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 21 week experiment was conducted with male SPF Ico/Shoe: WIST rats to study the influence on diagnostic parameters of toxicological studies of (i) acidification of drinking water by hydrochloric acid (untreated tap water vs. pH 3 vs. pH 2), (ii) individual vs. group caging (5 animals/cage), and (iii) ad libitum vs. 10 ml restrictive water supply. Acidification to pH 2 resulted in a slightly but significantly reduced excretion of phenol red, lowered proteinuria and a decreased urine volume, whereas all other parameters remained unchanged. Individual caging was less stressful than expected from published data. Red blood cell counts were increased, water consumption and urine volume were somewhat lowered, but stress-sensitive parameters like adrenal weight, leucocyte and lymphocyte counts were not altered. A 10 ml restrictive water supply decreased urine volume, food consumption, body weight development and organ weights. Furthermore transient increases in red blood cell counts and hemoglobin contents, leucopenia and--most important--an impaired renal function were observed. In conclusion acidification of drinking water with hydrochloric acid should not be lower than pH 3, male Ico/Shoe: WIST rats can be regarded as minimum susceptible to individual caging, and reduced water intake might give false positive nephrotoxic effects.
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PMID:Effects of drinking water acidification, restriction of water supply and individual caging on parameters of toxicological studies in rats. 252 65

The correlation between 24-hour urine protein excretion and the protein-to-creatinine ratio (U-P/C) from random, voided urine specimens was assessed in 16 healthy Beagles (9 to 11 months old) and in 14 dogs with suspected renal proteinuria. Initially, a voided urine specimen was obtained from each dog, and the U-P/C was determined. An attempt was not made to standardize the time of collection of the voided urine. Subsequently, each dog was placed in a metabolism cage, and 24-hour urine specimens were collected for quantitative protein analysis. The Coomassie blue technique was used to measure urine protein. The correlation between the U-P/C and the 24-hour urine protein excretion (mg/kg/24 hr), evaluated by linear-regression analysis, was found to be significant (r = 0.975, P less than 0.01). These results substantiate previous findings and indicate that random, voided urine specimens may be used to compute the ratio and to accurately reflect 24-hour urinary protein loss in the dog.
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PMID:Estimation of quantitative proteinuria in the dog, using the urine protein-to-creatinine ratio from a random, voided sample. 406 15

In 1976 we isolated a novel glycoprotein labeled EDC1, Mr 27,500, which is immunologically related to the normal plasma protein inter-alpha trypsin inhibitor (IATI, Mr 160,000) and which is the major component of cancer-associated proteinuria. Urinary excretion of EDC1 (mg/g creatinine) may be classified in four ranges: i) low (less than 15); ii) light (15-30); iii) intermediate (31-45); and iv) heavy (greater than 45). Normal healthy women excrete 8.0 +/- 2.2 mg/g creatinine (average +/- SEM), whereas patients with metastatic breast cancer excrete 98.2 +/- 11.6 mg/g creatinine. Patients with a variety of non-malignant disorders excreted 14.6 +/- 4 mg EDC1/g creatinine, but patients with renal failure, rheumatoid arthritis, and infectious diseases averaged 130.3 +/- 60. Sixty-five to 95 percent of urinary immunoreactive EDC1 in the latter group was of higher molecular weight, perhaps reflecting increased renal clearance of plasma IATI. In patients undergoing excisional biopsy of breast lesions, preoperative EDC1 excretion was 21.5 +/- 3.4 in those whose lesions were benign and 43.1 +/- 7.6 in those whose lesions were malignant. Eight of these latter patients were heavy excretors; EDC1 excretion fell postoperatively in these patients. In normal serum the immunoreactive IATI (IR-IATI) exists in three molecular weight forms 160,000, 120,000 and 58,000. In patients who were heavy excretors of EDC1, the IR-IATI corresponding to Mr 58,000 was absent and total serum IR-IATI was about two-thirds of normal. There was also a negative correlation between serum levels of IATI and urinary EDC1 in these patients. These data suggest that urinary EDC1 may arise as a result of interaction between IATI and tumor-associated proteases.
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PMID:Urinary cancer-related protein EDC1 and serum inter-alpha trypsin inhibitor in breast cancer. 608

The development of proteinuria with increasing age was studied in three groups of male Wistar rats: ad libitum fed and isolated, ad libitum fed and group housed 6 to 8 rats per cage, and food restricted (one-third of the isolated ad libitum food intake) and isolated. Studies were begun at age 50 days and continued throughout life. Ad libitum fed rats when isolated ate more food, grew faster, had larger maximum body weights and developed proteinuria at a faster rate than those that were group housed. There was a small increase in the severity of glomerular pathology in old age. However, systolic blood pressure was not affected significantly by isolation, nor was life duration. Food restriction of isolated rats inhibited body growth, prevented the development of proteinuria, reduced the incidence of glomerular and tubular pathology in old age and prolonged life. Electron microscopic examination of the kidneys of old food-restricted rats revealed a much lower incidence of foot process retraction and spreading on the basement membrane of the glomerulus than in ad libitum fed rats. Cardiac enlargement was also prevented by long-term food restriction.
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PMID:Effects of isolation and food restriction begun at 50 days on the development of age-associated renal disease in the male Wistar rat. 667 Aug 91

