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)

Cushing's syndrome with pregnancy is rare, and only about 60 cases have been reported. In the recent 4 years, 3 cases were diagnosed in Chang Gang Memorial Hospital. They presented with serious maternal complications early in the second month of pregnancy, including hypertension, proteinuria and lower leg edema. Unfortunately it was not diagnosed until the 20th week of pregnancy. They had the same hormone profile as other Cushing's syndrome patients who were not pregnant. Under the supportive treatment they had outcomes of two premature deliveries and one still birth. Just after delivery all patients received left adrenalectomy and pathology showed adenoma. All of them had good recovery courses. According to the literature, early treatment (surgical operation, medical treatment, or irradiation) could decrease maternal morbidity and fetal loss rate.
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PMID:[Cushing's syndrome with pregnancy. Report of three cases]. 129 59

A 45-year-old Turk had a year ago noticed a submandibular and a retroauricular node-like swelling, about 2 cm in diameter each, firm and freely mobile. During the preceding two months he had polydipsia and polyuria. Recently he developed a nephrotic syndrome with lower-leg oedema and proteinuria (14 g albumin in 24-hour urine). The concentrations of IgE (250 IE/ml) and IgA (745 mg/dl) were raised, and there was eosinophilia of 14%. Renal needle biopsy revealed glomerulonephritis with minimal proliferation. Excision of part of the nodular tumour revealed histologically the typical signs of Kimura's disease (eosinophilic follicular lymphadenitis of the skin; subcutaneous angiolymphoid hyperplasia with eosinophilia). During treatment with prednisolone, 20 mg daily by mouth, the clinical and biochemical findings regressed within two weeks. But eight weeks later, after dose reduction to 10 mg daily, the nephrotic syndrome recurred so that the dosage had to be increased again to 20 mg prednisolone daily. On this treatment the patient has now been symptom-free for six months. This case demonstrates the unusual association of Kimura's disease with minimally proliferative glomerulonephritis.
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PMID:[Kimura disease with minimally proliferative glomerulonephritis]. 204 61

A 54 year-old woman who had had 4 years history of ulcerative colitis (UC) was admitted to our hospital because of recently developed proteinuria and leg edema. On admission, laboratory findings disclosed massive proteinuria, hypoalbuminemia, acceleration of ESR and elevated of CRP. Her abdominal symptom was remitted. Renal biopsy showed amyloid deposition in glomeruli and arteriole. Amyloid deposition was also found on rectal biopsy. She had no evidence of familial amyloidosis and multiple myeloma. In this case, amyloid deposition might be developed after UC. Secondary amyloidosis due to UC was extremely rare, only 3 cases including ours were reported in Japan.
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PMID:[A case of secondary amyloidosis complicated with ulcerative colitis]. 237 13

A 35-year-old man developed leg edema, marked hypoalbuminemia, and proteinuria. Subsequent renal biopsy revealed a diffuse membranoproliferative glomerulonephritis and, on electron microscopy, typical electron-dense deposits characteristic of an immune complex pathogenesis. Although protein wasting might have readily been explained on the basis of his nephrotic syndrome, the concomitant symptom of diarrhea led to the diagnosis of celiac sprue, another disorder with a possible immune-mediated pathogenesis. While reports of immune complex glomerulonephritis in celiac sprue are rarely recorded, the potential significance of gastrointestinal symptoms in patients with the nephrotic syndrome may have important nutritional implications, especially if underlying occult celiac sprue is recognized.
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PMID:Celiac sprue-associated immune complex glomerulonephritis. 294 90

A 34-year-old female presenting with bilateral lower leg edema and distended abdomen was admitted to our hospital. The serum albumin was 1.42g/dl. Renal function and hepatic function were normal. Urinalysis did not show proteinuria. Tc-99m albumin scintigraphy was arranged for this patient to rule out protein-losing enteropathy. The results demonstrated loss of albumin into the intestines. We conclude that Tc-99m albumin scintigraphy of the abdomen is a valuable adjunct in the diagnosis of protein-losing enteropathy.
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PMID:Technetium-99m albumin scintigraphy in the diagnosis of protein-losing enteropathy: a case report. 762 22

A 69-year-old female was admitted to our hospital because of leg edema, proteinuria (2.1 g/day), and gross hematuria. She had non-alcoholic liver cirrhosis of unknown etiology. Esophageal varices also were found. Examination of the renal biopsy specimen revealed mesangial proliferative glomerulonephritis with IgA deposits. Propranolol was administered orally to reduce portal hypertension, resulting in a progressive decrease in urinary microalbumin excretion. This case suggests that portal hypertension is involved in the pathogenesis of IgA nephropathy in liver cirrhosis.
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PMID:IgA nephropathy associated with portal hypertension in liver cirrhosis due to non-alcoholic and non-A, non-B, non-C hepatitis. 780 17

