Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028754 (obesity)
124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The association between massive obesity and nephrotic syndrome has been rarely reported. We herein describe a patient with massive obesity (209 kg) and nephrotic proteinuria who had a normal renal biopsy. The patient was initially polycythemic and had a supranormal creatinine clearance. After losing 89 kg, his hemoglobin and creatinine clearance returned to normal, and proteinuria decreased to 300 mg/24 h. We postulated that increases in glomerular hydrostatic pressure may result in local alterations of glomerular basement membrane sieving characteristics (biologic membrane thixotropy) with resultant nephrotic proteinuria. Prompt remission of proteinuria with weight loss supports a reversible glomerular hemodynamic alteration as a mechanism for the proteinuria of massive obesity.
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PMID:Massive obesity and nephrotic proteinuria with a normal renal biopsy. 400 Mar 54

Advances in our understanding of the mechanisms of proteinuria in humans have depended on a variety of animal models. Most of these have been partially satisfactory because they require pretreatment of the animal with chemicals or toxins or they depend on an aging-related glomerular protein leakiness. The strain in this study was obtained by Koletsky after selective inbreeding of the offspring from a hypertensive Kyoto-Wistar and a normotensive Sprague-Dawley rat. The affected animals appear in 25% of the litters, indicating an autosomal recessive gene, and present with a spontaneous and progressive nephrotic syndrome detected as early as 3-5 weeks and associated with obesity, hypertension, hypoalbuminemia, hypercholesterolemia, and hyperlipidemia. Preliminary morphologic and immunofluorescence studies of their kidneys show progressive glomerular segmental sclerotic lesions and prominent mesangial deposition of IgM, a picture which resembles a steroid-resistant form of idiopathic nephrotic syndrome in humans, namely, focal glomerular sclerosis.
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PMID:Spontaneous nephrotic syndrome in a genetic rat model. 650 87

Nephrotic syndrome in children is a very common disease in Thailand. Most of the patients respond well to oral prednisolone treatment but side effects of the drug especially adrenal insufficiency remains a threat to all. We studied the adrenal function by studying the response to ACTH stimulation test in 14 Thai children, nine girls and five boys, with idiopathic nephrotic syndrome: immediately, 3, 6 and 9 months after discontinuation of oral prednisolone treatment. Average age on entry to the study was 104.4 months (25-183 months). Prednisolone was given every day for 29 days (6-64 days) then every other day for 542 days (178-1,562 days). Side effects of steroid treatment were gross obesity BMI > 30 (one patient), moderate hypertension (one patient), and marked cushingoid features (two patients). ACTH stimulation tests were normal in 64 per cent of patients within 7 days, 64 per cent at 3 months, 73 per cent at 6 months, and 90 per cent at 9 months after discontinuation of oral prednisolone. We suggest that adrenal insufficiency has to be considered in all children on prolonged prednisolone unit at least 9 months of treatment-free period.
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PMID:Adrenal function after prednisolone treatment in childhood nephrotic syndrome. 779 46

The authors define pro-thrombotic states as conditions associated with a high frequency of thrombosis; this association is based on pathogenetic or simply clinical and epidemiological relationships. Thrombophilic states have well-defined, specific causes: antithrombin III, protein C and S and similar deficiencies for inherited thrombophilias, and lupus anticoagulant, antiphospholipid antibodies for the acquired forms. Another identifiable group is made up of several conditions predisposing to thrombosis (CPT) characterized by less specific and multiple mechanisms (e.g. malignancy, inflammatory bowel disease, nephrotic syndrome, diabetes, obesity, etc.). These conditions may induce thrombosis by themselves or contribute to its clinical onset in patients with true thrombophilic states. This is especially the case for patients who are taking contraceptive drugs, are pregnant, have undergone surgery or trauma. The term hypercoagulability states is by no means equivalent to either thrombophilia or CPT. In fact, hypercoagulability may be defined as "activation of blood coagulation" in the presence of specific markers such as fibrinopeptide A and prothrombin fragment F1 + 2. Hypercoagulability is therefore a laboratory rather than a clinical condition and can be a transient feature appearing during certain phases of thrombophilia or CPT. Lastly, conditions involving the presence of hemostatic risk factors for atherothrombosis are simply terms used to describe a statistical-epidemiological relationship between certain hemostatic variables (fibrinogen, factor VII, PAI, etc.) involving the risk of cardiovascular morbidity and mortality but not necessarily indicating a hypercoagulability state.
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PMID:Pro-thrombotic states and their diagnosis. 800 87