F1 hybrid offspring of New Zealand Black mothers and New Zealand White fathers [(NZB X NZW)F1] female mice develop antibodies to single-stranded (ss) and native DNA, immune complex glomerulonephritis, massive proteinuria, and premature death with renal failure. By a series of matings, congenic (NZB X NZW)F1 . xid/xid mice were prepared. These mice were different from (NZB X NZW)F1 mice in having the X chromosome-linked immune deficiency gene, xid, in homozygous form. Such congenic (NZB X NZW)F1 . xid/xid females failed to develop antibodies to single-stranded or native DNA. They also failed to develop fatal renal disease as measured by proteinuria, glomerular histology, glomerular immunofluorescence, and survival. To control for unknown genetic factors, studies were performed with littermates that were derived by mating NZB . xid/+ females with NZW . xid/Y males such that the resulting offspring were either (NZB X NZW)F1 . xid/xid (and therefore "defective") or (NZB X NZW)F1 . xid/+ [phenotypically like (NZB X NZW)F1]. In these and in additional studies, mice were housed in the same cages and identified by ear tagging so as to avoid possible environmental variations from cage to cage. In these studies, xid/xid mice failed to develop the characteristic signs of autoimmunity, whereas the controls did. Similar results were also obtained with (NZW X NZB)F1 xid/xid mice compared with (NZW X NZB)F1 xid/+ mice. The effect of xid/xid upon (NZB X NZW)F1 mice was further investigated by assessing responses to immunization and polyclonal B cell activation in vivo. The xid/xid mice failed to produce anti-ssDNA following immunization with ssDNA complexed to a protein carrier in fluid form or even emulsified in adjuvant. Finally, the xid/xid mice failed to produce antiDNA in response to multiple injections of the polyclonal activator, bacterial lipopolysaccharide (LPS), or the polyclonal activator, polyribose inosinic acid . polyribose cytidylic acid. However, the xid/xid mice were neither generally hyporesponsive nor unable to recognize LPS because they made normal antibody responses following immunization with LPS to which multiple trinitrophenyl groups were chemically attached. We conclude from these studies that xid/xid, which is known to cause the deletion of a B cell subset, has a profound affect upon (NZB X NZW)F1 mice, rendering them insusceptible to the naturally occurring autoimmune disease characteristic of (NZB X NZW)F1 mice, and preventing them from producing antibodies to DNA despite purposeful immunization and polyclonal B cell activation. These results force a reevaluation of previous concepts regarding the mechanisms by which xid/xid might interfere with the development of autoimmunity, and a consideration of therapeutic implications.
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PMID:Ability of the xid gene to prevent autoimmunity in (NZB X NZW)F1 mice during the course of their natural history, after polyclonal stimulation, or following immunization with DNA. 698 Sep

The association of a spondyloepiphyseal dysplasia tarda (SED-T) with the nephrotic syndrome (NS) was found in three siblings. They have counsaguineous (first cousins) healthy parents. Patient 1 was a boy who was admitted to hospital for oedema at the age of 8 years; NS was diagnosed, renal biopsy revealed mesangioproliferative glomerulonephritis. After 4 years he developed end-stage renal failure and died whilst on haemodialysis. Combined therapy with cyclophosphamide and prednisone was of no benefit. At the age of 11 years his height was 122 cm (< 3rd percentile -3.2 SD); he had a short neck, broad and prominent chest and a short wide trunk. Patient 2, another male, had non-nephrotic proteinuria in a 24-h urinary sample at the age of 11 years; this was confirmed in a later analysis; mild lymphopenia and a reduction of helper T cell (OKT4)/suppressor T cell (OKT8) ratio was also detected. At 22 years of age he was admitted to hospital with end-stage renal failure. He was on haemodialysis for a few months until his mother donated a kidney. At the age of 22 years his height was 157 cm (< 3rd percentile), he had a short trunk with the thoracic cage increased in anteroposterior diameter and shoulder elevation. Roentgenograms revealed a disostosis of the spinal column and pelvis and a slight lombar platyspondylia. Patient 3, a girl, was admitted to hospital at 12.5 years for pain and restricted mobility of the right hip. X-rays showed deep acetabula and short femoral necks and mild dysplastic changes, especially in the right hip.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Spondyloepiphyseal dysplasia tarda and nephrotic syndrome in three siblings. 774 15

