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)

A nephrotic syndrome caused by immune-complex glomerular disease was diagnosed in a 4-year-old male Great Dane. The syndrome was characterized by proteinuria, hypoproteinemia, hypoalbuminemia, hypercholesterolemia, and subcutaneous edema. Renal biopsy revealed segmental membranous glomerular disease. The edema underwent complete remission 18 days after admission. Two months after admission, there was no clinical or laboratory evidence of glomerular disease. Periodic reevaluation of the dog during the next 2 years revealed recurrence of proteinuria, but no other clinical or laboratory abnormalities. Serial renal biopsies revealed persistence, but no appreciable increase, in the severity of the segmental membranous glomerular disease. The natural course of the nephrotic syndrome and immune-complex glomerular disease has been associated with unpredictable variability. It was concluded that the widespread use of corticosteroid or immunosuppressant therapy in dogs with immune complex glomerular disease should be withheld until the natural course of the disease has been evaluated in a significant number of patients and until the results of well-controlled clinical studies confirm or deny their therapeutic value.
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PMID:Natural remission of nephrotic syndrome in a dog with immune-complex glomerular disease. 12 46

Intravenous administration of the aminonucleoside of puromycin produces the nephrotic syndrome (proteinuria, hypercholesterolemia, hypoproteinemia and edema) in rats. This model is very similar to human nephrotic syndrome caused by various disease states. The current study was designed to assess the nature of urinary lipoproteins in the urine of nephrotic rats, including studies related to the urinary loss of the "activator" apolipoproteins for the lipoprotein lipase-triglyceride interaction. Sprague-Dawley rats were given a single intravenous injection (10 mg/100 g) of puromycin aminonucleoside. Plasma and urine were collected before and 7, 18, 29, 36, and 53 days after injection of puromycin. Urine was fractionated in the preparative ultracentrifuge into density (d) fractions less than 1.006 (very low-density lipoproteins), d = 1.006-1.063 (low-density lipoproteins), and d = 1.063-1.210 (high-density lipoproteins--HDL). The cholesterol, triglyceride, phospholipid, and protein content of these fractions was analyzed. Lipoprotein electrophoresis was performed in agarose agar. Urine from normal and nephrotic rats was added to an in vitro system containing lipoprotein lipase and triglyceride. The free fatty acids (FFA) liberated were then measured as an index of urinary activator property on this system. Measurable urinary lipoproteins were present only on days 7 and 18 after induction of the nephrotic syndrome. Coelectrophoresis of these urinary lipoproteins with rat plasma revealed a single band having alpha- (HDL) electrophoretic mobility. The total mean protein content of day-7 urinary lipoproteins (64.3%) was greater than the content of plasma HDL (52.9%). The protein content of urinary lipoproteins also increased with time. When day-7 and day-18 postinjection urine at nephrotic rats was added to the lipoprotein lipase system, the hydrolysis of triglyceride yielded a mean of 0.320 and 0.235 muEq FFA/ml/20 min, respectively. Control rat urine yielded 0.030 muEq FFA/ml/20 min and 0.000 muEq FFA/ml/20 min 7 and 18 days after injection of normal saline, respectively. It is inferred that in this experimental model (1) high-density lipoproteins are probably excreted in the glomerular filtrate, (2) alterations in the composition of the excreted lipoproteins may occur during their passage through the nephron. The possibility that only a selective portion of the HDL spectrum is excreted into the glomerular filtrate cannot be excluded. It is suggested that the urinary or renal loss of this functionally important lipoprotein may contribute to the pathophysiology of hyperlipoproteinemia in the nephrotic syndrome.
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PMID:High density lipoproteinuria in nephrotic syndrome. 18 67

