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)

Reported are the concentrations of beta-endorphin, beta-lipotropin, and adrenocorticotropic hormone (ACTH) in the amniotic fluid and plasma of 40 healthy pregnant women at different stages of gestation. Moreover, the amniotic fluid levels of the three peptides were evaluated in 20 other pregnant women affected by different pathologic conditions (Cooley's disease, gestosis, diabetes, placental insufficiency, etc.). A silicic acid extraction procedure was performed on the samples. Each extract was subjected to Sephadex G-75 column chromatography, and the two fractions corresponding to beta-lipotropin and beta-endorphin were collected, freeze-dried, and assayed by two specific radioimmunoassays. Levels of ACTH were measured by radioimmunoassay directly on the extracts. Levels of beta-endorphin in amniotic fluid showed the highest values in the first trimester (173 +/- 30 fmol/ml, mean +/- SEM) but were significantly decreased in the second (75.2 +/- 14) and third trimesters (14.3 +/- 1.8). An inverse trend characterized plasma levels of beta-endorphin, which showed a progressive increase from the first trimester to term (10.4 +/- 11.1). Amniotic fluid levels of beta-lipotropin remained stable during the first (48.6 +/- 6.3) and second (54.6 +/- 11.1) trimesters, but decreased significantly in the third trimester (17.9 +/- 2.3). The plasma concentrations of beta-lipotropin showed the highest levels in the first trimester (10.9 +/- 0.9), and decreased significantly at term (8.9 +/- 1.3). Last, amniotic fluid levels of ACTH decreased from 55.3 +/- 4.75 fmol/ml in the first trimester to 12.5 +/- 1.16 in the second trimester, and rose again in the third trimester to 34.4 +/- 6.6 fmol/ml. Plasma levels of ACTH were characterized in the first two trimesters by values twice those recorded for nonpregnant women, and decreased at term to 8.9 +/- 1.4 fmol/ml. In the pregnant patients with fetuses affected by Cooley's disease (second trimester) and in those with edema-proteinuria-hypertension (EPH) gestosis (third trimester), amniotic fluid levels of beta-endorphin, beta-lipotropin, and ACTH were in the same range as those in healthy pregnant women.
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PMID:Lack of correlation between amniotic fluid and maternal plasma contents of beta-endorphin, beta-lipotropin, and adrenocorticotropic hormone in normal and pathologic pregnancies. 631 61

In order to investigate the effects of lovastatin on adrenal and gonadal function, we prospectively determined the basal and gonadorelin-stimulated concentrations of testosterone, follicle-stimulating hormone (FSH) and luteinizing hormone (LH) and the cortisol response to adrenocorticotropic hormone (ACTH) in a sample of 25 male patients with advanced chronic renal failure, hypercholesterolemia and proteinuria. Hormone studies were done prior to and after lovastatin treatment. The values of these patients were compared with those of a matched healthy control group. Before starting treatment with lovastatin, the patients showed significantly lower testosterone concentration and higher LH concentration than the control group. After stimulation with gonadorelin, they also showed a lower increase in testosterone and LH. After 12 months of lovastatin treatment, a significant decrease in the concentration of cholesterol, LDL C, VLDL C and apo B was observed, but neither the basal testosterone concentration nor the response to gonadorelin stimulation was modified. Before treatment, basal and ACTH-stimulated serum cortisol levels did not differ from those of the control group. After lovastatin treatment, neither the basal serum cortisol levels nor the response to ACTH was modified. We conclude that in the patients studied, although the decrease in testosterone concentration may be partially attributable to a decrease in its synthesis, lovastatin treatment does not increase testosterone deficit. This is either because this drug does not inhibit gonadal hydroxymethylglutaryl CoA reductase at the does given or because the cholesterol which LDL C provides the cell with is enough to maintain testosterone synthesis.
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PMID:Prospective case control study to determine the effect of lovastatin on serum testosterone and cortisol concentrations in hyperlipidemic nephrotic patients with chronic renal failure. 877 42