A number of factors have been implicated in the pathogenesis of acute poststreptococcal glomerulonephritis (APSGN). The lack of a reliable animal model has made it difficult to further examine the role of these factors in the pathogenetic process. In this report, we present a tissue cage model in mice for the study of APSGN. Morphological and immunohistological changes in the kidney, resembling those of APSGN in man, were induced at high frequency in the experimental model after infection with group A streptococcal nephritis isolates. Nephritis-associated strain induced hypercellularity, occlusion of capillaries, and C3 deposition at high frequencies compared to the changes induced in animals infected with a non-nephritis-associated strain and non-infected controls. In animals infected with a nephritis isolate, hematuria and proteinuria were also detected. If penicillin treatment was initiated on the third day of infection, the development of the nephritis process was prevented. Streptokinase, as well as preabsorbing antigen and streptococcal pyrogenic exotoxin B (SpeB), have been implicated in the pathogenesis of APSGN. These proteins, as well as SpeA and SpeF, were detected in the fluids of the infectious focus, regardless of the origin of the strains and whether or not glomerulonephritis was seen. Antibodies to streptokinase were evoked in the majority of the infected animals. This immune response did not correlate with the nephritic process since hypercellularity was also seen in animals which lacked detectable streptokinase antibodies. The results show that the mouse tissue cage model can be used to study APSGN and to evaluate factors involved in the pathogenesis of the disease.
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PMID:An experimental model for acute poststreptococcal glomerulonephritis in mice. 898 44

We report a case of squamous cell lung cancer with nephrotic syndrome. A 69-year-old man was admitted because of proteinuria and microhematuria. A plain chest X-ray film on admission showed a large mass in the left-lower lung field. The patient was given a diagnosis of minimal-change-nephrotic syndrome and squamous cell lung cancer. We first treated the nephrotic syndrome with glucocorticoid therapy, and then treated the lung cancer with chemo-radiotherapy. This reduced the lung cancer, alleviated the proteinuria, and completely resolved the nephrotic syndrome. Nephrotic syndrome is generally associated with malignant lymphoma and other nonepithelial neoplasms. As the underlying disease, epithelial neoplasms are less common, but lung cancer is one of the most widely reported. Histologically, most cases of cancer-associated nephrotic syndrome exhibit membranous nephropathy; Minimal-change nephrotic syndrome is rare. Deposits of immunocomplex on glomerular basement membrane are considered to play a pathogenic role in membranous nephropathy. However, the pathogenesis of minimal-change nephrotic syndrome is different.
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PMID:[Squamous cell lung cancer with minimal-change nephrotic syndrome]. 1006 57

The association between membranous nephropathy (MN) and cancer is often mentioned in textbooks but poorly substantiated, and the characteristics of cancer-associated MN are unknown. To address these questions, we studied a cohort of 240 patients with MN, among them 24 had malignancy at the time of renal biopsy or within a year thereafter. The incidence of cancer was significantly higher in these patients than in the general population (standardized incidence ratio 9.8 [5.5-16.2] for men and 12.3 [4.5-26.9] for women). The frequency of malignancy increased with age. At the time of diagnosis, clinical presentation did not differ between the patients with cancer-associated MN and those with idiopathic MN, but smoking was more frequent among patients with cancer. Analysis of renal biopsies revealed that the number of inflammatory cells infiltrating the glomeruli was significantly higher in patients with cancer-associated MN (P = 0.001). The best cutoff value for distinguishing malignancy-related cases from controls was eight cells per glomerulus. Using this threshold led to a diagnosis of cancer-associated MN with a specificity of 75% and a sensitivity of 92%. In patients with cancer-associated MN, there was a strong relationship between reduction of proteinuria and clinical remission of cancer (P < 0.001). In conclusion, our study provides epidemiologic evidence of an excess of cancer risk in patients with MN. It also shows that age, smoking, and the presence of glomerular leukocytic infiltrates strongly increase the likelihood of malignancy in MN patients.
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PMID:Membranous nephropathy and cancer: Epidemiologic evidence and determinants of high-risk cancer association. 1694 Oct 21

Widespread eruptive purpura, hematuria and proteinuria developed in a 56-year-old woman. A skin biopsy showed leukocytoclastic vasculitis. During a 31-month follow-up, the purpura repeatedly cleared with corticosteroid treatment only to flare with tapering of the medication. Awareness of possible cancer-associated vasculitis led us to search for an occult malignancy, and an asymptomatic lung tumor was discovered. During a 32-month observation period, after resection of a well differentiated peripheral pulmonary adenocarcinoma, the purpuric skin eruption did not recur, although steroid therapy was withheld.
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PMID:Paraneoplastic leukocytoclastic vasculitis. 1907 38


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