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)

To evaluate long-term benefits and risks of CyA therapy in renal transplantation, we analyzed the 10-year experience with all 59 patients who had received a first cadaveric renal graft until August 1983 and were immunosuppressed with CyA. We compared their actual graft survival with that of all 213 patients who had received a first cadaveric graft from 1967 until August 1983, but were immunosuppressed initially with azathioprine and prednisone (AzaP). For comparison of p-creatinine, proteinuria, blood pressure, lipids, uric acid and skin malignancies we evaluated the patients staying unchanged on initial therapy for 10 years (CyA = 12, AzaP = 53). RESULTS. (1) Actual graft survival at 10 years was 34% (20/59) with CyA and 27% (58/213) in AzaP treated patients (intention to treat) (P = .09 = ns). At 1 to 5 years, graft survival was 15% superior with CyA, but after 7 years the survival curve of the CyA-group has closely joined the chronic decline seen in the AzaP group. This behaviour could neither be explained by chronic CyA-nephrotoxicity nor by chronic rejection after switching from CyA to AzaP. (2) P-creatinine at 10 years was significantly (P < .03), but mildly elevated under CyA (130 +/- 52; AzaP = 109 +/- 65). (3) Proteinuria (g/d) at 10 years was not significantly different (CyA = 0.41 +/- 0.58, versus AzaP = 0.83 +/- 1.61). (4) Systolic blood pressure was higher at 10 years under CyA (152 +/- 19) than under AzaP (136 +/-) (P < .02), but diastolic pressure was not (89 +/- 10 versus 84 +/- 12; ns). Antihypertensive drug/patient was twice as high under CyA (1.25 versus 0.64 P < .02). (5) Cholesterol, triglyceride, HDL were not different. 75% of the CyA-patients were steroid free at 10 years, none of the AzaP-patients. (6) P-uric acid was not significantly different in both groups (494 +/- 192 vs 400 +/- 124), but 42% of CyA-patients were on uric acid lowering drug (given after at least one gout attack) as compared to 9% under AzaP (P < .006). (7) Seventeen percent of patients under CyA for 10 years had at least one skin cancer, not different from 15% of AzaP-patients. CONCLUSIONS. The main benefit of CyA was the better graft survival up to 5 years and the chance to stay free of steroids. The main risks of CyA were nephrotoxicity, hypertension and symptomatic hyperuricemia. No difference was found for hyperlipidemia and skin-malignancies.
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PMID:Long-term benefits and risks of cyclosporin A (sandimmun)--an analysis at 10 years. 794 Jul 65

Several factors promote the progression of renal disease, including glomerular hypertension and hypertrophy, molecular factors such as cytokines and growth hormones, proteinuria, acidosis, and hyperlipidemia. Regardless of the underlying etiology, many patients with chronic renal insufficiency will ultimately require kidney replacement therapy. Your goal is to delay the progression of renal failure, mainly through aggressive control of blood pressure. Other possible interventions include protein restriction, bicarbonate therapy, and lipid-lowering drugs.
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PMID:Chronic renal disease: new therapies to delay kidney replacement. 803 27

Because of the high rate of spontaneous remission, treatment of membranous nephropathy with prednisolone and chlorambucil is still controversial. The aim of this study was to give this therapy only to those patients at risk of developing renal insufficiency and to test the efficacy of a low-dose therapeutic regimen. Seventeen patients with more than 10 g protein excretion per day (mean 16.9) and/or a deterioration in renal function (mean serum creatinine, 162 mumol/l) were included. Serum total protein, serum lipids, proteinuria, serum creatinine, and blood pressure were measured, along with the diuretic and antihypertensive medication. The observation time before the start of treatment was 27 +/- 27 months. Steroids were given during months 1, 3, and 5 (methylprednisolone 3 x 500 mg intravenously) prednisolone 0.5 mg/kgBW daily per os for 1 week, then tapered by 0.1 mg/kg BW/week for 1 month). Chlorambucil was given during months 2, 4, and 6 at a dose of 0.12 mg/kgBW daily. At the end of treatment proteinuria had significantly decreased (mean of all patients, 7.8 +/- 1.4 g/d) in all patients. Six months after the end of treatment proteinuria was significantly lower than at baseline in 14 of 17 patients. Hypoproteinemia and hyperlipidemia had improved; diuretic and antihypertensive medication were reduced. Elevated serum creatinine decreased in 7 of 9 patients (pretreatment, 227 +/- 39 mumol/l; 6 months, 176 +/- 28 mumol/l). Nonresponders with respect to serum creatinine responded with respect to proteinuria. Regarding adverse effects, two patients complained of dyspepsia while taking steroids; during chlorambucil treatment two patients experienced nausea and lack of appetite, and one developed leukopenia (1600/microliters).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Low-dose prednisolone/chlorambucil therapy in patients with severe membranous glomerulonephritis. 804 74

