Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We wish to determine what cellular and functional alterations are associated with the development of glomeruloscierosis when rats with one kidney are fed an excess of salt or protein. Rats with one kidney are more likely to develop pronteinuria and glomerulosclerosis than control animals. Blood pressure recordings indicate that proteinuria and glomerulosclerosis occur before hypertension is evident. Fluorescent antibody studies disclose that albumin accumulates in the epithelial cells of glomeruli and tubules. Ultrastructural examination shows that vacuolozation of epithelial cells and basement membrane thickening precede the sclerotic collapse of capillary loops. Increased concentrations of sodium or urea that are found in urines of these rats favor the point of view that an elevation of solute load when combined with a reduction of renal mass will on some unknown manner accelerate the deterioration of glomeruli.
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PMID:Protein overload nephropathy in rats with unilateral nephrectomy. A correlative light immunogluorescence and electron microscopical analysis. 4 49

Focal glomerular sclerosis was diagnosed in nine patients by renal biopsy. Proteinuria, hematuria, hypertension, and slowly progressive renal insufficiency unresponsive to corticosteroid and immunosuppressive therapy were consistent clinical findings. Focal, segmental, and global glomerular sclerosis with intraluminal deposits of hypereosinophilic and strongly PAS-positive material, intracapillary foam cells, and moderate interstitial involvement were consistent morphologic findings. The importance of this clinicopathologic entity in the spectrum of renal diseases has only recently been appreciated.
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PMID:Focal glomerular sclerosis. 18 92

Ten years' experience of renal transplantation in 40 children (aged 5--18 years) is reviewed. Including 3 second transplantations 40 cadaver grafts and 3 living donor grafts were transplanted. Mean graft survival was found to be 19 months, the longest being 8 years. At the time of last examination 24 children were alive wtith a functioning graft (mean serum creatinine level 1.5 mg/dl). After graft failure 9 children were again on intermittent hemodialysis. 7 children had died mainly because of infections or cardiovascular complications. Cumulative survival rate of patients and cadaver grafts after 2 years was 84 and 53% respectively. Growth velocity was variable but improved in the majority of patients compared to the previous dialysis period. Full social rehabilitation could be achieved in every case. Main complications were acute rejections (irreversible in 7 of 67), chronic rejections (irreversible in 6 of 10), side effects of immunosuppressive drugs (infections; hematologic, metabolic, and bone disorders), hypertension (60%), recurrence of primary renal disease (in 5 of 9 patients with focal segmental glomerulosclerosis) and surgical complications (28%). Therapeutic guide-lines are given emphasizing the role of specialized children's centres and the cooperation between pediatric nephrologists, immunologists, urologists and psychologists including the time before, during and after transplantation.
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PMID:[Kidney transplantation in children]. 38 67

The wide utilization of renal biopsy and the introduction of electron microscopic and immunohistologic methods has allowed better definition of the clinico-pathological conditions associated with the nephrotic syndrome (NS). Two major categories of facts can be differentiated. In the first one, diffuse lesions of glomeruli, either secondary to specific diseases, or apparently primary diseases such as membranous or membrano-proliferative glomerulonephropathy (GN) are responsible for the increased permeability of the glomerular capillaries. In most of these, there is evidence that immunological mechanisms play a role in the injury of the glomerular capillary. Any of the following clinical symptoms are suggestive of this category of NS: an acute nephritic onset, a moderate NS, macroscopic hematuria, marked hypertension and/or renal insufficiency, poorly selective proteinuria and decreased plasma C3 levels. Patients affected with any of these glomerulopathies usually do not respond to steroids. In the second one, usually referred to as the idiopathic nephrotic syndrome (INS) the mechanism of glomerular capillary alteration is unknown and the nephrotic syndrome is more marked. Minimal change NS (MCNS) accounts for the great majority of INS and is characterized in most cases by a selective proteinuria, the absence of hematuria, a good response to steroids and a good prognosis. However, in some instances, renal biopsy reveals either diffuse mesangial proliferation (DMP) or focal glomerular sclerosis (which may be superimposed on MCNS or on DMP). In both instances, hematuria may be present and 50--75% of patients do not respond to steroids and have a poor prognosis. There is still considerable controversy about the exact relationship between these 3 patterns. We believe that they are not distinct entities but represent variants of the same disease. In addition to these 2 major categories of NS, there are, in infancy, 2 conditions associated with a NS of poor prognosis: congenital NS of Finnish type and infantile mesangial sclerosis. Since steroid-sensitive nephrosis is by far the commonest cause of NS especially in young children up to 8 years, a renal biopsy should be performed only in 2 instances: (a) when the clinical symptoms suggest diffuse glomerular lesions, and (b) when steroid resistance has been demonstrated.
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PMID:Clinicopathologic correlations in the nephrotic syndrome. 39 6

