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)

In 15 out of 35 patients with myelomatosis histological examination showed intravascular fibrin within the glomeruli, and this was associated with proliferation of the mesangial complex in 12. The presence of intravascular fibrin and mesangial proliferation was not associated with any specific immunoglobulin abnormality or with the presence or absence of Bence Jones proteinuria. In addition to fibrin being present within glomerular capillaries it was also shown in intertubular capillaries in three cases of myelomatosis with acute tubular necrosis. It is suggested that intraglomerular coagulation and fibrin deposition may contribute to the genesis of renal failure in myelomatosis.
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PMID:The kidney and intravascular coagulation in myelomatosis. 460 Sep 4

Renal insufficiency occurs in some, but not all, patients with multiple myeloma and Bence Jones proteinuria. Many of these patients are found to have a distinctive renal lesion characterized by distal nephron cast formation. It has been proposed that the specific Bence Jones protein (BJP) which is produced by a myeloma tumor may play an important role in the genesis of this cast nephropathy and that patients excreting BJPs with the highest isoelectric points (pI) are those most likely to develop this cast nephropathy. We have utilized a rat model of multiple myeloma to further evaluate the relationship between Bence Jones proteinuria and the development of myeloma cast nephropathy. This model employed immunoglobulin-secreting tumors obtained from a unique strain of rats in which they spontaneously develop. These tumors were transplanted to a homologous strain of rats and the effect on renal function and morphology in these rats were evaluated. Four different kappa light chain synthesizing tumors were studied. Following transplantation of the tumors, all rats were maintained on a diet designed to produce an acid urine (pH 5.5 to 6.0) and maximal urinary concentration (2000 to 3000 mOsm/kg). Among the rats excreting BJP of pI 6.7, 17 of 18 had virtually normal renal histology. Of the 15 rats with BJP of pI 7.6, 11 also had normal renal histology. However, 12 of 12 rats excreting BJP of pI 5.2 developed a distal nephron, light chain containing cast nephropathy. In the pI 4.3 group, 6 of 12 rats developed acute tubular necrosis, and the remaining six animals sustained a less severe lesion which was characterized by the presence of bland hyaline casts. The mean serum creatinine level obtained at the time of sacrifice was elevated (compared to that found in sham-operated controls) in the pI 5.2 group (P less than 0.001) and the pI 4.3 group (P less than 0.01) but not in the pI 6.7 or 7.6 groups. These results do not support the concept that cationic BJP's are more nephrotoxic than those that carry a more negative charge and indicate that other factors must determine the nephrotoxicity of a given BJP.
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PMID:Myeloma kidney cast nephropathy in a rat model of multiple myeloma. 641 38

Immunological events in the acute, recovery and convalescent stages of typhoid fever were correlated with the occurrence of renal disease in 24 consecutively selected patients. Serum complement levels (C3) were significantly reduced in patients with renal disease during the acute state (p less than 0.01) and increased to normal levels in the recovery phase. IgG and IgM immunoglobulin levels were significantly lower than control values in all three stages (p less than 0.05). While IgA levels were elevated to above control levels in patients with and without renal disease in all three stages, IgA levels were lower in patients with renal disease compared to those without renal involvement in the acute stage (p less than 0.025). The percentage of T cells was increased significantly in all three stages (p less than 0.01). Seven patients showed renal abnormalities. All of them had glomerular disease demonstrated by proteinuria of 1.0 g or greater per 24 h, associated with significant haematuria. Almost all of these patients were glucose-six-phosphate-dehydrogenase (G.6.P.D.) deficient. Serum blood urea nitrogen was elevated in five of these patients who were G.6.P.D. deficient, and two of them developed classical acute tubular necrosis. It appears that renal involvement in typhoid fever commonly occurs as transient glomerular or tubular disease in G.6.P.D. deficient individuals. Glomerular disease is associated with a decrease in serum complement (C3) level in acute stage.
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PMID:Immunological and clinical aspects of kidney disease in endemic typhoid fever in Iran. 660 45