Elevated serum levels of the atherogenic and thrombogenic lipoprotein (a) (Lp(a)) have been recognized as a feature of the nephrotic syndrome associated hyperlipidaemia. To examine a possible relationship between serum Lp(a) concentration and proteinuria, serum albumin, or blood pressure, we studied nine patients with nephrotic-range proteinuria both at baseline and after various forms of antihypertensive and antiproteinuric treatment. In fixed order, patients received conventional antihypertensive treatment (either alpha-methyldopa or clonidine), subsequently ACE-inhibition therapy (lisinopril), ACE inhibition combined with an NSAID (indomethacin), and finally NSAID plus conventional antihypertensive therapy. Measurements were performed at the end of each 2-month study period. When compared to controls (n = 29), proteinuric patients before treatment showed increased levels of total cholesterol, very-low and low-density lipoprotein (VLDL+LDL) cholesterol, triglycerides and apolipoprotein B (apoB), while high-density lipoprotein (HDL) HDL cholesterol was lower. Lp(a) was significantly higher in patients (107 (95% CI: 55-208) mg/l) as compared to controls (25 (13-49) mg/l, P < 0.01). Conventional antihypertensive treatment did not reduce proteinuria, while Lp(a) remained unaffected. ACE-inhibitor treatment lowered proteinuria, raised serum albumin, while La(a) tended to fall (-11 +/- 8%). Addition of an NSAID induced a further fall in proteinuria and a rise in serum albumin. Lp(a) now fell by 40 +/- 5% from baseline values (P < 0.01). Both serum total, HDL and VLDL+LDL cholesterol fell significantly. Finally, during subsequent single therapy with NSAID most parameters, including proteinuria and Lp(a), returned towards values obtained during single therapy with ACE inhibiton.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Symptomatic antiproteinuric treatment decreases serum lipoprotein (a) concentration in patients with glomerular proteinuria. 805 29

Low-density lipoprotein apheresis (LDL-A) was performed for nine episodes of steroid-resistant nephrotic syndrome in eight patients. The clinical and immunohistological findings were analysed retrospectively. Six of the patients had focal glomerular sclerosis (FGS), one had minimal-change nephrotic syndrome (MCNS), and one had membranous nephropathy (MN) with FGS. The LDL-A treatment, carried out 2-13 times (mean 7.33 +/- 4.05) for one nephrotic episode, at average intervals of 3-16 days (mean: 8.5 +/- 5.1 days) and combined with steroid pulse therapy and the administration of an antihyperlipidaemic agent in some cases, led to rapid amelioration of hyperlipidaemia. In six nephrotic episodes (5 patients) more than 50% reduction of proteinuria occurred (less than 3.5 g/day) (response-group). A significant elevation of serum albumin (more than 3.0 g/dl) was obtained in five of these episodes. The other three patients were resistant (resistant-group). The number of and intervals between LDL-A treatments in the response group (5 +/- 2.8 times and 5.8 +/- 4.1 days) were significantly less than those in the resistant-group (12.0 +/- 0.8 times and 13.2 +/- 1.8 days) (P < 0.05). After LDL-A, significant reductions were observed in the serum total cholesterol (T-CHO), phospholipid (PL), triglyceride (TG), free-CHO (F-CHO), and beta-lipoprotein (beta-lipo) (P < 0.05). HDL-cholesterol (HDL-C) increased somewhat after LDL-A. Further, Ccr was elevated in all nephrotic episodes, except in one patient who manifested renal failure after 6 months.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Does LDL-apheresis in steroid-resistant nephrotic syndrome affect prognosis? 805 31

A 27-year-old female was admitted to our hospital in order to examine proteinuria and microscopic hematuria. Light microscopic findings of her kidney showed proliferation of mesangial cells and numerous interstitial foam cells. Immunofluorescent and electron microscopic findings revealed IgA nephropathy. Immunoperoxidase studies using monoclonal antibodies disclosed that interstitial foam cells were positive for antibodies of the monocyte/macrophage lineage and also expressed adhesion molecules (CD11a, b, c, LFA-1) and MHC-class II antigens. Hereditary nephritis as Alport syndrome was negated by her familial history and electron microscopic study. We considered that it was a rare and interesting case with numerous interstitial foam cells, because the patient did not have hyperlipidemia as in nephrotic syndrome.
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PMID:[A case of IgA nephropathy with numerous interstitial foam cells--analysis of infiltrating mononuclear leucocytes in renal tissue]. 808 80

Proteinuria is the primary manifestation of a variety of glomerular diseases which are characterized clinically by the nephrotic syndrome. In many cases there is little effective treatment for the primary disease process. However, reduction of proteinuria can frequently improve the hypoalbuminemia, hyperlipidemia and edema which are responsible for the morbidity of the nephrotic syndrome. Proteinuria can be reduced in nephrotic humans and experimental animal models by restriction of dietary protein intake, nonsteroidal anti-inflammatory drug, and by angiotensin-converting enzyme inhibitors. Each of these therapies modifies the activity of locally acting glomerular hormones, autocoids, suggesting that there is a component of proteinuria which is hormonally mediated. The effects of dietary protein, nonsteroidal anti-inflammatory drugs, and angiotensin-converting enzyme inhibitors on nephrotic proteinuria and their potential hormonal mechanisms of action is the subject of this review.
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PMID:Hormonal modulation of proteinuria in the nephrotic syndrome. 811 86