The hepatorenal syndrome is defined as the spontaneous onset of progressive renal failure in patients with far advanced hepatic disease, usually on the basis of cirrhosis. The clinical characteristics of the syndrome include azotemia, oliguria, hyponatremia, low urinary sodium excretion and the absence of abnormal findings in the urinary sediment. Although the results of a large number of studies suggest that abnormal histologic features in the kidneys are infrequent, changes such as glomerulosclerosis, degeneration of tubular cells and alterations in the basement membranes have been described. Theories on the pathophysiologic aspects of the syndrome, including reduced plasma volume, inferior vena cava hypertension and active renal vasoconstriction, are presented. The last of these is currently the most widely accepted theory in which there is a selective redistribution of blood flow away from the cortical nephrons to the medullary nephrons on the basis of selective cortical vasoconstriction. The role of the synpathetic nervous system, as well as that of plasma renins in the cause of this condition is explored. Therapy for the hepatorenal syndrome generally has failed to ameliorate extremely unfavorable mortality rates. Such factors as the effects of plasma volume expansion; various pharmacologic agents, including dopamine, Octopressin and metaraminol; portacaval shunt; transplantation of the liver, and steroids are discussed. Regardless of specific therapy, the few patients who do survive tend to demonstrate a significant reversible component with respect to hepatic disease.
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PMID:The hepatorenal syndrome. 78 80

Morphometrical and clinical investigations were performed in 34 patients with the so-called hypercellular form of focal glomerulosclerosis (FGS), i.e., a form showing clear diffuse mesangial hypercellularity beside focal sclerosis with the light microscopy. This form was compared with focal glomerulosclerosis without remarkable mesangial hypercellularity, with mild mesangioproliferative glomerulonephritis (gn), as well as with normal kidneys. The results were as follows: 1. Morphometrically both the increase in relative mesangial volume as well as in mesangial cell count is statistically significant in the hypercellular form compared with the nonhypercellular form and with controls. Comparison with mild mesangioproliferative gn shows no difference. 2. Even the so-called nonhypercellular form contains more mesangial matrix and mesangial cells than the controls. 3. The frequency of the hypercellular form is higher in males and in older patients. 4. All of our patients with hypercellular FGS had at the time of biopsy manifested nephrotic syndrome. The frequency of additional clinical symptoms (hematuria, hypertension, renal insufficiency) corresponds with the nonhypercellular form, but is different in mild mesangioproliferative gn. 5. Therapeutic response and prognosis is worse in the hypercellular form. The hypercellular form of FGS has to be separated from the nonhypercellular form as a defined entity.
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PMID:Diffuse mesangial cell proliferation in focal sclerosing glomerulonephritis. 82 13

A specific relationship between P. malariae and the nephrotic syndrome, originally postulated on epidemiologic evidence, has been substantiated by clinical, pathologic and immunologic observations. It would appear that quartan malaria causes an immune complex nephritis in some individuals that, once established, is sustained by mechanisms not yet fully explained but which may involve an autoimmune process. Evidence to support an immunologic pathogenesis of the renal lesions is provided by the presence of immunoglobulin, complement (C3) and quartan malarial antigen in biopsy specimens studied by immunofluorescence microscopy. In early cases in which some patients respond to treatment, fluorescence is coarsely granular but in late cases in which patients are unresponsive to treatment, fluorescence tends to be diffuse. Renal histology is distinctive and does not conform to any of the categories included in the conventional classification of the nephrotic syndrome in childhood. The basic lesion consists of thickening of glomerular capillary walls, leading to eventual obliteration of capillary lumina, and accompanying mesangial sclerosis leads ultimately to total glomerular sclerosis. A unique feature of electron microscopy is the presence of small lacunae scattered throughout the thickened capillary basement membrane. Histologic grading for severity of lesions shows positive correlation with response to treatment and immunofluorescence appearances. Prognosis is, in general, poor. The large majority of patients do not respond to treatment with prednisolone, azathioprine or cyclophosphamide, and prednisolone administration causes severe hypertension and other serious complications in a high proportion of patients.
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PMID:The quartan malarial nephrotic syndrome. 82 46

