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 total of 163 Japanese children (90 boys and 73 girls, ranging in age from 3 to 15) with proteinuria and/or hematuria were studied for renal histopathology using biopsy materials by light microscopy, electron microscopy, and immunofluolescence method. Eleven patients were diagnosed as membranous nephropathy (MN) while the other 152 patients had various renal diseases other than MN. All patients with MN did not have any known predisposing of associated caused. Hepatitis B virus surface antigen (HBsAg) in the serum, as determined by a reversed passive hemagglutination method (RPHA), was positive in 100% of the patients with MN, while it was positive in 4.6% of the patients with other renal diseases. The difference was statistically significant. Of the 11 mothers of the children with MN, six were positive for HBsAg, and one of the remaining 2 was positive for antibody to HGsAg (anti-HBs) and another was not examined. These findings suggest that MN among Japanese children are mainly, if not exclusively, caused by hepatitis B virus (HBV) and that the virus is transmitted from the mother to child in most instances. In each case of HBsAg-associated glomerulonephritis reported, HBsAg was detected, by immunofluorescence, in the glomeruli, with a distribution similar to that of immunoglobulins. However deposits of HBsAg could not be demonstrated in the glomeruli of the 9 patients with MN studied. Pathogenic immune complexes in the glomerular lesions with subepithelial deposits have been shown to weigh less than 1 million daltons. Since the intact 20-nm HBsAg has a molecular weight of more than 2.4 million daltons, probably most immune complexes containing it would be very large and rapidly cleared by the reticuloendothelial system. Therefore, this failure to detect glomerular staining with anti-HBs antiserum may mean that MN is caused by some other antigen, of a lower molecular weight, associated with HBV, but not necessarily by HB surface antigen.
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PMID:[Etiology of membranous nephropathy in children: Association between membranous nephropathy and hepatitis B virus infection (author's transl)]. 54 9

In seven patients on maintenance hemodialysis, de novo recurrent renal stone formation was observed. In all patients, the underlying disease was glomerulonephritis, with or without the nephrotic syndrome. All patients had considerable persistent proteinuria. The stones consisted predominantly of protein, as revealed by amino acid analysis, and had a negligible carbohydrate and lipid content. Only in some specimens, X-ray diffraction and scanning electron microscopy revealed the presence of small amounts of whewellit (calcium oxalate monohydrate) and/or uric acid. In semithin sections, the stones had a laminated texture and exhibited structural anisotropy under polarized light. With transmission electron microscopy, they were found to consist of peculair microfibrils. The proteinaceous material differed from fibrin or Tamm-Horsfall-protein, as indicated by ultrastructure, carbohydrate analysis, and amino acid analysis. Symptomatic de novo matrix stone formation constitutes another complication of dialyzed patients which has not been reported so far.
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PMID:Urinary matrix calculi consisting of microfibrillar protein in patients on maintenance hemodialysis. 54 10

A patient with a single functioning kidney presented with the nephrotic syndrome. On the basis of highly selective proteinuria, a diagnosis was made of lipoid nephrosis. Steroid therapy over a 2-year period did not control the disease. The patient eventually developed end-stage renal failure and malignant hypertension. Nephrectomy was performed to control the hypertension. Histological examination showed congenital dysplasia in one kidney and sclerosing glomerulonephritis, malignant nephrosclerosis, as well as dysplastic changes in the other.
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PMID:Sclerosing glomerulonephritis and malignant hypertension in a patient with congenital renal dysplasia: A case report. 55 Apr 41

A case of congenital syphilis is reported. It deals with a three-month-old girl suffering from a nephropathy clinically characterized by edema, hematuria, severe proteinuria and slight renal insufficiency. On light an delectron microscopy, a mesangial proliferative and focal extracapillary proliferative glomerulonephritis with abundant intermembranoepithelial deposits was observed.
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PMID:[Nephropathology caused by congenital syphilis. Report of a case]. 55 95

Two children with congenital fibroelastosis and recurrent episodes of heart failure had overt proteinuria and hematuria; one also had a reversible nephrotic syndrome. Urinary manifestations persisted during periods of cardiac compensation. Renal biopsies revealed mesangial hyperplasia by light microscopy, identical ultrastructural lesions in the glomerular basement membrane, and deposits of fibrin in one of the biopsy specimens studied by immunofluorscence. These changes detected by electron microscopy may result in an increase in glomerular permeability independent of the renal hemodynamic disturbances associated with cardiac insufficiency. The progression of the lesions appears to be slow, although urinary manifestations may simulate an intercurrent glomerulonephritis. Pulmonary hypertension and renal venous stasis with glomerular intravascular coagulation were discussed as possible pathogenic mechanisms.
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PMID:Glomerular lesions in congenital endocardial fibroelastosis: clinical manifestations and ultrastructural studies in two patients. 58 Aug 81

