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)

The excretion of the enzyme gamma-glutamyl-transpeptidase and its isoenzymes into the urine was investigated in patients with renal diseases and compared with the excretion of the enzymes leucine-aminopeptidase and lactate-dehydrogenase. In animal experiments an increased excretion of these enzymes was found after autotransplantation. Increased excretion of gamma-glutamyl-transpeptidase was also found in patients with glomerulonephritis and in the polyuric phase of acute tubular necrosis, but not in cases of pyelonephritis and in the oliguric phase of acute tubular necrosis. The alterations of the isoenzyme pattern during diseases with increased enzyme excretion are in accordance with the hypothesis that the enzymes are liberated from the kidney tissue into the urine, and only a minority stems from the blood. Investigation of the excretion of gamma-glutamyl-transpeptidase and its isoenzymes into the urine seems to be of both scientific and clinical interest.
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PMID:Investigations of the excretion of gamma-glutamyl-transpeptidase into the urine. 0 55

Although haematuria is a relatively common symptom of hemophilia A and B, renal disease seemed to be a rarity and it has usually been held that this symptom was benign in nature. However detailed studies of renal function in a series of such patients using radiological and biochemical tests of renal function show significant differences compared to normal. These abnormalities seem to be associated with recurrent haematuria but do not appear to be related directly to replacement therapy with plasma concentrate and do not occur more frequently in patients who have received long term fibrinolytic inhibitors. Other rare renal disorders associated with haemophilia include nephrotic syndrome, trauma, acute tubular necrosis, analgesic nephropathy and chronic pyelonephritis.
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PMID:Renal disorders in haemophilia A and B. 26 97

The clinical picture of an enlargement in kidney size, a decrease in renal function and an increase in temperature in a patient with a transplanted kidney into an ileal loop presents a problem in differential diagnosis among rejection, acute tubular necrosis and acute pyelonephritis.
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PMID:Acute pyelonephritis in a transplant patient with an ileal loop mimicking rejection. 78 33

We report a case of renal cortical microabscesses which presented as oliguric acute renal failure. Prior to the biopsy the patient was suspected of having acute pyelonephritis with acute tubular necrosis. Biopsy was performed to rule out rapidly progressive glomerulonephritis as a cause of his renal failure. To our surprise, we found multiple small microabscesses in the renal cortiex. Renal cortical microabscesses should be considered as a reversible acute renal failure.
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PMID:Renal cortical microabscesses as cause of reversible acute renal failure. 84 81

One hundred and seventy-five 67Ga-citrate scans were performed to detect suspected occult inflammatory processes. None of the patients had a known malignancy. Renal activity was noted in 12 patients (6.8%) on the 48-hr image. These patients had either pyelonephritis, acute tubular necrosis, vasculitis, or a renal abscess. Since delayed 67Ga uptake in the kidneys may be the first evidence of renal disease, further investigation, including either arteriography or biopsy, is necessary. In patients with a known malignancy, tumor involvement must be considered.
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PMID:Significance of delayed 67Ga localization in the kidneys. 96 53

We investigated the relationship between urinary prostaglandin E2 (UPGE2), kallikrein (UKal), graft function and complications after renal transplantation in 11 patients. Grafts of 9 patients were from living-related donors (LRD), and other 2 patients were from a cadaveric donor (CAD). UPGE2 was measured by the radio immunoassay, and UKal was measured by the amidolytic method using Pro-Phe-Arg-MCA. The results were as follows. 1. In 5 of 6 patients from LRD without acute rejection episode (ARE), both UPGE2 and UKAL were within normal and/or slightly less than normal. UKal values of the other patient were high in his donor. 2. In 2 of 3 recipients from LRD who experienced ARE, UKal increased prior to ARE. UPGE2 also increased at the time of ARE, but it showed a periodic rise in the stable condition. 3. In 1 of 2 recipients from CAD, UKal exhibited a transient elevation at the time of acute tubular necrosis (ATN) and pyelonephritis while UPGE2 was low. In another recipient, UKal was almost within normal range at the time of ATN, and UPGE2 showed a periodic rise. 4. A significant correlation was seen between UKal, UPGE2 and UAld in the recipients from LRD without ARE (except 1 patient who showed high UKal values). However, the correlation was blurred inclusive of values in the patients who experienced ARE or other complications. There was no relationship between UKal, UPGE2, creatinine clearance, urine volume and urinary sodium. 5. Soybean trypsin inhibitor (STI) was used for the confirmation of specificity of the amidolytic method.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Urinary prostaglandin E2 and kallikrein-like activity excretion in renal transplant recipients]. 235 62

