulin-secreting cells in peripheral blood provides a highly sensitive rejection marker. Evidence of rejection was obtained 1.7 +/- 0.4 (mean +/- SEM) days before a rise in creatinine, with a significant PFC rise in 95% (73/77) of rejection episodes. The PFC response was not influenced by HLA matching, number of preoperative blood transfusions, acute tubular necrosis, or uremia. A significant PFC rise in the absence of an ongoing rejection episode occurred in the presence of bacterial or viral infections, in case of posttransplant surgical complications, and regularly during the early posttransplant period (days 4-9). However, even early posttransplant the PFC peak was significantly higher in patients with an ongoing rejection episode than in patients without rejection (P less than 0.001).
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PMID:B lymphocyte response as an indicator of acute renal transplant rejection. I. Immunoglobulin-secreting cells in peripheral blood. 257 82

The neurotoxic potential of benzylpenicillin administered as a continuous intravenous infusion was studied in rabbits with intact blood-CNS barriers, experimentally established Enterobacter cloacae meningitis and experimental renal failure, secondary to cephaloridine-induced acute tubular necrosis after iv administration. The concentrations of benzylpenicillin in serum, CSF and brain tissue fluid were assayed at the onset of epileptogenic electroencephalographic activity. The brain tissue concentrations of benzylpenicillin were consistently higher than those in CSF in both infected and uninfected animals. The highest brain tissue fluid concentrations of benzylpenicillin were found in rabbits with renal failure after cephaloridine pretreatment. The brain tissue fluid concentrations of benzylpenicillin rather than the CSF concentrations were decisive for neurotoxicity. Cephaloridine-induced uraemia, but not the combination of uraemia and meningitis, resulted in a significantly increased tolerance of high intracerebral concentrations of benzylpenicillin before EEG-changes were precipitated.
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PMID:Neurotoxicity of benzylpenicillin in experimental renal failure and Enterobacter cloacae meningitis. 279 45

Metabolic clearance rate (MCR) and production rate (PR) of calcitriol were studied three and seven days after ischemic acute tubular necrosis (ATN). Creatinine clearance was decreased three days after clamping the renal arteries (0.42 +/- 0.03 ml/min/100 g, N = 6 in ATN vs. 0.68 +/- 0.09, N = 7 in sham controls; P less than 0.001). Plasma concentrations (24.1 +/- 1.9 pg/ml) and PR of calcitriol (9.8 +/- 0.91 ng/kg/day) were significantly lower in ATN rats three days after ischemic insult when compared to sham control rats, respectively (76.6 +/- 7.3 pg/ml, and 29.6 +/- 3.3 ng/kg/day; both P less than 0.01). The MCRs of calcitriol were not different between ATN (0.28 +/- 0.02 ml/min/kg) and sham control rats (0.27 +/- 0.01). By the seventh day after ischemic injury, when creatinine clearance of ATN rats returned to normal, both the PR and plasma concentrations of calcitriol also returned to normal values in these animals. In order to assess the effect of uremia on calcitriol metabolism, MCR and PR of calcitriol were measured in rats with reinfusion of their urines for 24 hours. The PR of calcitriol was significantly decreased (9.42 +/- 1.21; vs. controls, 20.5 +/- 2.9 ng/kg/day, P less than 0.001) in uremic animals. Since decreased PR of calcitriol was also accompanied by decreased MCR of calcitriol, plasma concentrations of calcitriol of the uremic rats with intact kidneys remained within normal values. We conclude that the PR of calcitriol is decreased early in ATN rats. Although the MCR was not decreased in mild ATN rats, it may decrease in severe acute renal failure.
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PMID:Production and metabolic clearance of calcitriol in acute renal failure. 336 54

Recovery of renal function after acute tubular necrosis usually begins within a few days or weeks, provided the patient does not succumb to the complications of uremia or of the precipitating illness. However, some studies suggest a high incidence of permanent renal failure perhaps reflecting the survival of patients who previously died because of less ideal treatment. Recently, we observed a patient with acute tubulo-interstitial nephritis whose course was notably different from the usual pattern since the patient required chronic dialysis. We believe that the cause of this permanent lesion is multifactorial including age, nephrotoxic agents (aminoglycosides, intravenous contrast media) and perhaps immunological mechanism. Treatment with prednisone did not produce improvement in our case and the patient has been treated by maintenance hemodialysis.
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PMID:[Chronic terminal renal failure: an unusual outcome of acute tubulointerstitial nephritis]. 344 94

The concentrations of serum amyloid A protein, a high-density lipoprotein-associated protein synthesized in the liver, were monitored in 66 recipients of cadaveric renal allografts. Acute graft rejection episodes were associated with dramatic elevations of serum amyloid A. Electrofocusing and immunoblotting of rejection sera showed a polymorphic serum amyloid A pattern similar to that obtained with control (apo) serum amyloid A isolated from the high-density lipoprotein fraction of plasma. Rejections in patients receiving cyclosporine alone as posttransplantation immunosuppressive medication were characterized by significantly higher serum amyloid A levels than in those receiving cyclosporine in combination with methylprednisolone. Due to the dramatic rejection-induced serum amyloid A elevation, limit values could be used which combined high sensitivity (87-96%) with reasonably high predictive value of a positive test (82%). The serum amyloid A test was applicable also in patients with initially nonfunctioning or poorly functioning grafts. It is concluded that monitoring of the serum amyloid A concentrations offers a valuable noninvasive aid in the early diagnosis of acute renal allograft rejection, including patients with acute tubular necrosis of the graft.
Uremia Invest
PMID:Posttransplantation monitoring of high-density lipoprotein-associated serum amyloid A protein: a new diagnostic aid in the detection of renal allograft rejection. 391 28

Ultrasound examination of a renal transplant was performed in 27 patients over a period of 28 months; there were kidneys from 12 living and 15 cadaveric donors. The ultrasonic scans were performed over a period ranging from 2 days to 12 years following transplantation. We were able to observe and describe the echographic findings of the normal evolution of a well functioning renal transplant, acute tubular necrosis, acute and chronic rejection, perirenal fluid collection, and obstructive uropathy. Ultrasound evaluation of renal transplant was accurate in the diagnosis of postoperative complications together with clinical and laboratory findings. Ultrasound imaging is independent of renal function and can be performed quickly as often as necessary. Percutaneous procedures, including fine needle aspiration, biopsy, aspiration of fluid collection, and positioning of the pyelostomy catheter can be performed under ultrasonic guidance.
Uremia Invest
PMID:Role of ultrasound in renal transplantation. 391 30

Of 48 patients with fulminant hepatic failure who progressed to grade III or IV encephalopathy 38 showed evidence of renal impairment. In 32 of these patients the underlying cause could be placed initially into one of three categories-prerenal uraemia (4 patients), acute tubular necrosis (16), and "functional renal failure" (12). The latter differed in several respects from that seen with liver failure secondary to cirrhosis. The frequency and type of renal impairment was the same in those patients in whom the fulminant hepatic failure had resulted from an overdose of paracetamol as in the other aetiological groups.Abnormalities in plasma electrolytes were common-in particular hypernatraemia occurred in 11 patients from an osmotic diuresis precipitated by hypertonic dextrose or fructose given intravenously, and from the sodium in the fresh frozen plasma used to correct the coagulation disturbance when renal excretion of this ion was inappropriately low.
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PMID:Frequency and type of renal and electrolyte disorders in fulminant hepatic failure. 481 48


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