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)

We studied the effect of dietary protein restriction on glomerular function and proteinuria in nine patients with membranous nephropathy. Patients were randomly assigned to a 3-month period of a normal protein diet (NPD, 1.3 mg/kg/d) or of a low-protein diet (LPD, 0.6 mg/kg/d), in a cross-over design. Dietary protein restriction did not affect glomerular filtration rate (47.8 +/- 10.7 and 49.0 +/- 13.5 mL/min/1.73 m2, LPD and NPD, respectively) and renal plasma flow (456 +/- 119 and 499 +/- 161 mL/min/1.73 m2, LPD and NPD, respectively), nor did it significantly improve glomerular permselective function, as shown by urinary protein excretion (3.1 +/- 2.2 and 3.5 +/- 2.8 g/d, LPD and NPD, respectively) and fractional clearance of albumin, IgG, and neutral dextran molecules of graded molecular size (radii ranging from 2.8 to 6.0 nm). These results indicate that reduction of protein intake to 0.6 g/kg/d does not improve glomerular size selectivity in membranous nephropathy. Thus, in current clinical practice, a protein-restricted diet does not appear to be effective in reducing proteinuria in this category of patients.
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PMID:Low-protein diet and glomerular size-selective function in membranous glomerulopathy. 199 76

A 42-yr-old woman with hypertension and renal involvement due to systemic lupus erythematosus (SLE) developed unilateral headache followed by the sudden onset of confusion and a grand mal convulsion. Cerebral computed tomography was normal. A magnetic resonance imaging angiogram revealed cerebral venous thrombosis and a venous infarct. Nephrotic syndrome had resulted in an acquired protein S deficiency. A review of previous cases suggests that either renal disease with proteinuria or features of the antiphospholipid syndrome are prerequisites for the development of cerebral venous thrombosis in SLE. Low free-protein S levels may be an additional risk factor. Furthermore it is likely that this condition is underdiagnosed.
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PMID:Cerebral venous thrombosis and acquired protein S deficiency: an uncommon cause of headache in systemic lupus erythematosus. 763 1

A 42-year-old female was admitted to a hospital, because of acute hepatitis A. Laboratory data were GOT 8210mU/ml. GPT 4650mU/ml, LDH 11860mU/ml, total bilirubin 4.7mg/dl, BUN 19.5mg/dl and creatinine 1.9mg/dl. Urinalysis showed proteinuria 3+ and occult blood 1+. Soon after admission, she suffered from anuric acute renal failure and was transferred to our hospital for hemodialysis. Her urine-volume was under 20 ml per day. Urinalysis showed proteinuria 4+, occult blood 1+ and casts. Laboratory data showed BUN 58.2mg/dl and creatinine 8.5mg/dl. She was treated by hemodialysis for 35 days, before recovering from renal failure. However, her renal function did not recover perfectly and her 24-hour creatinine clearance remained at 50ml/min after 6 months. Renal biopsy was performed on the 17th day after admission. Examination by light microscopy revealed the findings of acute tubular necrosis and examination by immunofluorescence antibody method was negative. Urinalysis of 8 patients with acute hepatitis A showed that all patients had proteinuria at the onset. Patients with acute hepatitis A have symptoms of appetite-loss, nausea, vomiting and/or diarrhea. These symptoms cause hypovolemia, and hepatic dysfunction causes discontrol of vasoactive hormones, which gives rise to disturbance of renal circulation. Subsequently, acute tubular necrosis and acute renal failure occur.
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PMID:[A case of acute hepatitis A associated with acute renal failure from the onset]. 823 Aug 22