Hyperlipidemia so commonly complicates heavy proteinuria that it has come to be regarded as an integral feature of the nephrotic syndrome (NS). Characteristically, total plasma cholesterol and triglyceride levels are elevated, as are very-low-density lipoprotein (VLDL) and low-density lipoprotein (LDL) cholesterol. Although high-density lipoprotein (HDL) concentrations may be normal, HDL subtypes are abnormally distributed, with a reduction of HDL2 and an increase in HDL3. In addition, lipoprotein (a) [Lp (a)] levels may be elevated. The mechanisms underlying these abnormalities are multifactorial, involving both increased rates of lipoprotein synthesis and defective clearance and catabolism of circulating particles. Although recent dietary and therapeutic studies have demonstrated that nephrotic hyperlipidemia can be effectively treated, the need for such intervention has not been clearly established. This pattern of lipoprotein abnormality is associated with an increased risk of cardiovascular disease in the general population, and several studies have suggested that nephrotic individuals are more likely to develop atherosclerosis. However, no prospective trials have evaluated the relationship between deranged lipid metabolism and coronary or cerebral artery disease in patients with NS. In addition, although recent experimental studies suggest that lipid abnormalities may accelerate renal injury and that lipid-lowering agents may protect renal function, there is little current evidence to suggest that such intervention is of value in preserving residual renal function in humans. Further studies are clearly required to assess the potential long-term benefits of lipid-lowering intervention in individuals with NS. In the meantime, based on data generated from other population groups, a rational approach to the clinical management of hyperlipidemia in these patients is presented.
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PMID:Lipid abnormalities in the nephrotic syndrome: causes, consequences, and treatment. 812 33

We treated hyperlipidemia in patients with nephrotic syndrome (NS) using pravastatin for more than one year. There were 7 cases consisting of 3 with minimal change nephrotic syndrome (MCNS), 1 with focal glomerulosclerosis (FGS), 1 with proliferative glomerulonephritis (PGN), 2 with membranous glomerulonephritis (MGN) and 1 of unknown origin. Three cases consisted of frequent relapsers, and 4 were steroid-resistant. Six randomly selected age- and sex-matched nephrotic patients were used as controls. The daily excretion of proteinuria was not decreased after pravastatin treatment, but, the serum albumin rose from 3.1 +/- 1.1 to 3.4 +/- 1.0 mg/dl. The serum total cholesterol level was significantly reduced from 401 +/- 174 mg/dl to 331 +/- 103 mg/dl in spite of an absence of marked change in the control group. However, there were no significant changes in the triglyceride and lipoprotein levels. The atherogenic index was 7.1 +/- 3.7 before and 2.8 +/- 1.7 after pravastatin treatment, respectively. Improvement of renal function defined by delta decrement of renal function per year (0.08 +/- 0.06 vs. 0.12 +/- 0.26) was observed after the discontinuation of pravastatin administration in 3 out of 4 intractable cases. We conclude that pravastatin has a potent effect in reducing the serum level of total cholesterol, but not triglyceride in NS. Furthermore, pravastatin can induce renal dysfunction especially in patients with intractable nephrotic syndrome.
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PMID:Pravastatin administration to hyperlipidemia in patients with nephrotic syndrome. 813 36

The nephrotic syndrome is a consequence of urinary loss of intermediate-sized plasma proteins and the resulting homeostatic responses to those losses. Plasma protein composition is changed greatly. Pathophysiologic changes are a consequence of the nature of the proteins lost and of the proteins that are increased in plasma to replace them. Plasma oncotic pressure (pi) falls because of the replacement of relatively small plasma proteins by larger ones. Decreased pi increases transudation of fluid into the interstitium and favors edema. This is exacerbated by causing renal insensitivity to atrial natriuretic factor (ANF), primary renal sodium retention, and plasma volume expansion. Many proteins lost in the urine, such as erythropoietin and IgG, are not defended by increased synthesis. Their loss may result in reduced immunity, anemia, and endocrinopathies. Albumin synthesis can be increased by dietary protein augmentation; however, urinary protein losses also increase, offsetting any palliative effect of increased albumin synthesis on albumin stores. The synthesis of many other proteins secreted by the liver is also increased, causing an elevation in plasma levels of several large proteins, including lipoproteins and elements of the coagulation cascade. This results in hyperlipidemia and, in conjunction with the urinary loss of smaller proteins that impede coagulation, a hypercoagulable state. Lipoprotein catabolism is also reduced as a consequence of proteinuria contributing to increased lipid levels.
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PMID:Nonrenal complications of the nephrotic syndrome. 819 77


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