Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033687 (proteinuria)
 24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Visceral leishmaniasis was diagnosed in a 5-year-old English Foxhound born and housed in an Ohio research colony. Physical examination revealed pyrexia, hematochezia, panuveitis, splenomegaly, and lymphadenopathy. Hematologic and serum biochemical abnormalities consisted of anemia, thrombocytopenia, hypoalbuminemia, hyperglobulinemia, azotemia, and proteinuria. Postmortem examination revealed widely disseminated (spleen, bone marrow, lymph node, liver, kidney, lungs) Leishmania amastigotes within macrophages.
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PMID:Visceral leishmaniasis in an English foxhound from an Ohio research colony. 319 62

We report a patient with polycystic kidney disease, advanced renal failure, and nephrotic-range proteinuria. Kidney biopsy revealed IgA nephropathy with lesions of focal and segmental glomerular sclerosis. This association had not been previously described and is probably coincidental. This case supports the assumption that the nephrotic-range proteinuria observed in some polycystic patients could be the consequence of another superimposed glomerular disease. This glomerulopathy can worsen the course of azotemia in these patients.
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PMID:IgA nephropathy and polycystic kidney disease. 321 62

Renal involvement is well described in patients with mucocutaneous lymph node syndrome (MCLNS), or Kawasaki disease and is manifested by mild azotemia, hematuria, pyuria or cylinduria, and more often, proteinuria. Renal morphology during the acute stages of the illness has never been reported. In this paper we describe the renal histopathologic changes in a child with MCLNS. The glomerular histopathologic findings suggest immune complex damage to the kidney as a possible mechanism of nephrotoxicity in MCLNS. Presence of kidney lesions, which speak in favor of the injurious role of immune complexes in MLCNS may be relevant to the understanding of the pathogenesis of the vascular lesions that are characteristic of this disease.
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PMID:Renal histology of mucocutaneous lymph node syndrome (Kawasaki disease). 328 6

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

Five children with acquired immunodeficiency syndrome (AIDS) and clinically significant renal disease had detailed pathologic examination of renal tissue (biopsy specimens, autopsy specimens, or both). All patients had proteinuria, hypoalbuminemia, and edema; one patient had persistent azotemia. In two cases, renal disease was the first manifestation of human immunodeficiency virus (HIV) infection. All patients had progressive renal disease, and four of the five died. Pathologic studies revealed focal glomerulosclerosis and mesangial proliferative glomerulonephritis with deposits of immunoglobulins and complement demonstrated by immunofluorescence and electron microscopy. Characteristic tubuloreticular structures were also demonstrated in the glomerular endothelial or epithelial cells in two cases. Renal disease is part of the multisystem involvement in children with AIDS. The pathogenesis of renal disease is not known, but circulating immune complexes are known to occur in children with HIV infection and may be involved.
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PMID:Acquired immunodeficiency syndrome-associated renal disease in children. 338 27

Borrelia burgdorferi infection was diagnosed serologically in a dog with lethargy, stiffness, and anorexia. Treatment with ampicillin and chloramphenicol did not alleviate the signs. Azotemia, proteinuria, cylindruria, pyuria, and hematuria developed over a 3-month period. Antibody titer for B burgdorferi remained high (1:8,192) during this time. Renal histopathologic findings included severe, chronic, diffuse, membranoproliferative glomerulonephritis and moderate chronic, multifocal, interstitial nephritis. Borrelia burgdorferi organisms were identified in renal tissue and in urine by results of immunofluorescent studies and bacteriologic culture, respectively.
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PMID:Renal lesions associated with Borrelia burgdorferi infection in a dog. 340 55

67 patients with multiple myeloma with different duration and stage were studied. In 12 patients (17.91%) the onset of the disease was manifested by renal symptoms which were mistaken for primary renal disease. This group of patients was compared with the patients with usual onset of the disease by clinical, paraclinical and immunologic parameters. 75% of the patients with renal onset were in the III stage of the disease when the correct diagnosis was made. A tendency toward normal proteinuria (80.6 +/- 12.04 g/l), stable azotemia (creatinine 497.83 +/- 313.96 mmol/l), significant and non-selective proteinuria, positive correlation with light-chain secretion (r = +0.77) and lack of therapeutic response in 41.66% of the patients were found. Suggestions about the frequency, characteristics, diagnostic problems, therapeutic responses and the unfavourable prognosis of multiple myeloma with renal onset are put forward.
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PMID:[Renal onset of multiple myeloma]. 341 4

We determined the concentrations of immunoreactive epidermal growth factor (irEGF) and creatinine in urine samples from 47 adult patients with various kidney diseases and wide ranges of azotemia and proteinuria. In most of the patients, urinary irEGF concentrations (nanograms per mg creatinine) were markedly subnormal. In the entire group, urinary irEGF correlated with creatinine clearance (r = 0.79; P less than 0.001) and serum creatinine concentration (r = -0.85; P less than 0.001). In the subgroups of patients with primarily glomerular or tubulointerstitial diseases, similar correlations were found. By contrast, there was no correlation with proteinuria. We also determined the concentrations of plasma irEGF in five patients with azotemia. In four patients, the irEGF to creatinine concentration ratio was 1.9- to 8.9-fold higher in urine than in plasma, indicating that plasma irEGF was not the main source of urinary irEGF in these patients. Our data are compatible with the theory that urinary irEGF originates from nephrons per se.
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PMID:Subnormal concentrations of urinary epidermal growth factor in patients with kidney disease. 348 88

Familial juvenile nephronophthisis (FJN) is a frequent cause of chronic renal failure in children and adolescents. Typically it presents after 6 years of age through adolescence, but may become apparent in early childhood. The clinical presentation is insidious, and the early symptoms of polyuria and polydipsia are often overlooked in the presence of a relatively normal urinalysis and in the absence of proteinuria, azotemia, and hypertension. Thus most patients are not diagnosed until after the onset of renal failure. These children are excellent candidates for properly selected transplantation.
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PMID:Familial juvenile nephronophthisis. A review and differential diagnosis. 351 Jul 94

Experimental autoimmune glomerulonephritis with pulmonary hemorrhage was induced in rats of 4 inbred strains, F344/DuCrj, LEW/Crj, WKY/NCrj and SHR/NCrj, by the injection of a nephritogenic antigen from bovine glomerular basement membrane. The severity and clinical course of glomerulonephritis within the strains were very similar, but those between the strains were different. Among them, F344 rats demonstrated mild glomerulonephritis with petechial pulmonary hemorrhage. LEW rats showed more severe symptoms from pulmonary hemorrhage than F344 rats and had heavy, long-lasting proteinuria that caused nephrotic syndrome. WKY rats showed very severe glomerulonephritis with pulmonary hemorrhage, and had azotemia by 4 weeks after the injection. SHR rats had both severe glomerulonephritis and severe pulmonary hemorrhage. Investigation of the dose-effect relationship of the nephritogenic antigen in F344 and WKY rats revealed that the minimum dose required to induce nephritis in F344 and WKY rats was 10 micrograms and 3 micrograms respectively, and that the injection of more than a certain amount (i.e., 30 micrograms in F344, 10 micrograms in WKY) of the antigenic material induced almost the same severity of disease. These results indicate that genetic differences in experimental animals influence the severity of renal damage, suggesting that the use of inbred strains is necessary for adequate study of experimental glomerulonephritis.
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PMID:Strain specific responses of inbred rats on the severity of experimental autoimmune glomerulonephritis. 352 18


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