To determine the nature and frequency of renal disorders in AIDS we reviewed the records of thirty-two patients hospitalized over a twenty-two month period. Group I, including all patients with AIDS who demonstrated proteinuria and/or renal insufficiency, numbered thirteen patients, in ten of whom renal tissue was available. Renal abnormalities included proteinuria in twelve patients, which exceeded two grams per day in seven. The glomerular histologic lesions included focal glomerulosclerosis, diffuse mesangial hypercellularity, diffuse proliferative glomerulonephritis, and membranoproliferative glomerulonephritis. The nonglomerular histologic lesions included acute tubular necrosis, nephrocalcinosis, focal interstitial nephritis, and one case each of intrarenal cryptococcal infection and renal cell carcinoma. Nine of these thirteen patients developed renal insufficiency, and four of them required dialysis. Their mortality by the end of the study period was eleven of thirteen patients (85 percent), significantly worse in the short term than AIDS patients without renal problems. The patients in Group I were compared to the nineteen AIDS patients without renal abnormalities in Group II. The Group I patients had a higher incidence of oral and esophageal candidiasis, other fungal infections, and infections with Mycobacterium avium-intracellulare. They also had a higher incidence of exposure to aminoglycoside antibiotics and amphotericin B, and experienced more clinical shock than their Group II counterparts. It is concluded that patients with AIDS may demonstrate renal abnormalities on the basis of immune, hemodynamic, infectious, and neoplastic derangements.
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PMID:Renal disease in patients with AIDS: a clinicopathologic study. 673 86

A collaborative study including seven kidney transplant centers in Paris recorded 19 new cases of "de novo" membranous glomerulonephritis (MGN) in a series of 1000 kidney graft biopsies over 1550 renal transplantations. This study represents the largest series "de novo" MGN in the literature. The mean time for the onset of the proteinuria was 26 months post-transplantation (extremes 2-58 months). None of the following factors seemed to be linked with the presence of MGN: age, sex, donor-recipient HLA phenotype, 1st graft vs 2nd graft, cadaver vs related graft, HLA matching, recipient treatment, number of transfused blood units, lymphocytotoxins, number of rejection episodes, number and length of acute tubular necrosis, viral or bacterial infections. These 19 new cases of MGN were compared to the other previously published 42 cases. They generally do not appear to be deleterious for the graft function.
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PMID:[Cooperative study of de novo extramembranous glomerulonephritis in renal allografts in humans: report of 19 new cases in 1550 renal transplant patients of the transplantation group of the Ile de France]. 675 63

Renal involvement during Brucella infections has been known for several years, and its real frequency appears to be higher than initially suspected. This case report deals with a patient with positive blood cultures and seroagglutination to Brucella mellitensis who presented transitory renal failure, proteinuria, and macroscopic hematuria. Renal histopathology disclosed the existence of acute tubular necrosis, and the immunofluorescence study revealed the presence of mesangial deposits of immunoglobulins and complement. Electron microscopy demonstrated the presence of electron-dense paramesangial deposits. These data suggest that immunological mechanisms are implicated in the glomerular involvement of Brucella infections.
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PMID:[Renal disease with glomerular involvement during Brucella infection (author's transl)]. 701 97