The purpose of the present paper was to study clinical, morphological and immunological aspects of late rejection of renal allotransplants. We have, therefore, analyzed the occurrence and nature of renal transplant disease and graft failure among 125 recipients surviving for 1 to more than 8 years after transplantation. In this population transplant disease as defined by the appearance of heavy proteinuria and/or steadily declining graft function occurred in 22 patients. At the closure date of the study on December 31, 1972 complete graft failure had occurred in 12 of these 22 patients and 4 of these have died. In addition two patients died in the presence of normal graft function, due to chronic hepatitis and metastatic cancer respectively. As based on clinical findings, pathophysiological features and renal lesions the patients with late transplant disease were classified into two groups and described accordingly. Group A, termed glomerular transplant disease, included a majority of 16 patients, constituting a rather homogenous idsease entity in relation to course of disease, clinical findings and renal lesions as studied by light-, immunofluorescence- and electron microscopy. All these patients presented with heavy proteinuria, which was non-selective in all but two, resulting eventually in complete loss of graft function in eight cases. All these patients developed hypoalbuminemia and hypercholesterolemia, and one half manifested a classical nephrotic syndrome. Arterial hypertension occurred in all patients except two. Glomerular structure as studied by light microscopy revealed a number of lesions of a rather polymorphous pattern in all patients in group A. Endomesangial proliferation, hyperplasia and segmental proliferation of epithelial cells and thickening of capillary walls were prominent features, although the degree of severity, extension and type of lesion occurred in such varying proportions that classification into any well characterized category of glomerulonephritis was not possible. All cases in group A revealed immune deposits, most frequently containing IgG, IgM, complement and fibrinogen. IgA, IgD and IgE were also demonstrated in a lesser proportion of cases in this group. The immunofluorescent pattern was a mixed granular and linear, and in no case strictly linear or granular alone. The ultrastructural investigation contains a detailed analysis of the
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PMID:Late failure or human renal transplants. An analysis of transplant disease and graft failure among 125 recipients surviving for one to eight years. 23 63

We describe 11 patients whose renal biopsies showed minimal changes with focal segmental glomerulosclerosis. These patients, in contrast to the majority of patients with similar renal histology, went into renal failure within 2 1/2 years of clinical onset. All were young, severely nephrotic, most hypertensive, with microscopic hematuria, non-selective proteinuria and extreme hypercholesterolemia. Treatment with corticosteroids and cytotoxic drugs was without effect in any patient. Despite rapid decline in renal function, profuse proteinuria and a nephrotic syndrome persisted into terminal uremia and continued even after dialysis had begun. Seven patients were given nine allografts; four grafts failed because of immediate vascular complications, and a persistant nephrotic syndrome was evident in two of the five surviving grafts. This did not, however, lead to graft failure. Two patients died on dialysis because of myocardial problems. These patients with rapid decline in renal function constitute a distinct clinical subgroup amongst those with focal and segmental glomerulosclerosis; it is possible that they have a different primarily vascular pathogenesis in contrast to other patients with similar renal biopsy appearances.
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PMID:Focal segmental glomerulosclerosis with rapid decline in renal function ("malignant FSGS"). 69

