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 59-year-old woman with retinal vein thrombosis and livedo racemosa had hematuria (4+) and proteinuria (1.7 g/day). Skin biopsy showed swollen blood vessel walls with infiltration of mononuclear cells, which were compatible with livedo racemosa (vasculitis). Magnetic resonance imaging (MRI) of the brain demonstrated multiple lacunar infarctions in the basal ganglia and white matter. Renal biopsy showed that small round cells had infiltrated into the interstitium, and a reticular structure was observed in the glomerular hilus. An amorphous substance composed of a single cell was present in the glomerular capillary lumen. Immunofluorescent study demonstrated the deposition of only IgA, in a segmental pattern differing from the diffuse global mesangial pattern seen in IgA nephropathy. After combined therapy including 40 mg/day prednisolone, 50 mg/day cyclophosphamide, antiplatelet drug, and anticoagulant was started, proteinuria and hematuria improved to 0.5 g/day and 2+, respectively, at the time of discharge. Sneddon's syndrome is a rare entity characterized by livedo racemosa and cerebrovascular lesions. In our patient with livedo racemosa, occlusion of cerebral blood vessels, and nephropathy with segmental immunoglobulin A (IgA) deposition, no antiphospholipid antibodies were detected on routine examination. Dermatologists, neurologists, psychiatrists, and nephrologists should be aware of the existence of Sneddon's syndrome with nephropathy (LI-O-N).
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PMID:A combination of livedo racemosa, occlusion of cerebral blood vessels, and nephropathy: kidney involvement in Sneddon's syndrome. 764 61

Although several clinical and morphological changes observed in overt systemic lupus erythematosus have been associated with the presence of antiphospholipid antibodies (aPL), the relation between these antibodies and lupus nephropathy (LN) is not clear. Twenty-three patients with biopsyproved LN were retrospectively studied (average age 28.5 +/- 12.3 years, all women) in order to investigate the relationship between the presence of aPL and clinical and immunobiological data. The average follow-up period was 55 +/- 42 months. The presence of aPL (IgG and IgM) was detected at least once in all patients by ELISA and/or lupus anticoagulant (kaolin time). Seven patients (30.4%) were aPL+, and the remainder aPL-. We did not find differences related to age, period of follow-up, blood pressure and livedo reticularis. However the prevalence of thrombosis, strokes and hemolysis was slightly higher in the aPL+ patients. The levels of antinuclear antibodies or anti-DNA antibodies, immunoglobulins and complement serum levels (C3, C4) were also similar in both groups. In the aPL+ group, proteinuria was significantly higher than in aPL- cases (2.21 +/- 1.5 and 0.91 +/- 1.07 g/24 h, respectively; p = 0.029). The renal histological pattern in both series was similar. However, microthrombosis in the glomerular capillary lumens was more frequent in the aPL+ group. The evolution of renal function was less favorable in aPL+ patients when compared with aPL- patients. We conclude that the presence of aPL in patients with LN is associated with several characteristics of renal impairment which may contribute to its evolution.
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PMID:The role of antiphospholipid antibodies in lupus nephropathy. 853 46

A case of SLE is reported in a 43-year-old female who had initial signs of the disease 10 years before (exudative pleuritis). SLE ran chronically with spontaneous remissions. Insolation in 1985 provoked exacerbation and further progress. The progression was accompanied with appearance of antiphospholipid syndrome (APS): habitual miscarriage, livedo, Raynaud's [correction of Raunald's] syndrome, recurrent thrombophlebitis. Aortic valve disease was more likely to be consequent to non-infectious endocarditis while arterial hypertension as well as proteinuria could be caused by renal thromboangiopathy. This case demonstrates not only a wide spectrum of SLE and APS symptoms but also difficulties which may be faced in the choice of the treatment policy.
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PMID:[The late diagnosis of systemic lupus erythematosus with the antiphospholipid syndrome]. 948 49