A 58-year-old woman with kidney-limited recurrence of microscopic polyarteritis (MPA) is described. The patient had a history of histologically-confirmed MPA 7 years previously, which had been in remission with corticosteroid treatment for 30 months followed by no medication thereafter. However, in February 1994, clinical manifestations including leg edema and proteinuria developed, followed by rapidly progressive renal insufficiency. Renal biopsy revealed crescentic glomerulonephritis with necrotizing vasculitis. Furthermore, at the same time antimyeloperoxidase antibody (MPO-ANCA) was detected in plasma. She was diagnosed as having kidney-limited recurrence of MPA without systemic presentation. Corticosteroid therapy was reinstituted, and the renal function improved, with a decrease in the titer of MPO-ANCA.
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PMID:Kidney-limited recurrence in a patient with microscopic polyarteritis. 856 91

A 66-year-old Japanese male, who suffered from persistent proteinuria and leg edema, underwent renal biopsy. Light microscopy revealed marked narrowing of the glomerular capillary lumen with a diffuse accumulation of weakly PAS-positive material. By electron microscopy, abundant abnormal collagen fibers were observed predominantly in the subendothelial space and occasionally in the mesangial matrix. The fibers had a periodicity of about 60 nm and were immunoreactive for anti-type III collagen. Subendothelial electron-dense deposits were also found in some of the capillary walls. The serum level of procollagen III peptides was elevated and changed in parallel with the amount of proteinuria during the patient's clinical course. On the basis of these findings, a diagnosis of the collagenofibrotic glomerulonephropathy was made. A review of the literature, including 29 similar or identical cases, failed to reveal the etiology and pathogenesis of this disease. We suggest that this disease may be divided into two different clinical subtypes, an adult-onset type and a pediatric type.
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PMID:Collagenofibrotic glomerulonephropathy associated with immune complex deposits. 956 56

A 26-year-old woman who presented facial and lower leg edema associated with massive proteinuria was admitted to our hospital in February 1992. Nine months before this admission, she exhibited myasthenia gravis and malignant thymoma, and underwent total thymectomy. On admission, there was no symptom of myasthenia gravis. She was diagnosed as having nephrotic syndrome and the first renal biopsy was performed. The histological findings showed membranous nephropathy. Immunofluorescent microscopy revealed that IgG and C3 were stained in a granular pattern in the periphery, and subepithelial deposits were observed in the basement membrane of the glomerulus by electron microscopy. With the administration of prednisolone, proteinuria disappeared and the nephrotic syndrome remitted. She was admitted again in January 1993 due to proteinuria and lower leg edema following cystitis. The findings of the second renal biopsy were unremarkable. She was administered cyclosporin A to improve the nephrotic syndrome and to reduce the side effects of prednisolone. The proteinuria disappeared again and this effect was dependent on the dose of cyclosporin A. Since the first administration, no symptoms of myasthenia gravis or malignant thymoma have been observed. The relationships among myasthenia gravis, malignant thymoma and nephrotic syndrome were examined. Although the first renal biopsy findings showed membranous nephropathy, from the therapeutic responses of both prednisolone and cyclosporin A, the main course of proteinuria in this case may have been due to minimal change nephrotic syndrome. We consider this case of nephrotic syndrome to be important considering its etiology and the relationship between the histological findings and its clinical course.
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PMID:[A case of nephrotic syndrome associated with myasthenia gravis and malignant thymoma]. 1036 23

We report an autopsy case of elderly-onset anticentromere antibody-positive pulmonary-renal syndrome. An 84-year-old woman was admitted to our hospital with complaints of leg edema and general malaise. Neither skin rush nor arthritis was seen. Because of hematuria, proteinuria with various casts, renal dysfunction and anemia, a clinically diagnosis of rapidly progressive glomerulonephritis was made. Slight pulmonary hypertension was observed in ultrasonic cardiography. Hypocomplementemia was not seen. Tests for MPO- and PR 3-anti-neutrophil cytoplasmic antibodies and anti-glomerular basement membrane antibody were negative, but a high titer of antinuclear antibody with a discrete speckled pattern on immunofluorescent staining was disclosed. Results for anticentromere antibody and anti-Ki antibody were positive, but for anti-Sm antibody and anti-double stranded DNA antibody were both negative. She did not present any clinical features of systemic sclerosis or CREST syndrome. Subsequently, prednisolone was administered, but pulmonary alveolar hemorrhage occurred and the patient died of acute respiratory failure caused by massive pulmonary hemorrhage. Autopsy revealed crescentic glomerulonephritis including glomerular capillaritis and pulmonary capillaritis with positive granular deposits of immunoglobulins and compliment on the glomerular and pulmonary capillary walls. Immunologically mediated crescentic glomerulonephritis and pulmonary capillaritis was then diagnosed histopathologically. The main pathological feature of the case was small-vessel vasculitis with immune-complex deposition. Although this case did not fulfill the clinical criteria for systemic lupus erythematosus (SLE), its histological features resembled those of lupus nephritis and acute lupus pneumonitis. We speculated that anticentromere antibody-positive pulmonary-renal syndrome without any other symptoms or signs of connective tissue disease, such as our case, is a clinical entity distinct from typical SLE or CREST syndrome.
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PMID:[Elderly-onset anticentromere antibody-positive pulmonary-renal syndrome: report of an autopsy case]. 1157 30


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