Renal artery infarction is a very rare complication in patients with systemic lupus erythematosus (SLE), even in patients with antiphospholipid syndrome which often causes thromboembolism: Renal infarctions have only been reported in 4 SLE patients with antiphospholipid antibodies (aPL). Here we report a case of SLE without aPL who accompanied by renal and cerebral infarctions. A 42-year old Japanese woman with 8 year history of SLE manifested by arthralgia, central nervous system symptoms, positive-antinuclear and anti-DNA antibodies was admitted to our hospital for the treatment of progressive lupus nephritis. Physical examinations revealed hypertension (130-160/80-110 mmHg) without pitting pretibial edema. Laboratory evaluations showed proteinuria (3.7 g/day), normal serum creatinine level (0.9 mg/dl), low serum albumin level (2.3 g/dl) and high cholesterol level (317 mg/dl). Old cerebral infarctions were recognized by magnetic resonance imaging. However, hematological and immunological studies revealed that this case has neither a prolonged activated partial thromboplastin time, lupus anticoagulant nor anticardiolipin antibodies. Prednisolone was increased from 30 mg/every other day to 30 mg/day, and oral azathioprine, 50 mg/day, was started for the treatment of lupus nephritis. On the 11th day, she suddenly complained severe abdominal pain, which gradually localized on the right side. Computed tomography of the kidney suggested right renal infarctions, and arteriography of right renal artery confirmed both an obstruction of the ventral branch and a narrowing of the dorsal branch of right renal artery. No intra-cardiac thrombus was demonstrated by echocardiography. Following to the treatment with fibrinolytic agent and anticoagulant, her symptoms have improved.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Renal and cerebral infarctions in a patient with systemic lupus erythematosus without antiphospholipid antibodies]. 823 16

A 42-year-old man with chronic myelogenous leukemia underwent allogeneic hematopoietic stem cell transplantation (allo-HSCT) from an unrelated donor in January 1998. About 100 days later, he developed skin eruption and a diagnosis of chronic graft-versus-host disease (cGVHD) was made by skin biopsy. The eruption improved with steroid therapy, and the dose of steroid was gradually tapered. On day 151, the patient developed nephrotic syndrome with proteinuria up to 20 g/day. A renal biopsy carried out on day 160 showed minimal change in the glomeruli. The proteinuria disappeared 19 days after the onset of nephrotic syndrome without any additional therapy, and no recurrence was observed upon re-tapering of the steroid. In this case, cGVHD might have been related to development of the nephrotic syndrome. Nephrotic syndrome after allo-HSCT is a rare complication, and only ten cases have been reported. The histological findings were mainly membranous nephropathy, and immunosuppressive therapy was effective. As seen in this case, transient nephrotic syndrome with cGVHD may occur after allo-HSCT, and care is necessary to ensure that treatment of cGVHD is sufficient.
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PMID:[Transient nephrotic syndrome after allogeneic bone marrow transplantation for chronic myelogenous leukemia]. 1140 Mar 4

A 42-year old housewife presented herself with flu symptoms and dry cough. Because of pregnancy test (chest x-ray) we accidentally detected a hematuria. Exact medical history revealed the presence of a known IgA-Nephropathy. Banal respiratory infections can exacerbate IgA Nephropathy. In addition, medical history and further investigations are important because of possible secondary IgA-Glomerulonephritis. Treatment of IgA glomerulopathy depends on blood pressure, renal function and degree of proteinuria. An acute renal insufficancy is uncommon (< 5%), but 25% patients develop during 20-25 years a terminal insufficandy.
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PMID:[Bronchitis, pregnancy test and hematuria--an atypical algorithm for diagnosis]. 1785 84

A 42-year-old woman was admitted to Kyushu University hospital because of 6 months' history of bilateral leg edema. Upon admission, ascites and pleural effusion as well as systemic edema were noted. Laboratory tests revealed hypoalbuminemia of 1.5 g/dl and massive proteinuria of 10 g/day. She was diagnosed with nephrotic syndrome. Renal biopsy revealed diffuse thickening of the glomerular basement membrane (GBM) and a crescent-like extracapillary lesion with segmental sclerosis in four of 11 glomeruli. Immunoglobulins and complements were negative by immunofluorescence examination. Therefore, we diagnosed this as focal segmental glomerulosclerosis (FSGS) rather than membranous nephropathy. Using an electron microscope, we observed a thickening of the GBM with numerous intramembranous vesicle-like microstructures and an infolding of the podocyte into the GBM. Since the microstructures were partly demarcated by a unit membrane and some of them were located very closely to the infolded podocyte, we speculated that the microstructures were derived from the podocyte. The unique electron microscopic finding of our case is a disease entity rather than a reactive phenomenon.
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PMID:Focal segmental glomerulosclerosis with intramembranous vesicle-like microstructures and podocytic infolding lesion. 1897 62

