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)

In 2 patients with the nephrotic syndrome, unsuspected solid tumors were found. One was a small cell lung carcinoma, accompanied with the syndrome of inappropriate ADH secretion. The other was a cancer of the breast with lymph node and bone metastases. In both, renal biopsy showed minimal change disease without immune complex deposits. There are only 14 other reported cases of paraneoplastic lipoid nephrosis complicating solid tumors. Such cases lead to the discussion on the respective roles of tumor cell gene product(s) inducing proteinuria and of lymphokine secretion by lymphocytes directed against the tumor itself. Cancer should be considered as a possible etiology of the minimal change nephrotic syndrome in the adult.
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PMID:Minimal change nephrotic syndrome revealing solid tumors. 813 50

A 60-year-old man with long-standing chronic myelogenous leukemia presented with renal insufficiency and proteinuria after more than 6 years of therapy with daily interferon alpha injections. He also manifested unusual skin lesions and a low-titer antinuclear antibody (ANA). Percutaneous renal biopsy disclosed an unusual glomerular lesion characterized by global, diffuse, and marked widening of the lamina rara interna, and focal segmental mesangial proliferation. Discontinuation of the drug resulted in resolution of the proteinuria, but not the renal insufficiency. These glomerular changes have not been reported previously as a complication of this form of malignancy and are similar to lesions reported in newborn rats and mice receiving interferon alpha. The potential role of interferon alpha in the development of this glomerular disease is discussed.
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PMID:Unusual glomerular lesion in a patient receiving long-term interferon alpha. 144 66

During the past several years, numerous laboratories have reported isolation and purification of proteinase inhibitors from human urine. Many of these molecules were incompletely characterized and some of them may have been artifacts in part because of harsh procedures used for their isolation. Consequently, there is disagreement and confusion regarding the biochemical characteristics of these inhibitors. We previously reported the isolation of a proteinase inhibitor, EDC1, from the urine of a leukemic patient. This molecule, M(r) 30 kDa, was antigenically related to plasma inter-alpha-trypsin inhibitor (IATI) and inhibited the growth of a virally transformed B cell line. Immunoreactive EDC1 was also the major component of low molecular weight proteinuria observed in cancer patients. We now report a new method for the isolation of EDC1 from urine of patients with adenocarcinomas of colon and lung and melanoma and compare its partial amino acid sequence with that of HI 30, a proteinase inhibitor previously isolated from pooled normal urine by Hochstrasser et al. [Hoppe-Seyler's Z Physiol Chem 357:153-162, 1976]. Our method involves i) a batchwise cation exchange, ii) gel filtration chromatography, iii) anion exchange chromatography on FPLC, and iv) reverse phase C18 chromatography on HPLC. This method is mild and results in an overall yield of 0.4 to 1.2 mg of EDC1/liter urine. On the basis of the partial N-terminal amino acid sequence of its N terminal (38 residues) and middle regions (29 residues), EDC1 appears to be identical with HI30. Surprisingly, during this isolation procedure, another proteinase inhibitor, M(r) 22 kDa, which cross-reacted with antisera to EDC1 and IATI, was also isolated. The 22 kDa molecule was a major component of the IATI related urinary molecules and was identical with the 30 kDa EDC1 in which first the 15 N terminal residues were clipped. The lower M(r) inhibitor was not an artifact formed during storage or isolation procedure because the Western blot analysis of fresh cancer and normal urine revealed the 30 and 22 kDa molecules. Thus, both the 30 kDa EDC1 (or HI30) and its clipped variant, the 22 kDa molecule, are physiologic components of IATI related urinary proteinase inhibitors and excretion of both forms may be increased in patients with advanced cancer.
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PMID:Cancer-related urinary proteinase inhibitor, EDC1: a new method for its isolation and evidence for multiple forms. 146 60

Little information is available about the clinical status and outcome of patients with a long history of lupus nephritis. We have reviewed the dossiers of 25 patients (23 women and two men) who have been monitored by our Unit for more than 10 years after the diagnosis of lupus nephritis. At presentation the mean age was 28.5 +/- 10.33 (SD) years, the mean plasma creatinine was 136.1 +/- 144.7 (SD) nmol/l, the mean proteinuria was 3.02 +/- 2.7 (SD) g/day. At initial renal biopsy 18 patients showed diffuse proliferative glomerulonephritis, six patients showed membranous glomerulonephritis and one showed focal proliferative glomerulonephritis. All patients but one were treated with corticosteroids and 18 were also given immunosuppressive agents. At the last observation (16 +/- 4.6 (SD) years after presentation), 19 patients have normal plasma creatinine (11 of them show proteinuria less than 0.2 g/day) and six patients show increased plasma creatinine (mean 203.3 +/- 61.9 (SD) mmol/l). Eleven patients have been without any treatment for 88 +/- 64 (SD) months. The incidence of lupus flare-ups fell significantly after the tenth year (0.31/patient/year between 0 and 10 versus 0.11 between years 11 and 27; p = 0.01). No case of pericarditis or cerebritis occurred after the tenth year. Only one case of cerebral thrombosis occurred before the tenth year, but ten severe atherosclerotic cardiovascular and cerebrovascular complications were seen after the tenth year (two cardiac infarcts, three angina pectoris, four cerebral thrombosis, one cerebral haemorrhage). Two cases of cancer (thyroid and lung) occurred after the tenth year. The professional rehabilitation was good in most patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Clinical status of patients after 10 years of lupus nephritis. 148 Jul 42