We have studied sodium retention during volume expansion in rats with autologous immune complex nephropathy (AICN), a model of nephrotic syndrome (NS) in which GFR after volume expansion was not different from that in adjuvant-injected controls (C). AICN rats developed heavy proteinuria (298 +/- 27 vs. less than 10 mg/day), hypoalbuminemia (2.14 +/- 0.15 vs. 3.08 +/- 0.12 g/100 ml) and hypercholesterolemia (181 +/- 22 vs. 58 +/- 4 mg/100 ml). After saline, there were no significant differences in blood pressure (119 +/- 2 vs. 114 +/- 2 mm Hg), renal plasma flow (4.9 +/- 0.41 vs. 4.1 +/- 0.28 ml/min), inulin clearance (1.37 +/- 0.06 vs. 1.55 +/- 0.10 ml/min), or SNGFR (47 +/- 2 vs. 53 +/- 4 nl/min). Sodium excretion, however, was significantly lower in NS rats (4.7 +/- 1.1 vs. 9.2 +/- 1.2 muEq/min). Proximal sodium reabsorption was decreased in NS rats (35 +/- 2 vs. 41 +/- 2%, 2.5 +/- 0.2 vs. 3.3 +/- 0.2 nEq/min). Sodium delivery into the loop, however, was equal in NS and C, since the slightly lower filtered load in NS rats offset the depression in proximal reabsorption. Sodium reabsorption by the loop and by the distal convoluted tubules were equal in NS and C. Thus, sodium delivered into the cortical collecting ducts was the same in both groups (0.33 +/- 0.17 vs. 0.34 +/- 0.07 nEq/min; 4.5 +/- 0.6% of filtered sodium vs. 4.4 +/- 0.3%). The percent of filtered sodium excreted in the urine, however, was significantly lower in the NS rats, 2.18 +/- 0.48% vs. 4.0 +/- 0.58%. We conclude that antinatriuresis in this model of NS is determined beyond the superficial late distal convoluted tubule. The inability to excrete the sodium load during volume expansion is due to either enhanced reabsorption by the collecting duct or to abnormal function in deep nephrons.
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PMID:Renal sodium retention during volume expansion in experimental nephrotic syndrome. 75 Jun 93

The clinicopathologic correlation of 18 cases of idiopathic nephrotic syndrome (INS) with diffuse mesangial proliferation (MP), (over 3 cells per intercapillary space) showed clinical characteristics similar to INS with minimal glomerular lesions (MGL) in relation to age at onset, sex, period of evolution, intensity of proteinuria, hypercholesterolemia, hypoalbuminemia and edema. However, there was a greater incidence of cases with arterial hypertension, hematuria, azotemic retention and positive glomerular immunofluorescence. Out of the 18 cases, 10 were corticosensitive (group I) and 8 were corticoresistant (group II). Patients of I followed a similar course as those with MGL, while most cases of group II showed proteinuria through observation periods up to 5 years. No differences were found in the initial clinical presentation between these 2 groups. The only item with prognostic value was the intensity of the mesangial proliferation which in group I was of 3 to 5 cells per intercapillary space, while in group II, in the spaces of some glomeruli, there were up to 10 mesangial cells present. These findings suggest the convenience to practice renal biopsy before initiating treatment in children with INS and arterial hypertension, hematuria and/or azotemic retention in order to identify this group of patients that appears to be different from that with MGL.
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PMID:[Idiopathic nephrotic syndrome with diffuse mesangial proliferation]. 75 99

Unilateral renal perfusion with the aminonucleoside of puromycin (60 mg. per kilogram) was used to produce unilateral renal disease in rats characterized by marked proteinuria, hypoalbuminemia, and hypercholesterolemia. Urine albumin excretion increased from 0.21 plus or minus 0.16 mg. per 24 hours prior to perfusion to 126 plus or minus 30 mg. on the fourteenth day after perfusion. If the perfused kidney was removed after 10 days, urine albumin excretion immediately decreased to normal, whereas marked proteinuria continued after contralateral nephrectomy. Immunofluorescent studies revealed abundant protein reabsorption droplets (beta1C and albumin) in proximal tubules of aminonucleoside-perfused kidneys but not in contralateral kidneys thus indicating that the increased proteinuria was of unilateral origin. Less marked proteinuria was observed following unilateral renal perfusion with lower doses of aminonucleoside. Glomerular mesangial function was studied 10 days after renal perfusion. Renal specimens were obtained 12 hours after intravenous injection of 37.5 mg. per 100 Gm. of body weight of aggregated human IgG and evaluated by immunofluorescent microscopy. Glomerular mesangial staining for human IgG in aminonucleoside-perfused kidneys was markedly increased when compared to contralateral kidneys. In contrast, mesangial staining in kidneys perfused with saline was equal to that of contralateral kidneys and proteinuria following perfusion with saline was not increased. These studies provide further evidence that increased proteinuria following administration of aminonucleoside to rats is the result of a rapid direct on the kidney and that alterations of glomerular mesangial function are related to renal factors rather than changes in systemic milieu.
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PMID:Unilateral renal disease in the rat. I. Clinical, morphologic, and glomerular mesangial functional features of the experimental model produced by renal perfusion with aminonucleoside. 109 13

