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)

Proteinuria was studied in ten renal allograft recipients; it was defined as: (a) glomerular--characterized by predominant albumin excretion; (b) tubular--significant excretion of both albumin and low molecular weight (LMW) proteins; and (c) glomerulo-tubular or mixed type, a combination of the two. LMW protein and albumin were quantitated by polyacrylamide gel electrophoresis with sodium dodecyl sulfate. In the immediate posttransplant period, LMW protein and albumin excretion, expressed as a percentage of creatinine clearance, were high, revealing a mixed pattern, and excretion of both protein classes was higher than during both acute tubular necrosis and acute rejection crisis. Tubular proteinuria was observed in acute tubular necrosis; a glomerulo-tubular or mixed pattern of protein excretion in acute rejection crises.
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PMID:Proteinuria following renal transplantation. 32 83

Djenkolic acid was extracted from djenkol beans with 70% ethanol and water and was quantitatively determined by paper chromatography. Djenkol beans contained 0.3-1.3 gm% djenkolic acid and about 93% of this acid occurred in the free state. The toxicity of djenkol beans was studied in 5 rhesus monkeys, 9 albino rats and 22 mice fed with 70% ethanol extracts. The total urinary output decreased. There was an increase in specific gravity of the urine during the period of feeding monkeys with djenkol beans. Urinary samples of the experimental animals were turbid and contained some red cells, white cells, epithelial cells, albumin and amorphous particles. One of 22 mice excreted sharp needle-shaped crystals in the urine on day 3 after feeding. Histological examination of kidneys of rats and mice showed mild to severe acute tubular necrosis with some glomerular cell necrosis.
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PMID:Studies on djenkol bean poisoning (djenkolism) in experimental animals. 82 79

Reported was an aged woman (80-year-old) of minimal change nephrotic syndrome which was complicated with reversible oliguric acute renal failure. The patient presented massive proteinuria, anasarca, and severe azotemia. She recovered conservatively from the acute renal failure and subsequently remitted from the nephrotic syndrome after the treatment which comprised albumin infusion, diuretics, adrenocorticosteroid hormones (including the pulse therapy), antiplatelet drug, and anticoagulants. The histopathologic findings of renal biopsy were compatible with minor glomerular abnormalities and acute tubular necrosis with many tubular casts. The previously reported cases older than 80-year-old which remitted from minimal change nephrotic syndrome complicated with reversible acute renal failure, were very rare. The present case was the second case among the literatures.
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PMID:[An aged woman with minimal change nephrotic syndrome complicated with reversible acute renal failure]. 219 Nov 62

Male volunteers were infused with L-arginine dextran and Haemaccel. Arginine (0.5 g/kg body weight infused over 30 min) resulted in transient highly significant increases in urinary albumin (p less than 0.001), beta 2-microglobulin (p less than 0.001) and N-acetyl-beta-D-glucosaminidase [NAG] (p less than 0.001). These effects lasted less than 120 min. Dextran 40 and 70 (500 ml infused over 2 h) did not affect urinary albumin, beta 2-microglobulin or NAG excretion. Haemaccel (8 ml/kg body weight infused over 2 h) resulted in significant increases in urinary albumin (p less than 0.05) and beta 2-microglobulin (p less than 0.01) during the second hour of the infusion. It also caused a biphasic increase in urinary NAG excretion, the initial peak (p less than 0.05) coinciding with the peak of albumin and beta 2-microglobulin excretion. The second peak which was more defined (p less than 0.01) occurred 21-24 h after the beginning of the infusion. Neither arginine or Haemaccel have been reported to be nephrotoxic whereas dextran infusions are a well recognised cause of acute tubular necrosis. These data indicate that increases in urinary beta 2-microglobulin and NAG are not always reliable indicators of nephrotoxicity or renal tubular cell damage.
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PMID:The effects of arginine, dextran and Haemaccel infusions on urinary albumin, beta 2-microglobulin and N-acetyl-beta-D-glucosaminidase. 242 74

The secretory immune system has been well studied in the intestinal, bronchial, and biliary systems and breast. Tissue studies of secretory immunoglobulins in the kidney are scanty, mostly related to nephropathies with IgA. Renal tissues from 37 autopsies selected for any history of renal dysfunction were processed for immunohistologic studies on frozen sections with several antisera, including a purified rabbit anti-human secretory component (SC). By immunohistology, gel diffusion, and immunoblotting, the anti-SC antibody reacted appropriately with purified human SC, saliva, intestinal epithelium, and breast milk and did not cross-react with immunoglobulin heavy or light chains, lactoferrin, and other tissue proteins. IgA and SC were seen in tubular casts in 70% of patients, whereas less impressive staining with IgM, IgG, and albumin was seen, respectively, in 24%, 13%, and 22% of the patients. SC was present in the cytoplasm of distal tubule and Henle's loop cells in 78% of specimens. A control group of 10 healthy individuals who died suddenly showed minimal staining of casts and tubules in 2 specimens. Renal pathology in the group with IgA-SC+ casts included acute tubular necrosis (54%), severe chronic renal disease (61%), and mild chronic renal injury (38%). The group with negative IgA-SC casts included acute tubular necrosis (64%), infectious interstitial nephritis (36%), and negligible renal disease (36%). This study suggests that discrete distal segments of the nephron may have the capability of secreting SC, which is probably coupled with serum-derived IgA and incorporated into luminal tubular secretions. The low level of immunosecretions in kidneys which are normal or minimally damaged suggests that this system may need to be turned on by unknown, probably pathogenic stimulating factors.
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PMID:Secretory immune responses in human kidneys. 354 43

