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)

Bromoethylamine (BEA)-induced papillary necrosis is a reproducible model for analgesic nephropathy. We induced this lesion in groups of male Sprague-Dawley rats and followed the functional and histological changes for 1 year. We found that by 1 month, necrosis of the papilla was complete, glomerular filtration rate was depressed, and urine albumin excretion was increased. There was an extensive interstitial fibrosis characterized by a mononuclear cell infiltrate and patchy tubular atrophy. By 6 months, there was re-epithelialization of the papillary stump accompanied by a marked increase in albuminuria and an improvement in concentrating ability. Changes seen at 9 months were more advanced. There was extensive cortical fibrosis manifested by pitting of the surface of the kidney. At 1 year, renal function remained impaired (creatinine clearance reduced by 65% to 0.26 mL/min/100 g), and the animals were now markedly nephrotic, with albuminuria of 254 mg of albumin/24 h. In the BEA rats, there was selective destruction of the deep nephrons leading to an increase in the volume-ratio of superficial to deep nephrons. Glomerular changes, affecting approximately 60% of the glomeruli, were characteristic of focal segmental glomerular sclerosis. This model of papillary necrosis/interstitial fibrosis is associated with chronic renal insufficiency and leads to the development of focal glomerular sclerosis and nephrotic proteinuria by 6 to 12 months after its induction.
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PMID:Evolution of experimentally induced papillary necrosis to focal segmental glomerulosclerosis and nephrotic proteinuria. 1035 90

Morphological changes of the tubulointerstitial architecture are a major determinant in the progression of chronic renal disease. The evolution of the tubulointerstitial lesion includes early tubular hypertrophy, recruitment of inflammatory cells into the tubulointerstitial space, and proliferation of interstitial fibroblasts resulting in the irreversible changes of tubular atrophy and tubulointerstitial fibrosis. Many of these diverse effects are mediated by autocrine or paracrine release of growth factors, cytokines, and chemokines. Proteinuria, reduction in functional renal mass per se, alterations in tubular fluid reabsorption, and well as hemodynamic changes in the injured kidney may all stimulate local release of such growth factors. A more recent conception is that vasoactive substances, traditionally viewed to be only involved in the regulation of vascular tone, could actually mediate many of these functions of the more 'classical' growth factors and cytokines. In this regard, one of the most intensively studied vasoactive substances is angiotensin II which has been linked to the progression of renal disease by a host of mechanisms, including the induction of tubular hypertrophy and proliferation of interstitial fibroblasts. There is also increasing evidence that other vasoconstrictive factors such as endothelins and eicosanoids are involved in pathophysiological changes leading eventually to tubulointerstitial fibrosis. On the other hand, natriuretic peptides may exert antifibrogenic properties. Although interference with the renin angiotensin system is currently the only treatment being effective in attenuating the loss of function in patients with chronic renal insufficiency, it is likely that future studies will also investigate the role of other vasoactive substances in the progression of human chronic renal disease.
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PMID:Vasoactive factors and tubulointerstitial injury. 1035 9

When focal segmental glomerulosclerosis (FSGS) has reached the stage of chronic renal insufficiency, further progression is usually considered inevitable. African-American patients are believed to exhibit a particularly aggressive form of FSGS. We have treated five African-American patients, aged 11-18 years, with FSGS and reduced renal function using intensive intravenous methylprednisolone protocol, combined with chlorambucil in three cases. All patients had a pretreatment creatinine clearance of less than 50 ml/min per 1.73 m2. Three patients responded with normalization of creatinine clearance and serum albumin levels and had no or only minimal proteinuria at latest follow-up. One patient showed no improvement and one patient progressed to end-stage renal disease. These findings indicate, for the first time, that even severe FSGS may respond to aggressive methylprednisolone with or without alkylating agent treatment, and that African-American race does not preclude a favorable response.
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PMID:Aggressive treatment of severe idiopathic focal segmental glomerulosclerosis. 1045 77

Results are analyzed of a prolonged treatment with inhibitors of the angiotensin-converting enzyme (captopril, Capoten, 100 to 150 mg daily, Renitec, 10 to 20 mg daily) in 53 patients with chronic glomerulonephritis. Of these, 23 patients presented with nephrotic syndrome in prehypertensive stage, 30 were in the stage of chronic renal insufficiency. The time-related course of proteinemia was studied as were indices for systemic hemodynamics, azotemia. Shown in the study was a significant effect of ACE inhibitors on proteinuria, indicators of systemic hypertension. A tendency toward decline in indices for creatinemia was noted. A concept is considered of multifactor effect of ACE inhibitors resulting in inhibition of progression of renal insufficiency.
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PMID:[The use of angiotensin-converting enzyme inhibitors in patients with chronic glomerulonephritis]. 1067 90