We performed renal biopsies on eight patients who had benign essential hypertension but laboratory abnormalities suggestive of glomerulonephritis. Persistent microscopic hematuria was detected in four patients, proteinuria in five, RBC casts in two, and decreased glomerular filtration in seven. In all eight biopsy specimens, we detected hyaline arterionephrosclerosis, focal glomerular obsolescence, and segmental, afibrillar thickening of glomerular basement membranes. Direct immunofluorescence studies performed on all eight samples were negative for immunoglobulins, complement, and fibrinogen. Although the patients in our study had laboratory findings suggestive of glomerulonephritis, the morphologic changes were indicative of benign essential hypertension.
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PMID:Glomerular lesions in benign essential hypertension. A study of eight biopsy specimens with laboratory evidence suggestive of glomerular abnormalities. 58 47

A 60 year old hyperthyroid black woman with long-standing Graves' disease treated with methimazole presented with anasarca and congestive heart failure. She was found to have the nephrotic syndrome with a urinary protein excretion of 32 g/day. Light and electron microscopy revealed a stage II membranous glomerulopathy. Direct and indirect immunofluorescence demonstrated immunoglobulin G (IgG), immunoglobulin M (IgM), third component of complement and thyroglobulin in a granular diffuse pattern consistent with an immune complex glomerulonephritis. Total thyroidectomy led to a decrease in proteinuria with little change in glomerular filtration rate during an 11 month follow-up period. We believe this to be the first report of immune complex glomerulonephritis associated with thyroid antigen in Graves' disease.
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PMID:Thyroid antigen associated immune complex glomerulonephritis in Graves' disease. 58 94

Isolated glomerulonephritis with mesangial IgA deposits was the most common single finding encountered in a large biopsy series in an Australian community and was found in 50 patients, 18% of those presenting for the investigation of primary glomerular disease. A uniform histopathological picture of mesangial enlargement, with or without focal and segmental features was present. A tendency to progression was suggested by the frequent presence of glomerulosclerosis, interstitial scarring and vascular hyalinization. Because of the uniform histological immunofluorescence and ultrastructural appearances, the term IgA nephropathy has been used for this condition. The clinical picture, however, was heterogenous. Presenting symptoms included macroscopic hematuria (34%), proteinuria (32%) acute nephritis (10%), nephrotic syndrome (6%), malignant hypertension (8%), acute renal failure (6%) and chronic renal failure (4%). There was a striking correlation of increased blood pressure and decreased renal function with increasing age. While the period of follow-up was too short to assess individual patient data, a gradual and progressive decrease in renal function over several decades is suspected in patients with this condition.
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PMID:IgA nephropathy: a syndrome of uniform morphology, diverse clinical features and uncertain prognosis. 58 77

Rat-adapted Plasmodium chabaudi caused a syndrome characterized by hemolytic anemia, splenomegaly, and glomerulonephritis. All rats recovered and appeared normal after 4 weeks despite persistence of proteinuria. Serologic studies on the malarious rats revealed that the infection was associated with a soluble antigen which was present concurrently with antibody in plasma, in material eluted from blood cells, in extracts of kidney tissues, and in the urine. This antigen appeared to be identical with one extracted from P. chabaudi parasites and did not cross-react with antigens of Plasmodium gallinaceum. Tests for the cold-active hemagglutin (CAH) and the globulin associated serum antigen (SA) previously associated with acute malaria, revealed that CAH, but not SA, was present. From these observations it is suggested that soluble complexes of the parasite antigen and its antibody may have been causal in this syndrome.
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PMID:Experimental infection with Plasmodium chabaudi in rats: antigen and antibody associated with anemia and glomerulonephritis of acute infection. 59 39

A case of minimal change glomerulonephritis, associated with the nephrotic syndrome and prolonged acute renal failure requiring two months of dialysis, is reported. Complete recovery of renal function occurred, but proteinuria recurred, responding to a course of steroids. Normal renal function without proteinuria has been observed for two years subsequently. The full return of renal function without specific therapy demonstrates that spontaneous recovery is possible in this rare complication of minimal change glomerulonephritis.
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PMID:Reversible acute renal failure in the nephrotic syndrome with minimal glomerular pathology. 60 Jan 64


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