Eosinophiluria is considered a useful marker of drug-induced acute interstitial nephritis. However, recognition of eosinophiluria by Wright's staining is technically difficult, and the spectrum of disorders causing eosinophiluria is not completely defined. We have adapted Hansel's stain for the examination of urinary sediment. Whereas there was a variable uptake of Wright's stain by eosinophils in the urine, such eosinophils were readily recognized with Hansel's stain by the presence of bright red granules. The prevalence of eosinophiluria in acute interstitial nephritis was 10 of 11 patients, in acute tubular necrosis none of 30, in acute pyelonephritis none of 10, in acute cystitis 1 of 15, in postinfectious glomerulonephritis 1 of 6, in rapidly progressive glomerulonephritis 4 of 10, and in acute prostatitis 6 of 10. Eosinophiluria in acute interstitial nephritis was demonstrated by Hansel's stain in 10 of 11 patients but by Wright's stain in only 2 of 11 patients. We conclude that Hansel's stain substantially improves the recognition of eosinophiluria as compared with Wright's stain. Eosinophiluria is useful in distinguishing acute interstitial nephritis from acute tubular necrosis. The clinical spectrum of eosinophiluria also includes rapidly progressive glomerulonephritis, acute prostatitis, and occasionally, acute cystitis or postinfectious glomerulonephritis.
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PMID:Eosinophiluria--a new method of detection and definition of the clinical spectrum. 1842 May 15

A sandwich ELISA assay has been formatted from two commercially available murine monoclonal antibodies, URO-4 and URO-4a, directed against a 120,000 dalton glycoprotein, the adenosine deaminase binding protein (ABP), found on the brush border of the renal proximal tubular epithelial cell. Untimed urine samples from 37 normal individuals and urinary ABP less than 0.1 AU; 37 patients with pure glomerular disease had ABP less than 0.4 AU (with 29, or 76% less than 0.2 AU); 10 patients with pre-renal azotaemia had ABP less than 0.6 (with 8, or 80% less than 0.3 AU). In contrast, 79 patients with post-ischaemic acute tubular necrosis had ABP greater than 0.6 AU. Acute renal failure due to myoglobinuria, contrast dye, and aminoglycoside toxicity were all associated with urinary ABP greater than 1.0 AU. In addition, all six patients with acute bacteraemic pyelonephritis had ABP greater than 0.7 AU, as opposed to ABP less than 0.2 AU in the urines of 12 women with acute cystitis. We conclude that this monoclonal antibody based urinary assay is a sensitive measure of renal proximal tubular injury, reliably distinguishes acute tubular from glomerular disease, and may be helpful in differentiating forms of urinary tract infection.
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PMID:Diagnosis of renal proximal tubular injury by urinary immunoassay for a proximal tubular antigen, the adenosine deaminase binding protein. 288 57

Duplex Doppler ultrasound (US) examination of the renal vasculature has proved valuable in assessing the kidney transplant. The normal renal allograft exhibits low-impedance arterial inflow similar to that seen in the normotopic kidney. The authors and others previously reported that a high vascular impedance, defined as either a pulsatility index (PI) greater than 1.8 or a resistive index greater than 0.9, indicates acute vascular rejection (AVR). Although AVR remains the most common cause of increased PI, the authors noted ten episodes among 180 serially followed-up transplants in which abnormal waveforms were clearly not due to rejection. Four other causes of increased vascular impedance are reported, including renal vein obstruction, severe acute tubular necrosis, pyelonephritis, and extrarenal compression of the graft. These new causes only slightly decrease the specificity of high vascular impedance for rejection. Furthermore, the cause can usually be recognized from the clinical history or other US findings.
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PMID:Unusual causes of increased vascular impedance in renal transplants: duplex Doppler evaluation. 305 Nov 13

Acute renal failure is a most challenging clinical problem when it occurs in pregnancy. It requires an understanding of the normal physiology of the kidney in pregnancy and the natural history of different underlying renal diseases when pregnancy occurs. Because patients with chronic renal disease may present with worsening proteinuria, hypertension, and renal function, these disorders must be excluded from those conditions that cause acute deterioration of renal failure in otherwise normal women during pregnancy. As in all patients who develop acute renal failure, prerenal and obstructive causes must be excluded. Particularly important causes of prerenal azotemia in pregnancy include hyperemesis gravidarum and uterine hemorrhage, especially if it is unsuspected as in abruptio placentae. Infectious causes of acute renal failure in the pregnant woman include acute pyelonephritis and septic abortion. The clinical presentation of both these conditions should be apparent, and appropriate diagnosis and treatment can then be promptly instituted. Renal cortical necrosis is another cause of renal failure that occurs more frequently in pregnancy, and it must be differentiated from the many causes of acute tubular necrosis that may be associated with pregnancy. Those conditions that cause renal failure unique to pregnancy must always be considered when renal function deteriorates in the last trimester or the postpartum period. Severe preeclampsia, acute fatty liver of pregnancy, and idiopathic postpartum acute renal failure may all present similar complications, but the approach to each of these clinical disorders must be individualized. By understanding the causes of renal functional deterioration in pregnancy, a logical differential diagnosis can be established, allowing appropriate therapeutic decisions to preserve both maternal and fetal well-being.
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PMID:Acute renal failure in pregnancy. 305 11


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