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)

A 23 year old female, born in 1957, was diagnosed as having idiopathic thrombocytopenic purpura at the age of 3 and treated with prednisolone during her childhood with no response. On her regular check-up in 1978, facial edema and proteinuria suggested renal disease. The family history was negative for bleeding diathesis or renal disease. Close examination revealed the following: WBC 4,200/microliters without leukocyte inclusions, RBC 3.42 x 10(6)/microliters, Hb 11.7 g/dl. PT 10.6 sec, APTT 28.9 sec. Platelet count 4,500/microliters by HEMATRAK 360, and 40 x 10(3)/microliters measured by microscopic method. Giant platelets were noted on peripheral blood smear with an average diameter of 6.1 microns. Bleeding time (Duke) was 12.0 min. Number of megakaryocytes was increased although platelet production was remarkably decreased. Results of platelet aggregation and retention tests were normal. Platelet life span (T1/2) was 2.3 days. Sensory neural hearing loss, congenital cataract, double ureter and short small intestine were also found. Chromosome analysis showed 46XX. She underwent splenectomy resulting in increase of the platelet count to 226 x 10(3)/microliters. The increased platelet count, however, gradually decreased to the initial count in 2 years although the bleeding tendency was improved. In 1987, renal function deteriorated, causing intractable hypertension. The serum creatinine was 4.8 mg/dl. The following year she developed cerebral bleeding and died 4 days after the episode. The serum creatinine was 8.6 mg/dl.
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PMID:[Macrothrombocytopenia with deafness, nephritis, cataract, short small intestine, and double ureter]. 221 83

A rare case of idiopathic plasmacytic lymphadenopathy with polyclonal hyperimmunoglobulinemia (IPL) associated with chronic renal failure was described in this report. A 73-year-old male was admitted and diagnosed as IPL. IPL is proposed by Mori et al. in 1980. Clinical entity of IPL is (1) Polyclonal hyperimmunoglobulinemia (2) Systemic Lymphadenopathy characterized by remarkable mature plasmacytosis without atypism and by no destruction of the structures. (3) All disease with polyclonal hyperimmunoglobulinemia can be excluded. In this patient, physical findings showed enlarged lymph nodes (1-2 cm) in bilateral nuchal, submandibular, axillary and inguinal lesions. Laboratory examinations showed polyclonal hyperimmunoglobulinemia (especially IgG, IgA), anemia and renal dysfunction. Microscopic observation of hematoxylin-eosin staining in the axillary lymph node showed increased mature plasma cells without evidence of malignant growth. Immunoperoxidase staining showed intracytoplasmatic polyclonal immunoglobulins. IPL is known as invading other organs besides lymph node, for example skin, lung or kidney. This patient showed renal dysfunction (Cr clearance 11 ml/min, severe proteinuria). Nine cases of IPL and multicentric plasma cell type Giant Lymphnode Hyperplasia (GLH) concurrent with renal dysfunction were reported. Only in two of them chronic renal failure were reported. Twice a week hemodialysis improved his condition and laboratory findings.
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PMID:[A case of idiopathic plasmacytic lymphadenopathy with polyclonal hyperimmunoglobulinemia associated with chronic renal failure]. 228 6

Nine patients with the unusual combination of renal failure, nephrotic-range proteinuria, and biopsy-proved interstitial nephritis are described. Six of these patients had received nonsteroidal anti-inflammatory agents (three fenoprofen, one ibuprofen, one zomepirac, and one tolmetin). The remaining three patients had no history of exposure to drugs known to cause interstitial nephritis. Immunologic characterization of the infiltrating cells with monoclonal antibodies showed that the majority of cells in most cases were cytotoxic T cells, although some B cells were present in all cases. Giant collecting duct cells were seen in half the patients with drug exposure but in none of the others. Otherwise, there were no conspicuous morphologic differences between patients with and without drug exposure. Many of the patients had associated glomerular abnormalities. Only the zomepirac and tolmetin recipients showed pure interstitial disease. The three fenoprofen recipients and the zomepirac and tolmetin recipients regained normal renal function after the drug was discontinued. The combination of renal failure, nephrotic range proteinuria, and interstitial nephritis is one form of nephrotoxicity observed in patients treated with nonsteroidal anti-inflammatory agents. However, this lesion, which may be mediated by cytotoxic T cells, may also be seen rarely in patients with no apparent drug exposure.
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PMID:Interstitial nephritis, proteinuria, and renal failure caused by nonsteroidal anti-inflammatory drugs. Immunologic characterization of the inflammatory infiltrate. 637 63

Very large macrophages, which we have termed "giant macrophages" (G-M phi), have been found in renal tubules, some containing cytoplasmic vacuoles. To elucidate their pathophysiological roles, we examined renal biopsy tissues from various primary glomerulonephritis (GN) and tubulointerstitial nephritis (TIN) using immunohistochemistry with monoclonal antibodies against M phi and other cell surface markers. Giant macrophages were absent or rare in TIN, minimal change nephrotic syndrome, and minor glomerular abnormalities, but G-M phi was plentiful in progressive glomerulonephrides such as IgA nephropathy with crescents, membranoproliferative GN, focal segmental glomerulosclerosis, and especially in crescentic GN. These G-M phi were usually seen in the lumen of renal tubules, but occasionally were found in the Bowman's spaces and glomerular tufts, and similar cells were also found in urine. Moreover, they frequently made contact with tubular epithelial cells expressing intercellular adhesion molecule-1, and the tubular epithelial cells in such lesions often had degenerative changes. Giant M phi may damage tubular epithelial cells from the luminal side. Phenotypically, G-M phi showed activated (CD71+) and mature (25F9+) characteristics along with features of M phi (CD68+), and the cytoplasm contained a great deal of lipids. The numbers of G-M phi in renal tissues closely correlated with the degree of hematuria (rho = 0.5, P < 0.001), serum creatinine value (r = 0.63, P < 0.001) in GN patients (N = 96) and with proteinuria in IgA nephropathy patients (r = 0.89, P < 0.001, N = 27). These data suggest that G-M phi are M phi that were activated and matured in certain active inflammatory sites, which flowed into tubules and then into urine. Thus, the existence of G-M phi in biopsy tissue or urine reflect the activity of GN and may have a predictive value for the progression of GN.
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PMID:Clinicopathological significance of intratubular giant macrophages in progressive glomerulonephritis. 957 33

We report a case of acute tubulointerstitial nephritis with giant cell tubulitis and tubular basement membrane immune complex deposits in a patient with membranous lupus nephritis. The patient, who had no prior evidence of lupus nephritis, developed acute kidney failure and mild proteinuria after cardiac valve replacement surgery. Giant cell tubulitis with tubular basement membrane immune complex deposits has been described in 4 patients after cardiac surgery, 3 of whom received cefuroxime, suggesting the possibility of a drug hypersensitivity reaction. The present case suggests there may also be a pathogenetic role for autoimmunity in this condition.
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PMID:Giant cell tubulitis with immune complex deposits in a patient with lupus nephritis. 1899 77