An episode of acute pustular psoriasis in a middle-aged man was associated with cholestatic jaundice and followed by acute tubular necrosis. It is suggested that renal failure was due to oligaemia after the loss of albumin into and from the skin. Fluid balance, central venous pressure, and arterial blood pressure should be monitored in patients with acute pustular psoriasis.
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PMID:Oligaemia, renal failure, and jaundice associated with acute pustular psoriasis. 483 97

The impact of nonlinear plasma protein binding of a drug on its removal by haemodialysis has been quantified. Prednisolone 10-100 mg was given i.v. to 10 renal transplant patients on haemodialysis for acute tubular necrosis. Dialysate and afferent and efferent blood samples were collected simultaneously in 67 instances. Total and unbound prednisolone in plasma and its total concentration in blood and dialysate were assessed by high performance liquid chromatography and equilibrium dialysis. The amount of prednisolone lost, as measured directly in the dialysate (21.8 +/- 4.4 micrograms/min, mean +/- SE), was predictable from the afferent-efferent blood concentration differences (20.1 +/- 4.8 micrograms/min), but not from measurements of total afferent-efferent prednisolone concentrations in plasma (13.1 +/- 3.0 micrograms/min). The amount of prednisolone lost in the dialysate increased linearly with unbound (r2 = 0.96) and hyperbolically with the total prednisolone concentration in plasma. The latter hyperbolic relationship is adequately described by the equation for nonlinear plasma protein binding, using the affinity and capacity constants of albumin and transcortin for prednisolone (r2 = 0.98). Thus, the haemodialysis clearance of total prednisolone is concentration-dependent, while the clearance of unbound prednisolone is constant (76 ml/min). Free clearance values or measurements of afferent-efferent blood concentrations are mandatory for a drug showing nonlinear plasma protein binding in order to predict the amount lost in the dialysate.
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PMID:Nonlinear plasma protein binding and haemodialysis clearance of prednisolone. 675 35

The hemodynamic status of renal transplant patients is important for achieving early diuresis. Many reports have demonstrated that overload infusion can reduce the frequency of acute tubular necrosis (ATN). We studied the effect of overload fluid infusion using pulmonary arterial pressure (PAP) and pulmonary wedge pressure (PCWP) monitoring on forty patients undergoing cadaveric renal transplantation. Patients were divided into two groups. Group 1 received general anesthesia by nitrous oxide-isoflurane. Group 2 received continuous epidural anesthesia. Mean PAP > 15 mmHg and mean PCWP > 10 mmHg were achieved with the infusions of normosmotic saline, colloid solution and human albumin. Systolic arterial pressure (SAP) > 150 mmHg was achieved by intravenous administration of dopamine when required. Hemodynamic stability and diuresis in the early postoperative period were maintained in both groups. Group 1 required lower doses of dopamine than Group 2. Blood loss and infusion requirements were lower in group 1 than in group 2. No patient in either group developed pulmonary edema. We conclude that overload infusion using PAP and PCWP monitoring during general anesthesia can achieve safe diuresis immediately after cadaveric renal transplantation.
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PMID:[Hemodynamic changes secondary to overload infusion during cadaveric renal transplantation--comparison between nitrous oxide-isoflurane anesthesia and continuous epidural anesthesia]. 832 Aug

We present a 72-year-old man who had episodes of severe, acute renal failure during severe attacks of diarrhea caused by Vibrio cholerae. Patterns of acute tubular necrosis and tubulointerstitial nephritis developed following hypotension and decrease in renal blood flow, causing secondary renal ischemia. There was severe dehydration with profound hypovolemia and infection. The clinical picture included fever, weakness, arthralgia, pedal edema, mild bilateral pleural effusions, anemia, leukocytosis, azotemia with a maximum of 330 mg/dl of urea, creatine to a maximum of 9.8 mg/dl, hypoproteinemia, severe metabolic acidosis, marked increase in lactate dehydrogenase (LDH) and creatine phosphokinase (CPK), microscopic hematuria, sterile leukocyturia, normoglycemic glucosuria and phosphaturia with diminished tubular reabsorption of phosphorus. A short oliguric phase was followed by a polyuric phase lasting about 10 days, and glomerular and tubular function became normal after about 3 weeks. Treatment was by intensive infusions of fluids, electrolytes, sodium bicarbonate, salt-free albumin and antibiotics. To the best of our knowledge, this renal complication of cholera has not yet been described in Israel.
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PMID:[Acute renal failure as a complication of cholera]. 868 55

Acute renal failure (ARF) associated with idiopathic nephrotic syndrome has been reported in adults with advanced age but is a rare event in children. We have reviewed the literature on this subject and report an additional pediatric case. The pathogenetic mechanisms which may lead to ARF during the course of idiopathic nephrotic syndrome are reviewed with a brief discussion of the role of angiotensin II and angiotensin converting enzyme inhibition in this setting. Although no consensus has emerged for the prevention and treatment of ARF in patients with nephrotic syndrome, a combination of salt-poor albumin and diuretics to reduce interstitial edema may be beneficial as a preventive measure. Once acute tubular necrosis is diagnosed, dialysis may be indicated. In the majority of reports the prognosis for recovery of renal function has been good even in patients in whom long-term dialysis was required.
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PMID:Acute renal failure in idiopathic nephrotic syndrome. 904 53


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