Gene/Protein Disease Symptom Drug Enzyme Compound
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 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In experimental membranous nephropathy, antibody binding to glomerular epithelial cell membrane antigens results in complement activation and formation of complement C5b-9 membrane attack complexes in glomeruli. During active disease, the C5b-9 complexes are shed into the urine. To test the hypothesis that a similar mechanism might be operative in human membranous nephropathy, we measured urinary excretion of C5b-9 and C5 in 146 proteinuric patients with biopsy-proven glomerular diseases or diabetes mellitus. Urinary excretion of C5b-9 relative to C5 excretion was higher in 40 patients with membranous nephropathy than in 106 patients with proteinuria due to non-membranous glomerulonephritis when analyzed by covariance analysis (P less than 0.0002). Urinary C5b-9 excretion was higher in membranous nephropathy than in membranoproliferative glomerulonephritis (N = 13, P less than 0.05), minimal change-focal sclerosis (N = 33, P less than 0.001), mesangial proliferative glomerulonephritis (N = 9, P less than 0.02) and IgA nephropathy (N = 7, P less than 0.025). Urinary C5b-9 excretion was also higher in patients with lupus nephritis (N = 18, P less than 0.02) compared to those with non-membranous glomerulonephritis. The lupus patients with the highest excretion had clinical or pathological features of membranous nephropathy. Nine patients with membranous nephropathy and elevated urinary C5b-9 excretion had a shorter duration of disease (P less than 0.05), lower serum creatinine levels (P less than 0.05) and more proteinuria (P less than 0.02) than the 31 membranous nephropathy patients with normal values.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Elevated urinary excretion of the C5b-9 complex in membranous nephropathy. 178 50

This essay describes the rich tradition of research in the English-speaking Caribbean and the possibilities for meaningful collaboration between Caribbean researchers and scientists from developed countries. Significant contributions include work related to the human T-lymphotropic virus type I (HTLV-I), Jamaican vomiting sickness, veno-occlusive disease of the liver, J-type diabetes, and the role of skin sepsis and streptococcal infection in the etiology of glomerulonephritis. In the fields of malnutrition, human metabolism, child development, and sickle cell anemia, the Caribbean has been at the forefront of medical research internationally. Many characteristics of the Caribbean population, including the disease profile, offer advantages and unique opportunities for significant research, despite difficulties related to the "brain drain" and weaknesses of the infrastructure.
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PMID:Is serious research possible in the Caribbean? 184 51

The pediatric nephrologist has traditionally not been involved in the care of the diabetic child since diabetic nephropathy presents in adulthood. Recent studies suggest that diabetic kidney disease develops silently during childhood. Measurement of urinary albumin excretion (UAE) allows earlier detection of patients at risk of nephropathy, often in adolescence. In addition to diabetic nephropathy, diabetic children are at risk of urinary tract infections, renal papillary necrosis, and various forms of glomerulonephritis. The role of the pediatric nephrologist in the care of the child with diabetes might include advising on the administration and interpretation of screening for UAE and the measurement and interpretation of glomerular filtration rate, and blood pressure. Children with evidence of renal dysfunction should be evaluated and treated by the pediatric nephrologist. Frequently, renal biopsy will be necessary in these patients. Future research may allow the detection of diabetic kidney disease earlier in childhood, further expanding the role of the pediatric nephrologist. In particular, early renal biopsy may eventually be used to select those patients at risk of diabetic nephropathy for specific treatment alterations.
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PMID:The role of the pediatric nephrologist in the care of children with diabetes mellitus. 186 94

Platelet activating factor has been demonstrated in blood and urine and has a broad range of effects on kidney function. The kidney possesses the enzymes responsible for PAF synthesis as well as the specific acetylhydrolase which deactivates PAF. We used a radioactive assay to measure PAF-acetylhydrolase activity in urine samples obtained from normal individuals and patients with various nephropathies. Activity was detected in the majority of normal urines with a mean + 2 SD = 0.70 nmol/30 min/ml. Activity exceeding this value was measured in the urines of 11 of 14 patients with diabetes mellitus, 14 of 22 with glomerulonephritis, and 5 of 16 with hypertensive renal disease. Further study is necessary to relate urine hydrolase activity to specific functional and structural abnormalities of the kidney.
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PMID:Platelet activating factor acetylhydrolase activity in the urine of patients with renal disease. 187 13

