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)

1. The effect of inhibiting the rate-limiting enzyme (3-hydroxy-3-methylglutaryl-CoA reductase, EC 1.1.1.88) in cholesterol synthesis on plasma lipid and lipoprotein concentrations was investigated in 16 patients with primary glomerular disease, heavy proteinuria, well-preserved renal function and hypercholesterolaemia. 2. Detailed studies of low-density lipoprotein metabolism were performed on eight patients before and after 12 weeks of simvastatin therapy. Radioiodinated tracers were used to quantify the fractional catabolic rate of low-density lipoprotein by apolipoprotein B/E receptors and alternative pathways. 3. Simvastatin produced consistent reductions in total plasma cholesterol concentration (median 36.9%), plasma low-density lipoprotein-cholesterol concentration (43.6%) and apolipoprotein B pool size (29.9%). 4. In contrast, the changes in kinetic parameters of low-density lipoprotein metabolism showed no clear pattern. Although an increase in the receptor-mediated catabolism of low-density lipoprotein was demonstrated in five patients, no change or a slight decrease was seen in three patients. Production rates were not significantly altered, although there was a slight decrease in the median value (from 12.4 to 9.7 mg day-1 kg-1). Plasma lathosterol concentration was reduced in all eight patients (range 34-71%), indirectly confirming significant inhibition of cholesterol synthesis. 5. These results suggest that, as in patients with primary moderate hyperlipidaemia, the significant cholesterol-lowering effect of 3-hydroxy-3-methylglutaryl-CoA reductase inhibitors in the nephrotic syndrome is accompanied by variable changes in lipoprotein metabolism. The reasons for this heterogeneous response are unclear. This reflects our limited understanding of the metabolic basis of nephrotic hyperlipidaemia and the relationship between hepatic sterol synthesis and plasma lipoprotein kinetics.
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PMID:Effect of simvastatin on plasma lipid and lipoprotein concentrations and low-density lipoprotein metabolism in the nephrotic syndrome. 132 May 52

Lipoprotein(a) (Lp(a)) has recently been recognized to be a risk factor for coronary heart disease. Lp(a) median values in the absence of renal disease are around 10 mg/dl. Higher levels (greater than or equal to 30 mg/dl) correlate with the occurrence of coronary heart disease, particularly in the presence of elevated cholesterol. We have studied Lp(a) in 76 adults with proteinuria. Fifty had glomerular diseases and 26 non-glomerular diseases, with renal function varying from normal to advanced chronic renal failure. Lp(a) values were shifted to the right, with a median of 21.0 mg/dl, and 25% of patients had values of 30 mg/dl or more. Lp(a) did not correlate with cholesterol, age, lipoprotein subclasses, apoproteins A-I or B-100, albumin, creatinine, or creatinine clearance. Median Lp(a) values did not differ significantly comparing men versus women, or glomerular versus non-glomerular disease. Lp(a) may inhibit fibrinolysis, and is deposited in atherosclerotic lesions. Although the cause of these elevated Lp(a) levels is uncertain, we propose that they contribute to the increased risk of coronary heart disease in the nephrotic syndrome, and may play a role in progressive renal disease.
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PMID:Lipoprotein(a) in patients with proteinuria. 132 68

We studied the effects of symptomatic, antiproteinuric treatment with NSAID's (n = 28) and ACE-inhibitors (n = 14) in patients with proteinuria due to idiopathic membranous glomerulopathy (MGP). These two treatment groups were compared with a group of patients who did not receive antiproteinuric medication (n = 14). Urinary protein loss was effectively lowered by NSAID and ACE inhibitor therapy from 9.5 +/- 1.0 to 4.5 +/- 0.5 g/day (mean +/- SEM) and from 9.8 +/- 1.4 to 3.9 +/- 0.7 g/day respectively, whereas the control group showed a slight fall in proteinuria from 6.9 +/- 0.8 to 5.5 +/- 0.8 g/day. As a result of this treatment hypoalbuminaemia and hypercholesterolaemia improved significantly: serum albumin rose in the NSAID group from 25.4 +/- 1.2 to 29.0 +/- 1.0, and in the ACEi group from 29.9 +/- 1.8 to 32.7 +/- 1.2 g/l (control group from 27.4 +/- 1.6 to 27.8 +/- 1.6 g/l, while cholesterol was lowered in the NSAID group from 8.5 +/- 0.5 to 7.5 +/- 0.4 and in the ACEi group from 8.7 +/- 0.5 to 7.6 +/- 0.4 mmol/l (control group from 9.7 +/- 1.1 to 8.5 +/- 1.0 mmol/l). The antiproteinuric effect of both drugs was well maintained during an 18-month follow-up. Progression towards end-stage renal failure was observed especially in patients with impaired renal function at entry. Remission of proteinuria occurred particularly in patients with lower baseline values of proteinuria, irrespective of the treatment modality.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Antiproteinuric drugs in patients with idiopathic membranous glomerulopathy. 133 89

