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 58-year-old fisherman was admitted because of an abnormal chest X-ray shadow on the right side. Bronchoscopic examination revealed tumor of right B7. Transbronchial biopsy showed squamous cell carcinoma. He was treated with four courses of CDDP and PEP. Two years later, he developed nephrotic syndrome and relapse of lung cancer. Proteinuria and pedal edema continued. Renal biopsy revealed the characteristic light and immunofluorescent microscopic features of membranous nephropathy. Oral administration of low dose etoposide resulted in reduction of the carcinomatous lung lesion and a decrease in proteinuria as well as pedal edema.
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PMID:[A case of nephrotic syndrome associated with bronchogenic carcinoma]. 140 14

The course of eight pregnancies in seven renal transplant patients was analyzed. Immunosuppression consisted of Azathioprine and Prednisone. Pregnancy lasted from 32 to 39 weeks and the fetal development corresponded to the gestational age in every case. There were three cases which had complications during the pregnancy. One case had severe arterial hypertension, proteinuria and pedal edema, which was thought to be due to pre-eclampsia. Another patient had cholestatic jaundice and premature fissure of membranes and the third patient also had this last complication. Four patients had vaginal deliveries and in four cesarean section was performed. Renal function did not deteriorate during any of the pregnancies nor during the follow-up period, but the expected increase in creatinine clearance was not found. Clinical evaluation of the children, 4 months to 8 years of age, did not disclose any abnormalities.
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PMID:[Pregnancy in renal transplant recipients. Long-term evaluation of their children]. 145 32

A 26-year-old male with nephrotic syndrome (NS) due to alpha-mercaptopropionyl glycine (MPG) is described. In March, 1988, he was diagnosed as having familial cystinuria after receiving urolithiasis treatment since December, 1985. Massive proteinuria and slight pedal edema were noted. Nephrotic syndrome was suggested and renal biopsy was performed. The renal pathological finding demonstrated membranous glomerulonephritis (MN) at stage I. This case was defined as NS clinically associated with MPG, and glucocorticoid intake was initiated. The response to the glucocorticoids was fairly good with no clinical problems after discontinuation of MPG, and the cystinuria was maintained with alkaline medication. The patient's parents and younger brother were suggested and confirmed to have cystinuria based on urinary aminogram analysis, but displayed no symptoms. We present a rare case of NS due to MPG therapy in a patient with familial cystinuria. However, the mechanism of onset remains unclear.
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PMID:A case of nephrotic syndrome due to alpha-mercaptopropionyl glycine in a patient with familial cystinuria. 225 Apr 12

A 35-year-old Kashmiri male with a 12-year history of recurrent aphthous ulcers of the mouth and scrotal ulcers was admitted with pedal edema, facial puffiness and proteinuria. Kidney biopsy showed minimal change glomerulonephritis. During hospitalization he developed erythema nodosum and left renal vein thrombosis and features of right cerebral thrombosis. He improved with a course of heparin and prednisolone. In this report a case of Behcet's syndrome with minimal change glomerulonephritis and left renal vein thrombosis is presented.
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PMID:Behcet's syndrome associated with minimal change glomerulonephritis and renal vein thrombosis. 271 Feb 73

A 43 year old woman was admitted to our hospital in April 1987 due to shortness of breath and pedal edema. She had a history of sepsis associated with the crisis of hyperthyroidism 15 years prior to the admission. Physical examination revealed a badly nourished with ascites: weight was 56 kg and height 156 cm. The heart sounds were distant with mild holosystoric murmur (grade I/VI) at xiphoisternum. The chest X-ray showed cardiomegaly (CTR: 72.3%) with pleural effusion. The electrocardiogram showed atrial fibrillation, low voltage and right ventriculer hypertrophy. The echocardiogram showed marked dilatation of right atrium and ventricle with very short septal leaflet of tricuspid valve. The anterior and posterior leaflets were undetected. The tricuspid regurgitant doppler signal was recorded up to hepatic vein. No other abnormalities were noted in other valves. The white cell count was 4900 with lymphocytopenia (26%; T-cell 82%, B-cell 13%). Serum total protein was reduced to 3.4 g/dl with albumin 1.64 g/dl. Immunoelectrophoresis showed normal IgG, IgA and IgM. Proteinuria was not recognized. Fecal excretion of polyvinylpyrrolidone-131I (PVP) was elevated to 2.8%, The systolic pressure in pulmonary artery, right ventricle, right atrium, superior and inferior vena cave were almost equal as 26 mmHg. The pulmonary arterial scintigraphy disclosed multiple peripheral defects in both lungs. Two weeks after the operation of tricuspid valve replacement based on the diagnosis of protein-losing enteropathy due to isolated tricuspid regurgitation, serum total protein and albumin were normalized to 6.8 g/dl and 3.6 g/dl respectively, but the lymphocytopenia was persistent. She become very well, with free of ascites and edema.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of isolated tricuspid regurgitation associated with protein-losing gastroenteropathy]. 273 14