Studies addressing the epidemiological issues of end-stage renal disease (ESRD) and the implications for health resource allocations are valuable, especially because the Medicare ESRD program is expected to continue growing during the next decade. Studies on trends in the causes of renal failure have benefited from Medicare's extensive data files on ESRD patients. However, no studies have been published that validate the cause of renal failure field in the Medicare files. The primary disease causing renal failure for over 10,000 New York State patients in the Medicare ESRD program was compared with their hospital discharge diagnoses. Of these patients, 8,730 (83%) had a known cause of renal failure in the Health Care Financing Administration (HCFA) data files. Eighty-nine percent of these patients' primary cause of renal failure was matched with the same major hospital diagnostic code. Patients with diabetes and glomerulonephritis had the highest overall match rates (96% to 97%). Patients with polycystic kidney disease and causes of renal failure other than the four major causes had the lowest match rates (75% to 76%), but these match rates increased to 84% to 87% for patients hospitalized more than five times. Some differences in match rate by age and race were found. These findings suggest that HCFA data on the causes of renal failure of ESRD patients are reasonably accurate and can be used successfully to study a variety of issues related to the diseases leading to chronic renal failure.
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PMID:Validation of the cause of renal failure of patients in the Medicare end-stage renal disease program. 188 30

It is projected that the proportion of black Americans, American Indians, Asian Americans, and Hispanic Americans entering the ESRD program will continue to increase. Despite the increase in the average age of the ESRD population, the minorities entering the ESRD program are much younger. The major risk factors of ESRD--hypertension, diabetes, and glomerulonephritis--are affecting these minorities at a higher rate and in varying combinations. High prevalence and severity of hypertension followed by diabetes mellitus are the major risk factors in blacks, especially black women. Heroin and HIV nephropathies, tied to the epidemic of illicit drug abuse, have a major impact on young black men. The high prevalence of diabetes and the epidemic of glomerulonephritis in certain tribes are the major risk factors in American Indians. Hypertension and diabetes are the risk factors for the rapidly increasing Asian American population, especially for the elderly segment of this population. Diabetes predominates as the risk factor for the rapidly growing Hispanic American population, a group that needs to be identified separately within the ESRD program. Diabetes and hypertension are treatable, and adequate control can prevent progression of renal failure. However, with minority groups, it is difficult to fully implement the measures necessary to achieve this control. Outreach programs are necessary not only to provide medical treatment but to include instruction in socioeconomic and educational strategies. Programs that will seek out these patients and treat them should also educate them about their diet, about the detrimental effects of alcohol and smoking, and about the danger of substance abuse. Ultimately, these programs may be much cheaper than supporting a rapidly increasing ESRD program.
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PMID:End stage renal disease in minorities. 192 May 1

Dietary protein restriction has been shown to slow the rate of loss of kidney function in humans with progressive glomerulosclerosis due to glomerulonephritis or diabetes mellitus. A central feature of glomerulosclerosis is the pathological accumulation of extracellular matrix within the diseased glomeruli. Transforming growth factor beta 1 (TGF-beta 1) is known to have widespread regulatory effects on extracellular matrix and has been implicated as a major cause of increased extracellular matrix synthesis and buildup of pathological matrix within glomeruli in experimental glomerulonephritis. In the present study, it is shown that administration of a low protein diet to rats rapidly reduces the elevated expression of TGF-beta 1 mRNA and TGF-beta 1 protein that is known to occur within glomeruli after induction of glomerulonephritis. Compared to a normal protein diet, glomerulonephritic rats receiving the low protein diet did not develop an increase in glomerular extracellular matrix and showed significantly less proteinuria. Glomeruli isolated from glomerulonephritic rats fed the normal protein diet showed a marked increase in proteoglycan synthesis on day 7 of disease and were demonstrated to be secreting increased amounts of TGF-beta 1 into the medium, whereas glomeruli at the same point in time isolated from rats on a low protein diet showed no increase in proteoglycan production or TGF-beta 1 secretion. These results suggest that a mechanism of the rapid therapeutic effect of a low protein diet on experimental glomerulonephritis is through suppression of TGF-beta 1 expression and prevention of the induction of extracellular matrix synthesis within the injured glomeruli.
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PMID:Dietary protein restriction rapidly reduces transforming growth factor beta 1 expression in experimental glomerulonephritis. 194 1