We report the effect of 18-month ciclosporin (CS) treatment in 19 children with steroid-dependent frequently relapsing nephrotic syndrome. CS was started at 3-5 mg/kg per day after remission with steroid therapy, was adjusted to maintain a trough blood level of between 200 and 600 ng/ml and was administered for 6 months (high-dose CS). Then, the dosage of CS was decreased and 2.5 mg/kg per day was administered for the subsequent 12 months (low-dose CS). Only 2 patients had relapses during the initial 6 months of CS therapy. Eight patients had infrequent relapses, 4 had frequent relapses and 7 had no relapses during the 12 months of low-dose CS. Not only did continuation of CS at a lower dosage decrease the relapse rate, it also reduced steroid toxicity, allowed increased growth in 16 of the 19 patients and also decreased obesity scores in 12 of these patients. All of the side-effects that occurred during the 18-month period of CS treatment were reversible and none was serious enough to necessitate discontinuation of therapy. Our 18-month CS treatment was helpful in preventing relapses and reducing steroid toxicity in children with steroid-dependent frequently relapsing nephrotic syndrome.
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PMID:Long-term ciclosporin treatment in children with steroid-dependent nephrotic syndrome. 851 91

Serum lipoprotein(a) [Lp(a)] concentrations in chronic renal failure patients were investigated in relation to the degree of renal insufficiency, treatment by maintenance hemodialysis, and correction of uremia by renal transplantation with or without cyclosporin immunosuppression. Fast serum levels of Lp(a) (mg/100 mL) were determined in 34 chronic renal failure patients not in need of maintenance dialysis (16 with serum creatinine 2.0-4.0 mg/100 mL; 18 with serum creatinine higher than 4.0 mg/100 mL), 40 patients treated by hemodialysis, 55 successful renal transplant recipients (28 under cyclosporin treatment and 27 receiving no cyclosporin), and 34 healthy controls. Age and sex distributions were similar among groups. Pregnant women; non-White individuals; subjects with obesity, diabetes, nephrotic syndrome, and hepatic and thyroid diseases; and those treated with oral contraceptives or lipid-lowering drugs were excluded from the study. Compared to controls, median Lp(a) was increased in nondialyzed renal failure patients (11 vs. 47.5 p < 0.001) and this was the only lipid abnormally observed in the group. There was no significant difference in Lp(a) levels between nondialized renal failure patients with serum creatinine 2.0-4.0 and > 4.0 mg/100 mL (47 vs. 49, NS). Moreover, Pearson correlation coefficient (r = 0.01, NS) showed that Lp(a) values were not related to serum creatinine in nondialyzed patients, In hemodialysis subjects Lp(a) concentrations (median = 29) were intermediate between those observed in nondialyzed patients and controls but the differences were not significant. Lp(a) levels in renal transplant patients treated with cyclosporin (median = 6) and not receiving cyclosporin (median = 13) were similar and did not differ from controls. Serum Lp(a) increases and attains maximum levels with mild/moderate reduction in renal function, and does not seem to change through late renal failure stages or in relation to the introduction of maintenance hemodialysis treatment. Correction of uremia by successful renal transplant caused normalization of Lp(a) levels regardless of the use of cyclosporin. Increased Lp(a) levels may be the earliest and more consistent lipid alteration seen in predialysis renal failure.
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PMID:Early elevation of lipoprotein(a) levels in chronic renal insufficiency. 904 61

We observed that some patients do not develop hypoalbuminemia despite the presence of massive proteinuria. To investigate whether the absence or presence of hypoalbuminemia could be a marker in the distinction between idiopathic focal segmental glomerulosclerosis (FSG) and FSG secondary to hyperfiltration, we reviewed all our patients with biopsy-proven FSG and persistent nephrotic-range proteinuria (>3.5 g/24 h). Patients who met these conditions were then separated into those with hypoalbuminemia (serum albumin level <3 g/dL; group I; n = 19) and those with normoalbuminemia (>3.5 g/24 h; group II; n = 18). All group I patients had nephrotic edema in contrast with the absence of edema in all group II patients. Serum cholesterol and triglyceride levels were significantly greater in group I. All group I patients had been diagnosed with idiopathic FSG. The diagnoses of group II patients were FSG secondary to massive obesity in eight patients (44%), vesicoureteral reflux in five patients (27%), and renal mass reduction in three patients (16%); only two patients (11%) in this group had idiopathic FSG. The case histories of 19 other patients with nephrotic-range proteinuria associated with hyperfiltering disorders (reflux nephropathy, massive obesity, renal mass reduction), but without renal biopsy, were also reviewed; despite massive proteinuria (5.8 +/- 3.1 g/24 h), serum albumin and total protein levels were always within normal values. In conclusion, patients with FSG secondary to hyperfiltration do not develop hypoalbuminemia or the other characteristic complications of nephrotic syndrome, despite the presence of massive proteinuria values.
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PMID:Absence of hypoalbuminemia despite massive proteinuria in focal segmental glomerulosclerosis secondary to hyperfiltration. 991 67