Indications for renal biopsy are still ill defined. We recently sent a detailed questionnaire to 360 nephrologists in different areas of the world with the aim of providing information on this critical issue by evaluating the replies. The questionnaire was organized in four sections that included questions on renal biopsy indications in patients with normal renal function, renal insufficiency, and a transplanted kidney. In addition, the questions included methods applied to each renal biopsy procedure and to specimen processing. We received 166 replies; North Europe (50 replies), South Europe (47 replies), North America (31 replies), Australia and New Zealand (24 replies), and other countries (14 replies). In patients with normal renal function, primary indications for renal biopsy were microhematuria associated with proteinuria, particularly greater than 1 g/d of protein. In chronic renal insufficiency, kidney dimension was the major parameter considered before renal biopsy, whereas the presence of diabetes or serological abnormalities was not considered critical. In the course of acute renal failure (ARF) of unknown origin, 20% of the respondents would perform renal biopsy in the early stages, 26% after 1 week of nonrecovery, and 40% after 4 weeks. In a transplanted kidney, the majority of nephrologists would perform a renal biopsy in the case of graft failure after surgery, ARF after initial good function, slow progressive deterioration of renal function, and onset of nephrotic proteinuria. The last section provided comprehensive information on the technical aspects of renal biopsy. This survey represents the first attempt to provide a reliable consensus that can be used in developing guidelines on the use of kidney biopsy.
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PMID:Current indications for renal biopsy: a questionnaire-based survey. 1069 70

Clinical trials have shown the beneficial effects of angiotensin-converting enzyme (ACE) inhibitors in delaying the progression of diabetic renal disease. There is less evidence from primary clinical trials of nondiabetic renal disease. We performed an updated meta-analysis to determine the efficacy of ACE inhibitors in slowing the progression of renal disease over a broad range of functional renal impairment. We included published and unpublished randomized, placebo-controlled, parallel trials with at least 1 year of follow-up available from January 1970 to June 1999. In nine trials of subjects with diabetic nephropathy and microalbuminuria, the relative risk for developing macroalbuminuria was 0.35 (95% confidence interval [CI], 0.24 to 0.53) for individuals treated with an ACE inhibitor compared with placebo. In seven trials of subjects with overt proteinuria and renal insufficiency from a variety of causes (30% diabetes, 70% nondiabetes), the relative risk for doubling of serum creatinine concentration or developing end-stage renal disease was 0.60 (95% CI, 0.49 to 0.73) for individuals treated with an ACE inhibitor compared with placebo. Treatment of individuals with chronic renal insufficiency with ACE inhibitors delays the progression of disease compared with placebo across a spectrum of disease causes and renal dysfunction.
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PMID:Effect of ACE inhibitors in diabetic and nondiabetic chronic renal disease: a systematic overview of randomized placebo-controlled trials. 1073 92

Hypoproteinaemia, proteinuria and edema are the main features of Nephrotic syndrome (NS) and are the result of greater permeability of glomerular basal membrane for proteins. It is difficult to predict course of disease and outcome. During 1989-1998 year 18 children were followed up, 9 boys and 9 girls, at the age of 2 to 14 years and diagnosis of NS. Therapy with pronison was initiated in all children according to the protocol of ISKDC. Children were then divided in two groups, depending on success of therapy. In the first group (13 patients, 72.22%) were the patients that had remission, and the second group consisted of 5 patients that did not have remission. In the first group relapses occurred in 7 patients (53.84%), because of side effect of pronison therapy was discontinued in 3 patients. Those 3 patients along with 5 patients from second group were then turned to immuno-suppressive therapy. One patient responded well to cyclophosphamide, rest of them with regular follow up. Two years latter two of them had relapse but responded well on pronisone therapy in the full dose. Biopsies that were done showed that 2 had minimal changes, 2 had focal segmental sclerosis and one membranous proliferative glomerulonephritis. One patient developed chronic renal insufficiency. We conclude that our experience shows that if there is not favorable effect of corticosteroid therapy cyclosporine A is the first choice in NS, without regarding of the patho-hystological findings.
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PMID:[Remission of nephrotic syndrome in children treated with corticosteroids and other immunosuppressive therapy]. 1075 59