Class II major histocompatibility complex molecules are critical in both normal and abnormal immune responses. Both in mice and in humans, these molecules have been implicated in the development of various diseases, including insulin-dependent diabetes mellitus and systemic lupus erythematosus. The MRL/lpr mouse strain spontaneously develops a lupus-like illness with features that include anti-DNA antibodies, glomerulonephritis, and early death. We evaluated the structure of class II molecules from these mice, to investigate for unique sequences that might contribute to autoimmunity. Utilizing the polymerase chain reaction, we sequenced the second exons from the I-A and I-E genes of MRL/lpr and MRL-+/+ mice. We found that at the nucleotide level, there are several changes between MRL class II genes and the previously sequenced "k" haplotype, but at the protein level, they are identical. Furthermore, by comparing the sequences of class II genes from several strains of autoimmune mice, we found that there are conserved amino acids in the third hypervariable region of the I-E beta chain which may be important in the development of autoimmunity.
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PMID:Sequence of class II major histocompatibility complex genes from MRL mice. Conserved amino acids in the I-E beta chains from autoimmune mice. 195 19

Following 689 percutaneous renal biopsies, membranous glomerulonephritis was proved in 68 patients. In 16 (23.5%) an underlying primary disease was verified, and thus the glomerulonephritis the secondary form. The primary disease was SLE in 5 cases, diabetes mellitus in 5 cases, rheumatoid arthritis in 3 cases, chronic active hepatitis in 2 cases, an ulcerative colitis and eosinophilic angiolymphoid hyperplasia in 1 patient. As initial sign, nephrotic syndrome emerged in 87.5% of the 16 cases. Microscopic haematuria was observed in half of the patients, as was hypertension, while acute renal failure presented in only 1 case. Histologically, in 13 cases the predominance of early glomerular alterations was characteristic, while in 9 cases the picture proved to be equivocal and accompanied by some degree of interstitial alterations. During combined treatment, remission was achieved in 75%. Two patients with SLE died, but not as a consequence of renal failure. Transient side-effects of the treatment were registered in 5 cases. The principal pathogenetic and clinical differences between the individual secondary nephritis forms, and the difficulty of their differentiation from the idiopathic cases, even on repeated examination, are emphasized. In 3 patients the possibility of secondary renal processes was suggested by the histological picture, and this was proved by the detailed clinical findings.
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PMID:[Secondary membranous glomerulonephritis]. 199 1

Chemically induced autoimmunity is a recently recognized environmental hazard that may affect individuals genetically predisposed to autoimmune disease and chronically exposed to certain chemicals. For example, moderate concentrations of mercury may lead to renal autoimmune disease in a small but significant percentage of the exposed population. Mercury also induces autoimmune glomerulonephritis in susceptible Brown Norway (BN) and MAXX inbred strain rats. Autoimmune responses, directed to epitopes of the renal glomerular basement membrane (GBM), are rapid in onset and have a self-limiting course in mercury-treated rats. Both regulatory T cells and idiotype-anti-idiotype network have been implicated in the resolution of this autoimmune process. In our investigations of immune regulation of mercury-induced autoimmune glomerulonephritis, we have used flow cytometry to quantitate lymphocyte subpopulations in the spleen and lymph nodes of mercury-treated and control BN rats. Of particular interest was the RT6+ T cell subset, that appears to have important immunoregulatory properties in a rat model of autoimmune insulin-dependent diabetes mellitus. Spleen and lymph nodes from control BN rats contained 22 and 52%, respectively, RT6+ cells. Spleens from mercury-treated animals contained 21% RT6+ cells on Day 10 of treatment, 13% on Day 17, 16% on Day 24 and 20% on Day 30. Lymph nodes from the same rats had 36% RT6+ cells on Day 10, 23% on Day 17, 29% on Day 24, and 28% on Day 30. The decrease in RT6+ cells correlated inversely with autoimmune responses to GBM, which peaked on Days 17-24 and declined by Day 30. Moreover, autoimmune responses were also associated with elevated RT6-:RT6+ T cell ratios. Similar results were obtained in two additional groups of BN rats, comprising both younger and older animals, sacrificed at Day 18 of mercury treatment. Analysis of other lymphocyte subpopulations demonstrated a decrease of CD4+ and CD5+ cells, whereas B cells as well as CD8+, IL-2 receptor+, and MHC class II+ subsets showed no consistent correlation with the onset or resolution of the autoimmune process. These findings suggest that mercury-induced changes in RT6+ T lymphocytes may be related to the development of renal autoimmune disease in genetically predisposed BN rats.
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PMID:Reduction of the RT6.2+ subset of T lymphocytes in brown Norway rats with mercury-induced renal autoimmunity. 201 77


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