Hyperlipidemia (HL) is a common problem in adult renal transplant (TP) recipients, contributing to an increased risk of cardiovascular disease and chronic TP nephropathy. There are multiple causes of HL post renal TP in adult patients, including pre TP HL, immunosuppressive agents, renal dysfunction, hypoalbuminemia secondary to nephrotic syndrome, obesity, and conditions that lead to end-stage renal disease (ESRD). We evaluated the incidence and risk factors of HL in 62 pediatric renal TP recipients (15.4+/-4.2 years, range-3.0-22.3 years) with long-term (6.7+/-3.1 years) functioning [glomerular filtration rate (GFR) 66.7+/-23.2 ml/min per 1.73 m(2)] allografts. The mean serum cholesterol (C) level was 205. 5+/-43.6 mg/dl. Thirty-two patients (51.6%) exhibited elevated serum C levels. The mean serum triglyceride (TG) level was 157.3+/-88.4 mg/dl. Serum TG levels were elevated in 32 patients (51.6%). In patients with elevated serum levels of either C or TG, the mean low-density lipoprotein level (LDL) was 138.6+/-44.1 mg/dl (normal <130 mg/dl) and the high-density lipoprotein (HDL) level 54.6+/-15.9 mg/dl (normal>34 mg/dl). Of those patients studied, 45.5% had high LDL levels, whereas 9.1% exhibited low HDL levels. The two risk factors for elevated serum C levels in our patient population were pre-TP HL and increased years since TP. The only risk factor for elevated serum TG levels was reduced GFR. A family history of HL had a significant deleterious impact upon serum levels of C (P=0.01), but did not affect serum TG levels (P=0.7). Years on dialysis prior to TP, history of prior TP, gender, body mass index, and disease leading to ESRD had no influence upon the development of post-TP HL. We conclude that post-renal TP HL is a significant problem in pediatric renal TP recipients.
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PMID:Risk factors for hyperlipidemia in long-term pediatric renal transplant recipients. 1068 57

Numerous complications of nephrotic syndrome due to either the illness itself or repeated courses of high-dose corticosteroids have been well recognised for several score years. However, investigations concerning children of ex-patients are lacking. The purpose of this study was to assess physical development and health state in the group of children whose mothers had suffered from the idiopathic nephrotic syndrome during their childhood. 34 such children were studied. Thorough medical history was taken from children and their mothers and available medical documents data were obtained. Physical examination was performed and centile position of weight, height and their proportion was stated. The authors found that stillborn foetus, premature or low birth weight newborn incidence is much higher than in general population and the percentage of overweight and obesity is higher in the studied group than in general population. To confirm these findings further investigations with greater number of patients are necessary.
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PMID:[Health status and physical development of children delivered by mothers who suffered from nephrotic syndrome in their infancy]. 1089 16

Obesity is known as a risk factor for nephropathy, especially nephrotic syndrome and focal segmental glomerulosclerosis, and can aggravate renal dysfunction. However, whether these changes are caused by obesity itself or by the associated hypertension (HT) and hyperlipidemia (HC) remains unclear at present. We investigated the influence of HT and HC in obesity on glomerular morphometry. The study included cases with obesity alone (O, body mass index more than 25 kg/m(2), n = 16), O+HC (n = 8), O+HT (n = 17), HC (n = 10) alone, HT (n = 7) alone, and normal subjects (N, n = 11). Renal biopsies were examined and the glomerular diameter, and length and diameter of the glomerular capillary loop were determined using image analysis software. Clinically related data were obtained from medical records at the time of biopsy. Obesity was associated with dilatation of glomerular diameter due to glomerular loop elongation. However, end-stage renal disease (ESRD) was not noted in patients with obesity only. In contrast, ESRD requiring hemodialysis was noted in group O+HT within a 7.7-year follow-up period. Furthermore, enlargement of loop diameter was noted in group O+HC, but not in HC alone. These results suggest that obesity alone may not result in glomerular hyperfiltration or renal dysfunction, but obesity associated with hypertension or hyperlipidemia may accelerate renal damage.
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PMID:Obesity associated with hypertension or hyperlipidemia accelerates renal damage. 1175 5


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