Focal segmental glomerulosclerosis (FSGS) may be idiopathic or secondary to a variety of causes. Clinical distinction between primary and secondary forms of FSGS has crucial therapeutic consequences. Whereas the former may respond to immunosuppressive therapy, treatment of secondary forms of FSGS must aim to resolve the underlying diseases. Although the combination of nephrotic syndrome and Cushing's syndrome has been described anecdotally, the causal relationship between these two diseases remains controversial. We report herein a 37-year-old man who presented with lower extremity pitting edema. Heavy proteinuria and mild renal insufficiency prompted to perform a kidney biopsy and the specimen showed FSGS. On the other hand, admission physical examination was notable for a Cushingoid appearance. After endocrinological investigations, the patient was diagnosed as having Cushing's disease caused by pituitary adrenocorticotropic hormone-producing microadenoma. Immunosuppressive therapy for the treatment of FSGS was not carried out and we treated his Cushing's disease with transsphenoidal resection of the pituitary microadenoma. Surprisingly, resolution of heavy proteinuria occurred when the patient's physical features characteristic of Cushing's disease were gradually resolved 3 months later. This case suggests a possible association of Cushing's disease with FSGS.
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PMID:Focal segmental glomerulosclerosis in association with Cushing's disease. 1733 31

Thirty to forty percent of patients with idiopathic membranous nephropathy have persistent heavy proteinuria and may progress to end-stage kidney disease in 5 - 15 years. The ideal treatment for these patients is a matter of debate. Several nonspecific immunosuppressive regimens have been suggested with the aim of reducing proteinuria and to improve outcome, but all are burdened by significant toxicity. Therefore, more specific and less toxic therapies are needed. Promising results have been recently obtained with rituximab, a monoclonal antibody against the CD20 antigen of B lymphocytes that is able to deplete these cells and, thus, neoformation of pathogenetic antibodies. Other novel drugs, such as adrenocorticotropic hormone, mycophenolate mofetil and eculizumab have been proposed. This paper reviews the safety/efficacy profile of various agents that have been proposed as therapy for this disease, with particular focus on the latest, more specific and hypothesis-driven approaches.
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PMID:Latest treatment strategies for membranous nephropathy. 1803 60

Dogs diagnosed with sudden acquired retinal degeneration syndrome (SARDS) commonly are presented with concurrent clinical, physical, and historical findings consistent with hyperadreno-corticism (HAC) at the time of vision loss. Thirteen dogs diagnosed with SARDS on the basis of complete ophthalmic examination and extinguished bright-flash electroretinogram were evaluated for steroid hormonal abnormalities. Signalment, case history, physical examination, and clinicopathological findings were recorded. Serum cortisol and sex-hormone concentrations were measured before and after adrenocorticotropic hormone (ACTH) stimulation. Clinical signs of HAC, systemic hypertension, and proteinuria were commonly found in dogs with SARDS. Elevations in one or more sex hormones were found in 11 (85%) of 13 dogs (95% confidence interval [CI] 65% to 100%); cortisol was elevated in nine (69%) of 13 dogs (95% CI 44% to 94%). A minority of dogs (three [23%] of 13; 95% CI 0.2% to 46%) exhibited only an increase in adrenal sex hormones. Only one dog had completely normal ACTH stimulation test results. Symptoms of HAC were associated with abnormal ACTH stimulation results. Routine ACTH stimulation testing to evaluate cortisol and sex hormones, blood pressure screening, and urinalysis are recommended in these animals.
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PMID:Elevations in sex hormones in dogs with sudden acquired retinal degeneration syndrome (SARDS). 1972 43

A 23-year-old man was admitted to our hospital for fatigue, anorexia, proteinuria, and peripheral edema. Proteinuria was first pointed out at the age of 15, but no further studies were performed. Six years prior to admission, the patient noted becoming easily fatigued. Laboratory tests on admission showed marked peripheral eosinophilia (29.2%, count: 1,071/microL) and proteinuria. Endocrinological studies revealed isolated adrenocorticotropic hormone deficiency with primary hypothyroidism, but a lack of autoimmune thyroiditis. Renal biopsy showed focal segmental glomerulosclerosis. Hydrocortisone therapy (30 mg/day) for isolated adrenocorticotropic hormone deficiency resulted in marked improvement of adrenal and thyroid functions, and amelioration of proteinuria (from 2.8 to 1.0 g/day) over a two-month period. Renal function remains normal at five years after the start of hydrocortisone treatment. The findings suggest that both hydrocortisone therapy and normalized thyroid hormone status played a pivotal role in the improvement of proteinuria associated with focal segmental glomerulosclerosis.
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PMID:Focal segmental glomerulosclerosis in a patient with isolated ACTH deficiency and reversible hypothyroidism. 1980 85