A 49-year-old man noticed a swelling below the left ear. The histological diagnosis was chronic lymphadenitis with a small cell epithelioid cell reaction. A short time later he developed oedema of the legs, proteinuria and elevated serum creatinine levels (1.89 mg/dl). Renal biopsy showed mesangioproliferative glomerulonephritis. Over the next two years the tumour in the left side of the neck gradually increased in size. Computed tomography showed a space-occupying lesion 5 x 7 cm in the vicinity of the left parotid gland, with evidence of infiltrative growth. Histological examination of the tumour after removal revealed epithelioid cell tissue with numerous lymphocytes, and led to the diagnosis of a lymphoepithelial lymphoma (Lennert's lymphoma), a T-cell lymphoma of low malignancy. Complete remission was achieved after four chemotherapy cycles (COPP schedule) in reduced doses (creatinine concentration 2.09 mg/dl, creatinine clearance 36 ml/min); creatinine clearance subsequently improved to 63 ml/min. Later, however, the tumour recurred and the patient went into terminal renal failure, dying four years after the lymphoma first appeared. The glomerulonephritis may conceivably have been a paraneoplastic phenomenon.
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PMID:[Lennert's lymphoma and glomerulonephritis]. 171 46

There is no known biological requirement for germanium (Ge), germanates, or any organogermanium compound. Ge deficiency has not been demonstrated in any animal. The estimated average dietary intake of Ge in humans is 1.5 mg/d. Ge is widely distributed in edible foods, all of which, with few exceptions, contain less than 5 ppm Ge, since higher levels are toxic to most plants. Ingestion of Ge compounds has been shown to produce toxic effects in experimental animals. In recent years inorganic germanium salts and novel organogermanium compounds, such as carboxyethyl germanium sesquioxide (Ge-132) and lactate-citrate-germanate (Ge lactate citrate) have been sold as "nutritional supplements" in some countries for their purported immunomodulatory effects or as health-producing elixirs, resulting in intakes of Ge significantly exceeding the estimated average dietary intake. Since 1982, there have been 18 reported cases of acute renal dysfunction or failure, including two deaths, linked to oral intake of Ge elixirs containing germanium dioxide (GeO2) or Ge-132. In these cases, biopsies show vacuolar degeneration in renal tubular epithelial cells, without proteinuria or hematuria, in the absence of glomerular changes. Serum creatinine levels have been well above 400 mumol/L in such patients. In 17 of 18 cases, accumulated elemental Ge intakes reportedly ranged between 16 to 328 g over a 4-36 mo period, or between 100 to 2000 times the average estimated dietary intake for human. In surviving patients, renal function improved after discontinuation of Ge supplementation. However, in no case was recovery complete. One organogermanium compound, an azaspiran organogermanium compound, 2-aza-8-germanspiro[4,5] decane-2-propamine-8,8-diethyl-N,N-dimethyl dichloride (spirogermanium), has been found to cause both neurotoxicity and pulmonary toxicity in phase I and II studies examining its chemotherapeutic potential as an antitumor drug in the treatment of various malignancies. In cancer patients given the drug spirogermanium, 40% experienced marked, yet transient neurotoxicity. Two patients suffered from pulmonary toxicity. Results of phases I and II human cancer trials for spirogermanium have not been favorable, with the exception of moderate benefits for three types of malignancies. It is recommended that patients exposed to long-term (greater than 3 mo) Ge supplementation at levels well above the estimated daily intake be medically supervised and monitored for potential renal-, pulmonary- or neurotoxicity. Further study regarding the mechanism of Ge-induced nephrotoxicity in human is warranted.
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PMID:Nephrotoxicity and neurotoxicity in humans from organogermanium compounds and germanium dioxide. 172 9