Transformation of diffuse proliferative glomerulonephritis to membranous nephropathy 10 years later, in a patient with systemic lupus erythematosus, is reported. The original biopsy showed diffuse proliferative glomerulonephritis with epithelial crescent formation, 'wire loop' thickening of the capillary walls and moderately severe interstitial inflammation. Electron microscopy showed large subendothelial electron-dense deposits. Following treatment with a combination of prednisone and azathioprine for 2 years the 24-hour urine protein decreased from 8.8 g to 300 mg. In September, 1979, she again developed facial and pedal edema. With the exception of proteinuria of 6.0 g/24 h, the renal function remained normal. Repeat renal biopsy showed membranous glomerulopathy. On electron microscopy, electron-dense deposits were predominantly in a subepithelial position. The significance of the original biopsy as a predictor of eventual outcome and of sequential biopsies to the clinical management of patients with systemic lupus erythematosus is discussed.
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PMID:Transformation of diffuse proliferative glomerulonephritis to membranous nephritis in a patient with systemic lupus erythematosus. 726 28

A 6-year-old girl with Turner's syndrome presented with recent onset of proteinuria and pedal edema. There was no history of arthritis, fever, or abdominal pain. A physical examination revealed the stigmata of Turner's syndrome, hepatomegaly, and pedal edema. The urine contained 4+ protein without red blood cells or casts, and the BUN and creatinine were mildly elevated. The serum lipids were normal. An excretory urogram showed bilaterally enlarged, smooth kidneys without calyceal distortion. Because the proteinuria failed to respond after 1 month of steroid therapy, a diagnostic procedure was performed.
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PMID:A six-year-old girl with Turner's syndrome and proteinuria. 734 31

We retrospectively evaluated the clinico-laboratory features of 11 children and adolescents with Systemic Lupus Erythematosus between the period of 2001 and 2006. All of them (100.0%) had renal involvement at the first visit in the hospital. Female to male ratio was 10:1. Skin and or mucosal involvement (90.9%), periorbital puffiness and or pedal edema (81.8%), fever (72.7%), hypertension (72.7%), and reticuloendothelial involvement (72.7%), were the commonest presentations. All patients had anemia (8.6 +/- 1.5 gm/dl), raised ESR (46.7 +/- 9.4 mm in first hour), proteinuria, and in disease activity as evident by raised ESR and positive anti-dsDNA antibody at the first visit. The mean duration of disease was 7.6 months and the average duration of disease activity was 63.18 days. Renal biopsy was performed in 8 patients: class IV lupus nephritis in 4 patients (50.0%), class II in 2 patients (25.0%), class III and V in patient (12.5%) each. Nephrotic range proteinuria and hypertension was observed in all patients of class IV and V of lupus nephritis. Class II and III lupus nephritis patients' were normotensive and had non-nephrotic range proteinuria. Three out of 11 patients (27.2%) expired. The commonest primary determinant of mortality was uncontrolled disease activity in 2 patients (66.6%). The third one had infection and developed disseminated intravascular coagulation. The mean duration of disease activity in patients who died (mean 30 days) was statistically lower than the survival group (75.6 days) (p < 0.01). Renal involvement during first visit and mortality could be attributed by late referrals and diagnosis at hospital.
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PMID:Systemic lupus erythematosus in childhood--a review of 11 patients at a single center in eastern Nepal. 1809 38

Ankylosing spondylitis is a chronic inflammatory disease of the vertebral joints and soft tissues. Renal involvement, apart from amyloidosis, is rare in this disorder. Of the various glomerulonephritides reported in association with ankylosing spondylitis, IgA nephropathy is the most common. Membranous glomerulonephritis occurs very rarely in patients with ankylosing spondylitis, and only four such cases have been reported in the available English literature. Due to the rarity of this association, membranous glomerulonephritis may not initially be considered in patients with ankylosing spondylitis and proteinuria. We report the case of a 29-year-old man with ankylosing spondylitis who presented with pedal edema and was detected to have nephrotic syndrome. A percutaneous renal biopsy showed features of membranous glomerulonephritis with capillary wall granular deposits of IgG and C3 on immunofluorescence and subepithelial immune complex deposits on electron microscopy. No other secondary cause of membranous glomerulopathy was found on extensive investigations. Membranous glomerulonephritis is extremely rare in association with ankylosing spondylitis, the present case being the fifth such report. The exact relationship of these two entities (etiological or coincidental) still needs to be elucidated. The occurrence of this rare association needs to be recognized and differentiated from other more common causes of renal involvement in ankylosing spondylitis.
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PMID:Membranous glomerulonephritis in a patient with ankylosing spondylitis: a rare association. 1965 3

Nephrotic syndrome increases L-thyroxine requirements because of urinary loss of free and protein-bound thyroid hormones. We report 2 hypothyroid patients referred to us because of high serum TSH, even though the L-thyroxine daily dose was maintained at appropriate levels or was increased. The cause of nephrotic syndrome was multiple myeloma in one patient and diabetic glomerulosclerosis in the other patient. As part of the periodic controls for diabetes, urinalysis was requested only in the second patient so that proteinuria could be detected. However, as in the first patient, facial puffiness and body weight increase were initially attributed to hypothyroidism, which was poorly compensated by L-thyroxine therapy. In the first patient, the pitting nature of the pedal edema was missed at the initial examination. An endocrinologist consulted over the phone by the practitioner hypothesized some causes of intestinal malabsorption of L-thyroxine. This diagnosis would have been accepted had the patient continued taking a known sequestrant of L-thyroxine, i.e. calcium carbonate. The diagnostic workup of patients with increasing requirements of L-thyroxine replacement therapy should not be concentrated on the digestive system alone. Careful history taking and physical examination need to be thorough. Endocrinologists should not forget nephrotic syndrome that, in turn, can be secondary to serious diseases.
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PMID:Do Not Forget Nephrotic Syndrome as a Cause of Increased Requirement of Levothyroxine Replacement Therapy. 2628


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