In order to identify possible markers of cyclosporin A (CSA) efficacy, the use of CSA (6 mg/kg) in 47 children with refractory nephrotic syndrome was reviewed. Response was defined as remission of proteinuria within 2 months. Before CSA administration, nonresponders (N = 13) were found to have more proteinuria (6 versus 3 g/24 h; P less than 0.03) and higher serum creatinine levels (0.9 versus 0.6 mg/dL; P less than 0.03) compared with responders (N = 34). Also, a markedly elevated serum cholesterol level (545 versus 312 mg/dL; P less than 0.001) was noted among nonresponders. Logistic regression analysis of all three parameters isolated serum cholesterol (P less than 0.01) as the only significant predictor of CSA nonresponsiveness. Discriminate analysis identified serum cholesterol to predict 97% of responders and 77% of nonresponders (P less than 0.0005) to conventional CSA doses. The CSA whole-blood trough HPLC levels were subtherapeutic among nonresponders (71 ng/mL) compared with responders (162 ng/mL) (P less than 0.001). Thus, a high serum cholesterol level may prevent the achievement of therapeutic CSA blood levels with conventional doses. On the basis of this, seven of the nonresponders were re-treated by titration of the CSA dose (10 to 14 mg/kg) with their serum cholesterol level. Their mean highest trough CSA level was 286 ng/mL. Five patients responded within 2 months. No elevation in serum creatinine or evidence of nephrotoxicity on repeat biopsy was seen after 2 months of therapy in all seven patients. It was concluded that severe hypercholesterolemia in nephrotic syndrome patients necessitates the titration of the CSA dose with the serum cholesterol level to achieve remission.
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PMID:Severe hypercholesterolemia inhibits cyclosporin A efficacy in a dose-dependent manner in children with nephrotic syndrome. 139 23

Sixteen children with extensive crescentic glomerulonephritis and rapid renal deterioration were selected from 476 patients with glomerulopathy for study. The patients (1-14 yr, M:F = 5:11) presented with edema, oligoanuria, hypertension, gross hematuria and uremic symptoms in 81, 62, 62, 56 and 50 per cent, respectively. The mean Scr was 804 (+/- 436) micromole/L and BUN 38 (+/- 13.4) mmole/L. Anemia was found in 100 per cent, hematuria in 100 per cent, heavy proteinuria 75 per cent, hypoalbuminemia 40 per cent, hypercholesterolemia 38 per cent and low C3 40 per cent. The underlying causes of RPGN included idiopathic 9, PSAGN 6 and LE 1. Eight patients recovered with normal or slightly elevated Scr while the diseases progressed to ESRD in 8 patients. Idiopathic RPGN and extensive (greater than 80%) crescentic glomerulonephritis correlated with a poor prognosis.
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PMID:Rapidly progressive glomerulonephritis in Thai children. 140 80

Finding the proper balance between too much and not enough immunosuppression is just as important in the late posttransplant period as it is during the first year after transplantation. In general, too much immunosuppression leads to an increase in patient mortality, whereas inadequate immunosuppression can lead to an inordinately high rate of allograft failure (Fig 5). In the late posttransplant period, patient and allograft survival are both critically dependent on the degree of immunosuppression and on the long-term side effects of the agents used to achieve this immunosuppression. Adequate immunosuppression is important in treating and preventing the acute allograft rejection episodes that are common during the first year after transplantation (Fig 6). Some data suggest that the severity of early acute rejection episodes may influence the development of chronic rejection, the most common cause of graft failure in the late posttransplant period. Otherwise, the role of immunosuppression in treating and preventing chronic rejection is unclear. The discontinuation of immunosuppression by noncompliant patients is a major cause of late graft failure. Whether the nephrotoxicity of CsA will also result in graft failure in the very late posttransplant period is still unknown. The agents used to achieve immunosuppression, along with decreased graft function and proteinuria, contribute to hypercholesterolemia, hypertension, and hyperglycemia. These and other risk factors have a negative impact on both graft and patient survival. Thus, immunosuppression is directly, or indirectly linked to most of the common causes of death and graft failure after renal transplantation. Although potent new immunosuppression protocols have increased the rate of short-term patient and allograft survival after renal transplantation, future advances in long-term survival after renal transplantation will depend on improvements that are effective in the late posttransplant period. Currently, the best approach to preventing complications in the late posttransplant period is to maintain a vigilant, comprehensive program of on-going medical care. The minimal amount of immunosuppression required to prevent allograft rejection should be used, while adhering to the principle that it is better to lose the graft than to lose the patient.
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PMID:Patient and renal allograft survival in the late posttransplant period. 141 Aug 62