This is a study of a group of 23 patients from 16 families with a shared family tree, developing chronic renal insufficiency (CRI). Out of the 23 patients, 18 were female and five male with an average renal death age of 18.4 years old, showing fevo clinical manifestations. The main reason for consultation was the significant level of anemia. 17 patients had normal arterial tension, 1 patient manifested severe artery hypertension (AHT), 3 manifested mild AHT, and 2 manifested slight AHT. All the patients entered the final stage of CRI with a low level of hemoglobin overaging 6.5 g%. The urinalysis revealed an average SG of 1,010, without proteinuria or with slight proteinuria, lower than 500 mg in 24 hours. Three patients had microhematuria and the remainder had normal urinary sediment. A renal ultrasound in 18 cases revealed a bilateral reduction in the kidney size, loss of the cortcomedullar relation, an increase in the echogenety of the renal parenchyma, scattered in all cases, and the presence of corticomedullar cysts in 5 cases. The histopathological study performed in 8 cases revealed some findings which were compatible with chronic interstitial nephritis with corticomedullar cysts. The findings resemble those described in the literature in cases of familial juvenile nephronophthisis (FJN). An important aspect to be pointed out is the presence of an interstitial infiltrate with mononuclear cells, an even more significant feature than any previously reported. We can conclude that the members of these familial groups are carriers of FJN of recessive autosomic transmission, which, in view of some differences in the clinical presentation, age of onset of, CRI some biochemical and morphological findings, and the absence of genetic alterations as described in type 1 FJN, is a variant of this disease.
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PMID:[Familial juvenile nephronophthisis (report on 16 families with shared family tree)]. 1085 96

For people with chronic renal insufficiency, the therapeutic goal is to prevent progression to end-stage renal disease, a serious condition that can only be treated with dialysis and kidney transplantation. Although restriction of dietary protein slows the progression of renal disease somewhat, the principal treatment to slow chronic renal disease is appropriate reduction of blood pressure. Antihypertensive agents, particularly those that produce sustained, long-term reductions in proteinuria, such as angiotensin-converting enzyme inhibitors, not only decrease blood pressure but also preserve renal function. Clinical trials to evaluate these and other drug therapies in renal disease progression have used both "hard end points" (e.g., dialysis, transplantation, death) and intermediate end points of renal disease progression (e.g., doubling of serum creatinine concentration, reductions in proteinuria). Trials that have used hard end points typically recruited patients with advanced renal disease to demonstrate a difference in therapies within a period of 2 to 5 years. However, proteinuria reduction, along with a decrease in the time to doubling of serum creatinine in very early diabetic renal disease, could demonstrate an altered natural history of renal disease. Although hard end points are indicators of a drug's efficacy in reducing cardiovascular events or preserving renal function, they do not assess the impact of a treatment on altering the natural history of early renal disease. For clinical trials of people with all but the most advanced renal disease, use of intermediate end points of renal disease progression is the only practical option for assessment of treatment efficacy and effectiveness. Given the available data on proteinuria reduction and doubling of serum creatinine from clinical trials, these end points, taken together, appear to provide an acceptable means of assessing a treatment's impact on slowing renal disease progression.
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PMID:The future of clinical trials in chronic renal disease: outcome of an NIH/FDA/Physician Specialist Conference. Evaluation of Clinical Trial Endpoints in Chronic Renal Disease Study Group. 1093 65

To evaluate the prevalence and incidence density of heavy proteinuria and chronic renal insufficiency (CRI) and the factors related to disease progression, 10,288,620 urinary screenings of elementary and junior high-school students from 1992 to 1996 were studied retrospectively. Urinary screening included pH, protein, occult blood, and glucose measurements. Blood sample analysis included total protein, albumin, A/G ratio, blood urea nitrogen, creatinine (Cr), antistreptolysin O titer, C3, cholesterol, hepatitis B virus surface antigen, IgA, and fasting blood sugar. The results showed that the 4-year prevalence of proteinuria was higher in girls than in boys (6.87x10(-4) vs. 4.83x10(-4) respectively). There were 189 cases with disease progression into CRI among the 10,288,620 students screened and followed continuously, with the prevalence of disease progression into CRI higher in boys than in girls (2.24x10(-5) vs. 1.41x10(-5) respectively). Of the 119 cases (63%) presenting with CRI since the first urine screening and blood sampling, only 14 had serum Cr levels higher than 6.0 mg/dl. There were 1,289 patients (10.5%) with proteinuria in 1992 and 705 patients (7.1%) in 1996. The absolute number of patients with heavy proteinuria decreased. The percentage of underlying glomerulonephritis in children on dialysis also decreased from 63.2% in 1992 to 47.0% in 1996. Logistic regression analysis showed that a persistent serum cholesterol level higher than 220 mg/dl, an albumin level lower than 3.5 g/dl, total protein less than 6 g/dl, and diastolic pressure higher than 90 mmHg were the significant risk factors for disease progression to CRI. We conclude that early detection of students with heavy proteinuria by mass urinary screening, early appropriate treatment, and monitoring of significant risk factors may help to decrease or delay the progression of renal disease, delay the introduction of dialysis in these predialysis CRI patients and maintain their growth and development.
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PMID:The prevalence of heavy proteinuria and progression risk factors in children undergoing urinary screening. 1097 5


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