Dietary protein restriction is one major therapy in chronic kidney disease (CKD), and ketoacids have been evaluated in CKD patients during restricted-protein diets. The objective of the present study was to compare the efficacy of a low-protein diet supplemented with ketoacids (LPD+KA) and a low-protein diet alone (LPD) in halting the development of renal lesions in CKD. 5/6 Nephrectomy Sprague-Dawley rats were randomly divided into three groups, and fed with either 22 % protein (normal-protein diet; NPD), 6 % protein (LPD) or 5 % protein plus 1 % ketoacids (LPD+KA) for 24 weeks. Sham-operated rats were used as controls. Each 5/6 nephrectomy group included fifteen rats and the control group included twelve rats. Proteinuria, decreased renal function, glomerular sclerosis and tubulointerstitial fibrosis were found in the remnant kidneys of the NPD group. Protein restriction ameliorated these changes, and the effect was more obvious in the LPD+KA group after 5/6 nephrectomy. Lower body weight and serum albumin levels were found in the LPD group, indicating protein malnutrition. Lipid and protein oxidative products were significantly increased in the LPD group compared with the LPD+KA group. These findings indicate that a LPD supplemented with ketoacids is more effective than a LPD alone in protecting the function of remnant kidneys from progressive injury, which may be mediated by ketoacids ameliorating protein malnutrition and oxidative stress injury in remnant kidney tissue.
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PMID:A low-protein diet supplemented with ketoacids plays a more protective role against oxidative stress of rat kidney tissue with 5/6 nephrectomy than a low-protein diet alone. 1987 16

We report an unusual case of cerebral aneurysmal subarachnoid hemorrage (SAH) with Fabry's disease. A 42-year-old woman presented with aneurysmal SAH originated from a saccular aneurysm of the right posterior communicating artery. The patient was treated by an endovascular coil embolization of aneurysm. Postoperatively the patient recovered favorably without any neurological deficit. During her admission, the patient had a sign of proteinuria in urine analysis. The pathologic findings of kidney needle biopsy implied nephrosialidosis (mucolipidosis of lysosomal stroage disease), which is consistent with a Fabry's disease. It is uncommon that Fabry's disease is presented with aneurysmal SAH, especially in middle-aged patients, but could be a clinical concern. Further investigations are needed to reveal risk factors, vascular anatomy, and causative mechanisms of Fabry's disease with aneurysmal SAH.
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PMID:A Case of Cerebral Aneurysmal Subarachnoid Hemorrhage in Fabry's Disease. 2363 71

A 42-year-old Caucasian female with history of neurofibromatosis type 1 presented with nephrotic range proteinuria and focal segmental glomerulosclerosis (FSGS). On final dose of lisinopril 20 mg/day, protein-creatinine ratio declined to 0.33 within 10 months. We propose the hypothesis that development of FSGS in NF1 may be mediated by activation of mitogen-activated protein kinase (MAPK) and mammalian target of rapamycin (mTOR) signaling pathways secondary to up-regulation of ras proteins due to deficient neurofibromin. Since mTOR signaling pathway is partially mediated through angiotensin-II activation, angiotensin-converting enzyme (ACE) inhibition may serve as an effective initial treatment beyond anti-proteinuric properties of ACE-inhibitors.
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PMID:Focal segmental glomerulosclerosis in association with neurofibromatosis type 1: a case report and proposed molecular pathways. 2380 77


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