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 one-year period, drug-associated acute renal failure (ARF) was prospectively recorded in 398 patients, registered in 58 french nephrology Units. Drugs involved were primarily antibiotics, mainly aminoglycosides, glafenine, non-steroidal antiinflammatory drugs and contrast media. Hypersensitivity reactions were reported in 69 patients. Renal biopsy, performed in 81 instances, showed acute tubular necrosis in 42 and acute interstitial nephritis in 20 patients. Hypotension, sodium depletion and/or cardiac failure were predisposing factors in 198 cases. Fifty patients died, 251 recovered fully or regained previous renal function, and in 93 permanent renal damage remained. Advanced age, oliguria, severe ARF, and preexisting cardiac, hepatic or renal insufficiency were poor prognostic factors. Prevention of drug-associated ARF should be directed to high-risk patients, particularly those receiving aminoglycosides and contrast media.
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PMID:[Acute renal failure associated with drugs or iodinated contrast media. Results of a cooperative multicentric study by the Nephrology Society]. 287 11

A method to identify nucleated nonsquamous cells in urine using monoclonal antibodies and immunoperoxidase stain is described. Cells from washed deposits of midstream urine samples were transferred to gelatinized slides in a cytocentrifuge, air-dried, acetone fixed, and subjected to microwave irradiation. Slide preparations were then treated with monoclonal antibodies with the use of a four-layer peroxidase-antiperoxidase technique. It was possible to identify granulocytes, monocytes, lymphocytes, and renal epithelial and urothelial cells. This method was found to be helpful in determining the profiles of cells in urine in acute tubular necrosis, drug-related acute interstitial nephritis, and crescentic glomerulonephritis.
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PMID:Immunocytologic dissection of the urine sediment using monoclonal antibodies. 305 61

The pathogenesis of acute renal failure (ARF) in such common conditions as acute tubular necrosis, acute interstitial nephritis, and primary graft anuria (ischemic transplant ARF) is poorly understood. Animal models may not exactly mimic the situation in man and thus human morphologic studies are of particular importance. Non-replacement of individual sloughed tubular cells and simplification of the brush border and basolateral infoldings of tubular cells are prominent morphologic changes which correlate with the presence of renal failure. It is possible that the initial injury inhibits cell membrane synthesis, thus interfering with proximal tubular sodium reabsorption with resulting activation of the renin angiotensin system and afferent arteriolar vasoconstriction. Tubular backleak, tubular obstruction by casts and debris, and decreased glomerular ultrafiltration coefficient may also play a role. Although poorly studied until now, the renal failure in primary graft anuria may have a completely different pathogenesis from that in acute tubular necrosis and acute interstitial nephritis. Cyclosporine nephrotoxicity is an important component of primary graft anuria, as seen in many transplant centers in the 1980's.
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PMID:Acute renal failure in man: pathogenesis in light of new morphological data. 330 Nov 19

Urinary doubly refractile lipid bodies (DRLB) are a characteristic finding in patients with glomerular renal diseases causing heavy proteinuria. DRLB are felt to be an uncommon finding in glomerular diseases without heavy proteinuria, and a rare finding in nonglomerular renal diseases. In order to determine whether DRLB are found in nonglomerular renal diseases, we reviewed the medical records of all patients who had urinalyses performed in our laboratory from February 1975 to June 1983. Three hundred sixty one patients demonstrated less than or equal to +2 proteinuria, and at least two DRLB. Of these, 290 were identified as having a single renal diagnosis. One hundred forty eight patients (51%) had a variety of acute and chronic glomerular diseases, and 125 patients (43.2%) had nonglomerular renal diseases, including acute tubular necrosis (ATN), prerenal azotemia, chronic interstitial nephritis, polycystic kidney disease, acute interstitial nephritis, renal neoplasia, and acute myeloma kidney. Ten patients had transient proteinuria associated with acute illness, and seven patients had no renal disease at all. Only two patients with nonglomerular renal disease had more than five DRLB per 20 high power microscopic fields. The frequency of DRLB in patients with nonglomerular renal diseases was: chronic interstitial nephritis, 26%; polycystic kidney disease, 38%; prerenal azotemia, 20%; ATN, 15%; and acute interstitial nephritis, 33%. These data suggest that at lower levels of proteinuria, DRLB are found frequently in nonglomerular renal diseases, and that DRLB do not differentiate glomerular from nonglomerular renal diseases unless more than five DRLB are found on urinary sediment examination.
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PMID:Urinary doubly refractile lipid bodies in nonglomerular renal diseases. 335 69