Hyperlipidemic Imai rats spontaneously develop hypercholesterolemia, proteinuria and glomerulosclerosis. We investigated the effect of enalapril, an angiotensin-converting enzyme (ACE) inhibitor, on spontaneous hypercholesterolemia and the progressive renal injury in this rat strain. Male Imai rats (n = 7) were treated with enalapril at a dose of 50 mg/l in drinking water starting at 6 weeks of age. Body weight, blood pressure, urinary protein excretion and serum constituents were checked and compared with untreated controls (n = 5) up to 38 weeks of age. Enalapril treatment significantly reduced hypercholesterolemia (247 +/- 41 vs. 102 +/- 13 mg/dl, p < 0.01, at 38 weeks) and proteinuria (766 +/- 290 vs. 206 +/- 119 mg/kg/day, p < 0.01, at 38 weeks). The glomerulosclerosis index (SI) was significantly higher in untreated control rats than in the enalapril-treated group (227 +/- 57 vs. 27 +/- 9, p < 0.01). Although we could not clarify whether hypercholesterolemia is a primary event or secondary to the nephrotic syndrome, these results indicate that the ACE inhibitor has the property to protect remnant glomeruli from glomerulosclerosis in male Imai rats as well as in other animal models in which focal and segmental glomerulosclerosis is believed to represent a common pathologic pattern. This rat strain represents a unique model of a spontaneous proteinuria which can provide an important information on the pathogenesis of human focal and segmental glomerulosclerosis.
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PMID:Angiotensin-converting enzyme inhibition attenuates hypercholesterolemia and glomerular injury in hyperlipidemic Imai rats. 143 45

The nephrotic syndrome is characterized by proteinuria, hypoalbuminemia and hypercholesterolemia. Hypercholesterolemia is in some cases a risk factor for atherosclerosis in this group of patients. The lipid plasma spectrum was studied in 45 patients with the nephrotic syndrome. Most pronounced changes of the lipid composition of the plasma were revealed in patients with systemic lupus erythematosus and a special form of mesangio-proliferative glomerulonephritis which is characterized by a torpid course and rapid development of chronic renal failure. Plasma atherogenicity was calculated according to the index of plasma atherogenicity. A high atherogenicity index was revealed in patients with an association of the nephrotic syndrome and arterial hypertension. Plasma atherogenicity is determined mainly by the level of high-density-lipoprotein cholesterol.
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PMID:[Lipidemia in the nephrotic syndrome and the atherogenicity of the plasma]. 145 41

Renal amyloidosis was confirmed in 6 related male and female Beagles, ranging in age from 5 to 11 years. The most commonly reported signs of illness included lethargy, anorexia, vomiting, and weight loss. Common clinicopathologic abnormalities were normocytic, normochromic anemia; hypoalbuminemia; azotemia; hypercholesterolemia; proteinuria; and urine specific gravity values below the normal range. Histologic examination of renal tissue from the 6 Beagles revealed moderate to severe glomerular amyloidosis with inconsistently observed mild medullary interstitial amyloidosis. Congo red-stained kidney sections from 4 of 4 affected dogs were potassium permanganate-sensitive, suggestive of reactive amyloidosis. Hereditary predisposition for renal amyloidosis was suspected in these Beagles.
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PMID:Renal amyloidosis in a family of beagles. 151 31

The prevalences of risk factors and angiopathy were studied in 260 diabetic patients, 100 females and 160 males, 35-54 years old, in Uppsala. The prevalence, in females and males separately, of hypertension (WHO-criteria) was 46-34%, of hypercholesterolaemia (greater than or equal to 6.7 mmol.l-1) 32-29%, and of obesity (relative BMI greater than or equal to 120%) 25-20%. Those smoking greater than 15 cigarettes/day were 11-20%. Mean HbA1 was 10.6-10.5%. The prevalence of angina pectoris was 11-6%, of possible infarction 4-6%, and of major ECG abnormalities 6-4%. Large vessel (cardiovascular) disease was independently related to HbA1 (strongly), hypertension, cholesterol, age and familial NIDDM. The prevalence of severe retinopathy (blindness, new vessels or large hemorrhage) was 0% with 7-13 years of diabetes duration, and 26% with greater than or equal to 14 years of duration. The prevalence of severe proteinuria was 4% with 7-13 years of diabetes duration, and 15% with greater than or equal to 14 years of duration. Small vessel (retinopathy and nephropathy) disease was independently related to diabetes duration (strongly), HbA1 and hypertension. The data were discussed related to data from the London, Berlin and Tokyo centres of the WHO Multinational Study of Vascular Disease in Diabetics, using the same study protocol in the present study.
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PMID:Prevalences of risk factors and angiopathy in diabetic patients in Uppsala. 152 37


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