An intensive study of the course of lupus nephritis has been undertaken in 88 patients in whom strict morphologic criteria were utilized in classification. All were treated with steroid, and 17 received cytotoxic drugs in addition. Focal proliferative lupus nephritis generally follows a benign course except in the occasional instances when transition to the diffuse proliferative or membranous forms occurs. Membranous lupus nephritis, when characterized by persistent nephrotic syndrome, leads slowly to renal failure, but this progression is aborted in the one-third in whom remission of the nephrotic syndrome can be achieved. A fatal outcome occurs within five years in the majority of those with diffuse proliferative lupus nephritis and the nephrotic syndrome, often in association with necrotizing renal vasculitis, severe hypertension and accelerated renal failure. A small number with the diffuse proliferative form have a remission and then show only mesangial abnormalities, usually, however, with the appearance of glomerular sclerosis. Progressive glomerular sclerosis is observed in some patients and may be a sequel of the remission of the diffuse or focal proliferative lesions, or it may represent still another form of lupus nephritis. Mesangial immune deposits with or without proliferation, at times in the absence of clinical renal disease, are observed early in the course of systemic lupus erythematosus (SLE) and may proceed to the diffuse proliferative or membranous forms. The present observations serve to emphasize the importance of strict morphologic classification in the comparison of different treatment regimens for lupus nephritis. In view of the grave prognosis of established diffuse proliferative lupus nephritis, which probably evolves from a mesangial involvement common to all patients with SLE from its onset, early therapy may be the key to the management of lupus nephritis.
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PMID:Lupus nephritis. Clinical course as related to morphologic forms and their transitions. 83 80

In a retrospective clinicopathological study, 48 kidney biopsy specimens from 16 children (mean age, 7 years) and 17 adults (mean age, 33 years) with histological evidence of focal glomerular sclerosis (FGS) were examined using light, immunofluorescence and electron microscopy. The histopathological findings were related to the clinical course of each patient. At the clinical onset of the disease, the nephrotic syndrome was seen more commonly in children (12/16) than adults (7/17), while the incidence of both hypertension (children 1/16 versus adults, 9/17) and renal insufficiency (children, 0/16 versus adults, 7/17) was greater in adults. Despite a shorter average follow-up, (adults 3 10/12 years versus children, 7 years), the incidence of hypertension (adults, 13/17 versus children, 7/16) and renal functional impairment (adults, 13/17 versus children, 3/16) remained greater in the adult patients. One child and three adults died in renal failure while two adults underwent transplantation and on requires regular dialysis therapy. Nine of 15 pediatric patients treated with corticosteroids experienced partial or complete remission in either their nephrotic syndrome or level of urine protein excretion, while just 3 of 6 adult patients treated with corticosteroids experienced a partial remission, but never became protein-free. There was an excellent correlation in all patients between the degree of functional renal impairment and the extent of glomerular and nonglomerular histopathological damage in the kidney. It is concluded that in the adults, FGS represents a more severe and progressive disease process and is less responsive to therapy.
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PMID:Focal glomerular sclerosis: contrasting clinical patterns in children and adults. 110 46

From two groups of diabetics, i.e. an "invesitgation-group" of 40 cases and a "comparison-group" of 55 cases, the following characteristics of a state preliminary to proliferative diabetic retinopathy are resulting: early commencing of angiopathy by means of proteinuria (nephropathy), progression of retinopathy (pre-stage), pronounced progressiveness of the accompanying nephropathy and arterial hypertension, and finally uncommon diabetic heredo-familiarity. They all permit permature conclusion on proliferative retinopathy (and glomerulosclerosis).
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PMID:[Pre-conditions of proliferative diabetic retinopathy (author's transl)]. 114 87


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