A review of 85 patients aged 60 years or more, treated in a southern Indian hospital for conditions requiring renal biopsy, showed that diffuse poliferative glomerulonephritis was the most frequent diagnosis, being present in 24 cases of whom 11 had elevated serum streptococcal antibody titres. Infections were also important in 2 patients with amyloidosis secondary to tuberculosis, in 3 patients with acute tubular necrosis following infectious gastroenteritis and in a patient with acute pyaemic interstitial nephritis with septicaemia. Drugs including indigenous medicines were the other important cause of renal disease, being implicated in 11 cases.
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PMID:Medical renal disease in the elderly in a southern Indian hospital. 338 Feb 27

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

Indirect immunoperoxidase analysis using monoclonal antibodies (Mo Ab) was performed in 33 renal biopsies with interstitial cellular infiltration obtained from non-transplanted patients. We reviewed four acute interstitial nephritis (IN), three chronic IN, four granulomatous IN, four acute tubular necrosis, four vasculitis, seven primary glomerulonephritis and seven active lupus nephritis (LN). We used Mo Ab recognizing T and B cell markers [OKT3, OKT8, T4, B1, IOT14 (IL2 receptor)], HLA-DR related antigen (I2) and monocytes/macrophages (LeuM3). In all cases the interstitial cellular infiltrates were predominantly T cells, whereas the B cell population accounted for less than 20% of the infiltrate. LeuM3+ cells were present in 28 of 32 cases, usually in a lesser proportion than T cells. IOT14+ cells were exceptional. T4+/T8+ cells were clearly greater than one in three acute IN, three granulomatous IN, two LN and two vasculitis. The T8+ cell population predominated in one case of chronic IN related to a non-steroidal anti-inflammatory drug. In all the remaining cases T4+ and T8+ cells were equally present. Aberrant strong HLA-DR expression within tubular cells was noted in nine cases (4 LN) irrespective of the presence of tubular lesions. On the basis of the phenotypic analysis, our data do not support a specific pattern of the infiltrate in regard to a given etiology and thus cannot be used as a diagnostic tool. However, such analysis may aid in understanding the mechanisms of tissue injury.
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PMID:Characterization of mononuclear cell subsets in renal cellular interstitial infiltrates. 352 2

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

Non-narcotic analgesics have acute and chronic effects on the kidney. Until quite recently chronic effects have received much more attention than acute effects. Renal papillary necrosis attributed to prolonged intake of analgesic compounds was first described from Switzerland in the 1950s, and subsequently in many countries including Scandinavia, Australia, Belgium and Canada. Renal papillary necrosis is now accepted as an effect of over-the-counter analgesic compounds and has also been recorded with many individual non-steroidal anti-inflammatory drugs (NSAIDs). Evidence suggests that uroepithelial tumours also occur as a complication of prolonged abuse of analgesic compounds. Clinical evidence associating renal papillary necrosis with compound analgesics and NSAIDs has been backed up by experimental evidence showing that these drugs cause renal papillary necrosis in animals. Acute effects of non-narcotic analgesics have been described mainly in association with aspirin and NSAIDs. In high renin states, including salt-depleted normal subjects, NSAID administration may be associated with an acute decrease in renal function, which is more obvious in patients who have underlying renal disease. Clinical syndromes which occur in association with NSAIDs include oedema, hyperkalaemia and acute renal failure and the acute nephrotic syndrome. Acute renal failure may be associated with acute interstitial nephritis and the nephrotic syndrome or may be due to acute tubular necrosis. Patients who have the nephrotic syndrome show fusion of foot processes of glomerular epithelial cells on electron microscopy as well as acute interstitial nephritis. Patients who suffer these episodes of acute renal function deterioration associated with NSAIDs recover slowly after withdrawal of the drugs, and the recovery may not be complete.
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PMID:Effects of non-narcotic analgesics on the kidney. 355 79

The pathogenetic factors leading to acute renal failure (ARF) in 223 children between the ages of 20 days and 14 years were studied. Diarrhoeal diseases were responsible for ARF in 49.8%, acute glomerulonephritis in 34.1%, drug induced intravascular hemolysis in glucose -6-phosphate dehydrogenase deficiency in 4.5%, snake bite in 4%, hemolytic uremic syndrome in 2.2%, and miscellaneous causes in 5.4%. Dialysis was instituted in 178 children and the others were treated conservatively. Renal histology in 39 out of 76 children who presented with an acute nephritic illness revealed acute endocapillary proliferative glomerulonephritis in 27 and crescentic glomerulonephritis in 12. The histology in 79 out of 147 remaining patients showed acute tubular necrosis in 64, acute cortical necrosis in 13, and acute interstitial nephritis in 2. Overall mortality was 27.4%. This high incidence of ARF due to infective diarrhoeas and dysentery reflects poor socio-economic and hygienic conditions, inadequate facilities in rural areas, delays in seeking medical advice, and lack of knowledge about fluid and electrolyte therapy amongst the staff.
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PMID:Acute renal failure amongst children in a tropical environment. 358 35


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