In a population of 744 diabetics composed mainly of elderly female patients, 172 developed hypertension after the onset of diabetes. Compared to normotensive diabetics, they had an increased prevalence of diabetic retinopathy (p less than 0.001), cerebral accidents, ischemic disorders of the lower limbs and a decreased glomerular filtration rate (p less than 0.05); they are frequently insulin-dependent and difficult to manage. In 173 other indivuals the diabetes emerged several years after the hypertension. This group was characterized by relatively easily controlled blood sugar and increased prevalence of angina and myocardial infarction (p less than 0.001). The association of hypercholesteremia with hypertension increases the risk of coronary disease (p less than 0.02) and, to a lesser degree, of glomerular insufficiency. The prevalence of coronary symptoms increases with obesity (p less than 0.05) while retinopathy increases with insulin dependence (p less than 0.001). From this information it may be concluded that the importance of various risk factors in the diabetic chiefly varies according to the vascular territory involved: cerebral vascular accidents occur mainly in hypertensives, while the presence of retinopathies, proteinuria and peripheral ischemia is directly related to the diabetes and particularly to insulin dependence. The risk of coronary lesions increases considerably when hypertension is added to the diabetes, with an even greater risk in the case of a diabetic, hypertensive, hypercholesterolemic nexus.
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PMID:[Factors of arterial and renal complications in diabetes]. 112 60

Nephrosis was induced in Sprague-Dawley rats in two separate studies by injections of aminonucleoside with sacrifice of animals on days 20 and 54, respectively. Experimental animals in both studies showed the typical findings of nephrosis, i.e., hypoalbuminemia, hypercholesterolemia, and proteinuria. Biochemical findings included hypozincemia and hyperzincuria. A significant correlation between hypozincemia and hypoalbuminemia was noted in the short-term study. Proteinuria occurred on the 10th day in the short-term study and the 15th day in the long-term study and increased quantitatively over the remaining days. The hyperzincuria and proteinuria correlated significantly in the long-term study. Measurements of tissue zinc revealed no change in testes and kidney in the short-term study. Kidney and muscle zinc were increased, testicular zinc was unchanged and femur zinc was decreased in the long-term study. Our conclusions are that in the aminonucleoside induced nephrosis of the rat: 1) hypozincemia occurs probably as a result of hypoalbuminemia, 2) the hyperzincuria is likely due to proteinuria and 3) zinc deficiency is not observed in nephrotic rats who receive ample zinc in their diet and who are observed up to 6 weeks.
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PMID:Zinc metabolism in aminonucleoside-induced nephrosis. 114 20

A new strain of rat characterized by genetic obesity, endogenous hyperlipidemia, and hypertension was obtained in this laboratory. The abnormal phenotype is inherited as a homozygous recessive trait. The animals exhibit marked hypertriglyceridemia, moderate hypercholesterolemia, and an electrophoretic pattern resembling that of human Type IV hyperlipoproteinemia. The average life-span is less than 1 year, due largely to the development of premature renal and vascular disease. The kidney lesion has both glomerulonephritic and nephrosclerotic components and is accompanied by marked proteinuria. About 12% of animals develop urinary tract calculi. The vascular disease consists of fibrous and fatty-fibrous intimal plaques, and polyarteritis. The obese animal offers a useful model for investigating abnormal lipid metabolism and the etiology and pathogenesis of atherosclerosis.
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PMID:Pathologic findings and laboratory data in a new strain of obese hypertensive rats. 117 27


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