The early use of gold in medicine and dentistry dates back to the ancient Chinese and Egyptians. The discovery in 1890 that gold salts were toxic in vitro to tubercle bacilli led to the extensive treatment of tuberculosis with gold salts in the first three decades of this century. Eventually, gold therapy was extended to arthritis and lupus erythematosus, because of the belief that these diseases were forms of tuberculosis. Because of its beneficial effect particularly on active rheumatoid arthritis, chrysotherapy has remained one of the most widely used treatments of rheumatoid arthritis for the past half century. Toxicity of gold salts includes hypersensitivity reaction of skin and mucous membranes, bone marrow depression, and nephrotoxicity. The nephrotoxic clinical manifestations are renal insufficiency, proteinuria and hematuria, and the nephrotic syndrome. The pathologic changes are tubular degeneration, acute tubular necrosis or immune complex glomerulonephritis. The justification that any of these possible changes are the result of gold therapy rests clinically upon the time relationship of gold therapy and the renal symptoms, and pathologically upon the presence of gold inclusions (aurosomes) in proximal tubular epithelial cells. Aurosomes can at times be visualized by light microscopy, are usually seen by electron microscopy, and can be identified by microprobe analysis. Their pathology will be illustrated and pathogenic mechanisms discussed.
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PMID:Gold nephropathy. 703 39

The nephrotoxicity associated with mercury may be manifested as either acute tubular necrosis or an immune complex glomerulonephritis, depending upon the conditions under which the patient is exposed to the metal. Two patients with industrial exposure to mercury developed the nephrotic syndrome due to membranous glomerulonephritis. A multidisciplinary approach was used to define more precisely the pathogenetic mechanisms involved in the production of the glomerular lesion. Although glomeruli were normal by light microscopy, immunohistochemical studies demonstrated confluent finely granular epimembranous deposits of IgG and C3. This distribution was confirmed at the ultrastructural level with immunoelectron microscopy. High resolution elemental analysis of electron dense inclusions in tubular epithelial phagolysosomes demonstrated energy dispersion spectra characteristic of coexisting mercury and selenium. Eluates from the biopsy material were not immunoreactive against normal rat or human kidney. There was no immunoreactivity of epimembranous deposits with antibodies having renal tubular epithelial antigen or urinary uromucoid specificity. These observations suggest that a distinctive immunopathologic lesion is associated with mercury-associated membraneous glomerulonephritis, that the role of the metal itself may only be coincidental, and that the involved antigen remains unknown. Prednisone therapy had no documented persistent beneficial influence upon the level of proteinuria in one patient who has been lost to follow-up. In one patient not treated with steroid therapy, withdrawal of exposure to the metal resulted in disappearance of mercury from body fluids and clinical remission.
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PMID:Membranous glomerulonephritis associated with industrial mercury exposure. Study of pathogenetic mechanisms. 704 18

2 patients with systemic lupus erythematosus and mild renal functional impairment were treated with ibuprofen, one of the phenylproprionic nonsteroidal anti-inflammatory drugs. Within days after the onset of therapy, both developed renal insufficiency manifested by elevated serum creatinine levels, increased proteinuria, and active urinary sediments; 1 patient was oliguric. Renal biopsies disclosed mesangial proliferative lupus glomerulonephritis and acute tubular necrosis, the latter more pronounced in the oliguric patient. Renal failure resolved following discontinuation of ibuprofen and supportive therapy. It is postulated that altered blood flow, mediated through the well-known prostaglandin synthetase inhibitory effects of ibuprofen, resulted in tubular necrosis. This undesirable complication of ibuprofen therapy may be enhanced in patients with underlying renal disease, and may be a factor governing the limitation of its usage.
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PMID:Ibuprofen-induced acute renal failure with acute tubular necrosis. 718 Sep 1

Urinalysis is a simple, efficient, and accurate guide in the diagnosis of renal disease. By determining a patient's history and obtaining a physical examination, the physician is very often able to diagnose a patient's renal lesion. Heavy proteinuria and a microscopic sediment containing red cells and red cell casts strongly suggest acute glomerulonephritis. The causes of this nephropathy are legion. On the other hand, mild proteinuria and a lack of microscopic findings suggest nephrosclerosis, interstitial nephritis, or acute tubular necrosis in the proper clinical setting. When glomerular disease produces nephrotic syndrome, the various types of glomerular disease can be diagnosed accurately without biopsy in a high percentage of cases.
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PMID:Urinalysis and clinical renal disease. 721 37


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