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)

Morphometric investigations were performed in 18 biopsies from 16 patients with the nephrotic syndrome and 10 biopsies from 10 patients with mild proteinuria not associated with oedema. All biopsies showed normal glomeruli on light microscopy. The interstitial fibrosis was significantly increased in both patient groups compared with controls, and it was greater in the patients with mild proteinuria than in the group with nephrotic syndrome. A significant negative correlation was present between the degree of fibrosis and renal function in both groups of patients.
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PMID:Interstitial fibrosis of the renal cortex in minimal change lesion and its correlation with renal function. A quantitative study. 15 70

There is considerable circumstantial evidence relating neoplasia to glomerular injury. Recently, more convincing evidence has been derived from the demonstration of tumor-associated antigen or antibody to such antigen, in relation to glomerular basement membranes in four patients with glomerular injury and cancer. The most common form of glomerulopathy reported in patients with carcinoma has been membranous glomerulonephritis. However, increased mesangial cells and matrix have also been found in some patients with hematuria and progressive renal failure. In contrast, most patients with Hodgkin's disease and glomerulopathy have had the minimal lesion-type nephrotic syndrome, which has usually responded to successful treatment of the Hodgkin's disease. Glomerular abnormalities have also been reported with chronic lymphocytic leukemia, lymphosarcoma, Waldenstrom's macroglobulinemia, and benign tumors. When there is no apparent cause, proteinuria with or without hematuria or impaired renal function should suggest the possibility of associated neoplasia, particularly in elderly patients.
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PMID:Glomerular injury in patients with neoplasia. 18 Aug 69

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

A series of 29 cases of amyloidosis of the alimentary tract is reported. Five cases (17%) were primary amyloidosis; 14 cases (48%) were amyloidosis secondary to other diseases (such as chronic inflammatory and neoplastic diseases); 10 cases (35%) were amyloidosis of the heredo-familial type connected with Familial Mediterranean Fever. In 23 patients (79%) the diagnosis was established by biopsies, and in 6 more cases on autopsy. Gastrointestinal involvement was found in all age groups. Gastro-enterologic complications observed in the present series include: diarrhea, malabsorption, ileus and gastrointestinal bleeding. In addition other conditions such as jaundice (3 cases), esophagitis and acute hemorrhagic pancreatitis were observed. In 22 patients proteinuria was observed and in 13 patients the nephrotic syndrome. Among 17 patients, in 11 the clinical picture before death was that of terminal renal failure. The survival after diagnosis among 14 patients reached 4 years in 9 cases, and 19 years in one case. The diagnostic value of the rectal biopsy is emphasized.
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PMID:[Gastrointestinal amyloidosis]. 18 89

Serum lipids and their lipoprotein fractions were measured in 16 nephrotic syndrome patients. All component of lipids and beta-lipoprotein fractions (LDL) showed an increase in all uncomplicated patients. The increase in serum lipids were inversely proportional to the albumen level in these patients. In 3 patients, lipids and beta-lipoprotein fractions returned to near normal after treatment, the proteinuria diminished and serum albumen became normal. Most of these patients did not need any treatment for hyperlipidemia.
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PMID:The causal role of hypoalbuminemia in human nephrotic hyperlipidemia. 19 Sep 98

In 26 cases of myelofibrosis, the authors investigated for possible renal impairment that can be appraised from the usual clinical, laboratory, and roentgenographic signs. No anomalies were demonstrated in 12 of these cases. In 14 (or 53%) of the patients, some anomaly was discovered : essentially proteinuria with minor alteration of renal function, but also, two cases of poorly functioning left kidney evidenced on intravenous urograms, one case of acute anuric renal failure connected with hyperuricemia, one case of hypokalemic tubulo-interstitial nephritis, and one case of glomerulonephritis with, nephrotic syndrome. This study, when compared to the literature, indicates that besides nephropathy specific to myelofibrosis and attributed to myeloid metaplasia in the kidney, serious consideration must be given to lesions due to (1) compression of the left kidney by the enlarged spleen, (2) urate precipitation in the urinary passages, and (3) a possible glomerular disorder whose mechanism remains undefined.
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PMID:[Renal lesions in myelofibrosis (author's transl)]. 22 98

The authors report a case of acute nephritis which appears during a treatment with phenindione. The nephropathy described after this medication are now well known. Their manifestations are either a proteinuria associated or not with a nephrotic syndrome or an interstitial nephritis whose pronostic is reserved. In this observation the mechanism is different : the lesion is glomerular and complicates an allergic vasculitis which was secondary to the phenindione's therapy. The pronostic was good.
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PMID:[Acute nephritis and allergic vasculitis due to phenindione (author's transl)]. 22 9

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

Two major categories of membranoproliferative glomerulonephritis (MPGN) designated type 1 and 2 MPGN are currently recognized, largely on the basis of characteristic morphologic and immunofluorescence features. In contrast to experience reported from outside the United States, type 2 MPGN has been observed rather infrequently in this country. In a retrospective clinicopathologic study, 24 kidney specimens obtained from 10 children and young adults including seven females and three males (mean age: 13 years) with type 2 MPGN were identified using light, immunofluorescence, and electron microscopy. The histopathologic findings were related to the clinical course of each patient. When initially seen all patients had hematuria and proteinuria, three were nephrotic, and five were mildly hypertensive. A single patient was mildly azotemic. Eight patients had experienced an upper respiratory ifnection preceding their illness, although only one patient had evidence of a streptococcal pharyngitis. During a period of follow-up averaging 10 years, eight patients were nephrotic at some time during their illness and seven were persistently so. Hypertension was a major problem in eight patients and renal function declined markedly within a year of its onset in five. Persistence of the nephrotic syndrome from early onset of the disease, especially when associated with hypertension, was an additional sign of poor prognosis. Four patients developed chronic renal failure and three received one or more renal allografts. Histologic evidence of recurrent disease was found in allografts from the three patients as early as 7 months after transplantation in the absence of clinical features indicative of recurrent glomerulonephritis. It is concluded that type 2 MPGN is a chronic progressive renal disease of unknown etiology and pathogenesis which chiefly afflicts children and young adults. Hypertension and the early and persistent presence of the nephrotic syndrome suggest a poor prognosis. The disease appears to be largely unresponsive to conventional forms of therapy. The disease recurs with great frequency in allografts, often in the absence of clinical evidence of recurrent glomerulonephritis.
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PMID:Membranoproliferative glomerulonephritis with dense intramembranous alterations. A clinicopathologic study. 32 95

92 cases of extramembranous glomerulitis (EMG) documented by histology and immunofluorescence have been studied. At the time of renal biopsy the clinical and biologic picture was as follows: no proteinuria in 2%, isolated proteinuria in 18%, nephrotic syndrome without hypertension or azotemia in 41%, and hypertension and/or azotemia associated with proteinuria or nephrotic syndrome in 39%. A possible cause of the EMG was found in 27 cases: it was drug-induced or toxic in 10 instances, paraneoplastic in 7, lupus in 5 and parasitic (loasis) in 5.65 cases are regarded as idiopathic. The evolution is known in 66 cases and varies with the etiology: it is usually benign in secondary forms except the paraneoplastic cases. In the idiopathic forms it results in hypertension or more or less severe chronic renal failure in 62% of cases. The prognosis cannot be established on the basis of the initial histology. No treatment has proved effective.
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PMID:[Extramembranous glomerulitis. Apropos of 92 cases]. 32 37


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