Membranous nephropathy is one of the most common causes of nephrotic syndrome in adults. Recent reports suggest that treatment with adrenocorticotropic hormone (ACTH) reduces proteinuria, but the mechanism of action is unknown. Here, we identified gene expression of the melanocortin receptor MC1R in podocytes, glomerular endothelial cells, mesangial cells, and tubular epithelial cells. Podocytes expressed most MC1R protein, which colocalized with synaptopodin but not with an endothelial-specific lectin. We treated rats with passive Heymann nephritis (PHN) with MS05, a specific MC1R agonist, which significantly reduced proteinuria compared with untreated PHN rats (P < 0.01). Furthermore, treatment with MC1R agonists improved podocyte morphology and reduced oxidative stress. In summary, podocytes express MC1R, and MC1R agonism reduces proteinuria, improves glomerular morphology, and reduces oxidative stress in nephrotic rats with PHN. These data may explain the proteinuria-reducing effects of ACTH observed in patients with membranous nephropathy, and MC1R agonists may provide a new therapeutic option for these patients.
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PMID:Melanocortin 1 receptor agonists reduce proteinuria. 2050 42

Over the last two decades, adrenocorticotropic hormone (ACTH) has re-emerged as a potentially effective therapy for nephrotic syndrome, particularly for patients who have failed more conventional immunosuppressive therapies. The initial experience in Europe using synthetic ACTH in membranous nephropathy led to a randomized trial in which ACTH performed comparably to a combined regimen of steroids and alkylating agents. Observational data from American patients treated with natural ACTH gel for resistant nephrotic syndrome have also been promising. While we await larger clinical trials of ACTH in the nephrotic patient population, we still also await a more precise understanding of how the therapy achieves remission of proteinuria. We discuss a number of possible mechanisms for ACTH's beneficial effects on the inflammation and injury that occurs in nephrotic syndrome.
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PMID:Treatment of nephrotic syndrome with adrenocorticotropic hormone (ACTH). 2187 86

Idiopathic membranous glomerulonephritis is a frequent cause of nephrotic syndrome and may have a variable course, from spontaneous remission to progression on renal failure. The therapy is based on alternating steroids and chlorambucil or cyclophosphamide (Ponticelli protocol) for six months. In absence of complete or partial remission after protocol, cyclosporine, adrenocorticotropic hormone, mycophenolate mofetil, rituximab can be used for potential therapy. We report here the case of a woman with idiopathic membranous glomerulonephritis unresponsive to the Ponticelli regimen and treated with adrenocorticotropic hormone in association with azathioprine, showing a dramatic decrease of proteinuria and beneficial effects on lipid profile. After 36 months, no relapse of disease has occurred. Although larger cohorts of patients are needed to evaluate the long-term effects, adrenocorticotropic hormone plus azathioprine in association could be a possible therapeutic option for unresponsive idiopathic membranous glomerulonephritis.
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PMID:ACTH and azathioprine: antiproteinuric and lipid-lowering effect in the course of idiopathic membranous glomerulonephritis. 2247 5

Membranous nephropathy (MN) is an autoimmune disease usually associated with a nephrotic syndrome and it may progress to ESRD in the long term. Its etiology is often unknown (idiopathic MN), whereas other cases have a recognizable etiology (secondary MN). In idiopathic MN, the glomerular lesions are mainly caused by autoantibodies against a podocyte membrane protein, the M-type of phospholipase A2 receptor 1. The natural course of idiopathic MN is quite varied with spontaneous complete or partial remissions a relatively common occurrence. Patients with asymptomatic non-nephrotic proteinuria seldom progress and need only conservative management. Those with persistent full-blown nephrotic syndrome and those with declining renal function are candidates for specific treatment with any of several regimens. Cyclical therapy with alternating monthly intravenous and oral glucocorticoids combined with a cytotoxic agent can induce remission and preserve renal function in the long term. Cyclosporine or tacrolimus can induce remission, but relapses are frequent after the drug withdrawal. Mycophenolate mofetil monotherapy seems to be ineffective, but may be beneficial when administered together with steroids. The experience with adrenocorticotropic hormone, natural or synthetic, is limited to a few studies with short-term follow-up, but high rates of remission can be seen after prolonged treatment. A high rate of remission and good tolerance have also been reported with rituximab. Patients with moderate renal insufficiency may also benefit from treatment, but at a price of frequent and serious side effects. With these limitations in mind, idiopathic MN may be considered a treatable disease in many patients.
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PMID:Glomerular diseases: membranous nephropathy--a modern view. 2381 56


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