Spiroplatin was investigated in a multicentre phase I study. 67 patients with advanced solid tumours received 151 cycles either by short-term or prolonged infusion, repeated every 3 weeks, at 2.5-40 mg/m2. Myelosuppression and renal toxicity were dose-limiting. Proteinuria, which was dose- and schedule-dependent, indicated glomerular and tubular damage. The maximum tolerated doses (MTD) for poor-risk and good-risk patients were 35 and 40 mg/m2, respectively. The area under the curve (AUC) at the MTD did not correspond with the AUC at the LD10 in mice with ratios of 0.3 for free platinum and 2.6 for total platinum; these were not suitable for predicting the MTD. 1 complete response was observed in a patient with breast cancer and lung metastases and 1 partial response in a patient with adenocarcinoma of the lung. The recommended dose for phase II studies was 30 mg/m2 by 4 h infusion every 3 weeks.
Eur J Cancer 1991
PMID:Phase I study of spiroplatin. 182 11

A new staging system for multiple myeloma based on clinical and morphological features has been developed on the analysis of 190 patients. A score of "1" was assigned to each of the following clinical data, referred at the time of diagnosis, and selected by multivariate analysis: bone marrow plasma cells more than 30%, haemoglobin less than 110 milligrams, lytic bone lesions of degree 2 or 3, serum beta 2-microglobulin levels higher than 678 nmol/l, and presence of Bence-Jones proteinuria. Therefore, the score for each patient ranged from 0 to 5, and three clinical stages were provided: I = 0 or 1, II = 2 or 3 and III = 4 or 5. Substratification into A and B for each clinical stage was performed using multiple myeloma cellular score, calculated by the formula: total bone marrow myeloma cells per 500 cells x 0.752 + bone marrow plasmablasts per 500 cells x 0.709. Substage A corresponded to multiple myeloma cellular score value lower than 0.300, and substage B to a value greater than 0.300. Significant differences were found in median survivals (P less than 0.0001), in survival curves (P less than 0.0001), and in responses to treatment (P less than 0.0001) among the six staged groups. The use of this staging system for multiple myeloma could offer new prognostic information and could better quantify the picture of the disease in each patient. The substaging according to morphological criteria seems very useful in diminishing or eliminating the great prognostic variability observed within the same clinical stage. Confirmatory studies are required to validate this new staging system for multiple myeloma.
Eur J Cancer 1991
PMID:Prognostic factors in multiple myeloma: a new staging system based on clinical and morphological features. 183 21

A 19-year-old man with Philadelphia-positive chronic myelogenous leukemia treated with interferon-alpha (IFN-alpha) therapy for 45 months had systemic lupus erythematosus disease features: malar rash, migratory arthralgias, elevated antinuclear antibodies, elevated antinative DNA, hypocomplementemia, lymphopenia, and proteinuria. After discontinuation of the IFN and initiation of corticosteroids, there was gradual recovery of symptoms, a decline in antinative DNA and antinuclear antibodies to normal levels, and a decrease in proteinuria. The potential association between IFN therapy and the development of systemic lupus erythematosus, and the role of IFN in other autoimmune diseases, is discussed.
Cancer 1991 Oct 01
PMID:Development of systemic lupus erythematosus after interferon therapy for chronic myelogenous leukemia. 189 53

Seventy-two out of 102 consecutive patients autografted for various hematologic and lymphoid malignancies had a relapse-free survival of greater than 6 months after autologous bone marrow transplantation (ABMT) and were evaluated for long-term effect of the treatment on the renal function. The myeloablative therapy included total body irradiation (TBI) in a single fraction of 7.5 Gy in 41/72 patients. Mean glomerular filtration rate (GFR) showed a significant decrease (p less than 0.01) and serum creatinine and serum urea an increase (p less than 0.05) 6 months after ABMT. Twelve of 72 patients (17%) developed renal dysfunction defined as greater than 25% decrease in GFR, in most cases accompanied by hematuria and proteinuria. Onset was 3-6 months after ABMT. Some patients have later improved considerably, but others continue to deteriorate in renal function. The single most important risk factor for renal dysfunction after ABMT was irradiation. Renal damage was most frequent in lymphoma patients conditioned with BEAC (carmustine [BCNU], etoposide, cytarabine, cyclophosphamide) followed by irradiation, suggesting that this drug combination might have potentiated the toxicity of irradiation. Nephrotoxic antibiotics probably contributed to renal damage in individual cases. Young age did not appear to be a risk factor. Our data indicate that combined treatment with BEAC and TBI should be used with caution and that renal function should be monitored in all patients after bone marrow transplantation to detect any new toxicity patterns of the various conditioning regimens currently used.
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PMID:Renal function after autologous bone marrow transplantation. 193 54


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