Antiphospholipid antibodies (APA) were studied in 30 women with a history of recurrent fetal losses. An increased level of anticardiolipin antibodies was found in 7(23.3%) of them, being high and moderate in 4 women. Lupus anticoagulant was present in 9(30.0%) examinees. None cases of SLE were diagnosed. Diagnostically significant APA levels were associated with moderate symptomless thrombocytopenia. 12 of 13 women with antiphospholipid syndrome markers had definite (livedo reticularis, damage of cardiac valves, recurrent thrombophlebitis, leg ulcers, stroke, migraine) and possible (moderate arterial hypertension, proteinuria, retina angiopathy) extragenital features of this disorder. The most serious vascular complications took place in the group with high and moderate levels of anticardiolipin antibodies IgG.
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PMID:[Antiphospholipid syndrome in females with recurrent fetal losses]. 1048 65

We report our experience with a 62-year-old Japanese man with cholesterol crystal embolism after angiographic procedures performed because of intermittent claudication. In addition to progressive renal failure and nephrotic-range proteinuria, cutaneous ischemia, consisting of livedo reticularis in the lower limbs and digital necrosis at the tip of the right toe, and fundoscopic findings showing several white spots in the branches of retinal artery were also observed. Progressive renal failure and nephrotic-range proteinuria were halted just after treatment with simvastatin. Thus, simvastatin can exert a beneficial therapeutic effect on renal cholesterol embolism.
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PMID:Potential therapeutic effect of simvastatin on progressive renal failure and nephrotic-range proteinuria caused by renal cholesterol embolism. 1146 48

Cholesterol emboli are being increasingly recognized as an important cause of renal dysfunction in an aging US population. Irregularly shaped atheroemboli typically cause partial obstruction of small renal vessels resulting in ischemia. A vasculitis-like picture often evolves with an inflammatory reaction and giant cell formation. Cholesterol emboli may be temporally related to vascular manipulation, anticoagulant, or thrombolytic drug use. Spontaneous cases have been reported. Patients with cholesterol emboli may present with a spectrum of acute renal failure varying from mild and asymptomatic to life-threatening disease. The differential diagnosis includes radiocontrast nephropathy, endocarditis with left-sided emboli, vasculitis, and thrombotic emboli. The physical examination findings suggestive of cholesterol emboli include extrarenal emboli and livedo reticularis. The urinalysis is typically unremarkable. Some patients have hematuria and/or non-nephrotic proteinuria. Serology and hematology results may suggest an inflammatory-like picture with elevated erythrocyte sedimentation rate, hypocomplementemia, eosinophilia, and eosinophiluria. In the setting of a clear precipitating factor and suggestive physical findings, cholesterol emboli can be established purely on clinical grounds. Demonstration of cholesterol crystals by biopsy of the kidney, skin (if lesion present), or muscle is diagnostic in unexplained cases. The kidney is the organ most frequently involved in this order. Therapy is supportive with particular emphasis on management of hypertension and hypercholesterolemia.
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PMID:Atheroembolic Renal Disease. 1186 88

The prognosis of renal cholesterol crystal embolism (CCE) is poor, and many patients progressively develop to the end-stage of chronic renal failure. We herein experienced a 66-year-old male patient who recovered from hemodialysis (HD) shortly after an amputation of inflammatory toes. The patient complained of painful digital cyanosis at bilateral toes and livedo reticularis at right lower leg 4 weeks following aortic angiography. Laboratory examinations revealed eosinophilia and overt proteinuria (3.0 g/day). His serum creatinine level increased from 2.18 to 8.57 mg/dl over 6 weeks, and HD treatment was started. Treatment with simvastatin (5 mg/day) did not reverse renal failure and hypereosinophilia, but the amputation of right gangrene toes promptly increased urine output and eosinophilia completely disappeared concomitantly with a decline of C-reactive protein from 9.7 to 0.7 mg/dl. Serum creatinine level was also reduced to 3.46 mg/dl, and he eventually stopped HD totally after 32 sessions. This case suggested that the surgical amputation promptly recovered renal function. Reversal of inflammation may be more effective than lipid-lowering therapy for renal failure in our patient.
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PMID:Recovery from hemodialysis therapy in a patient with renal cholesterol crystal embolism. 1218 14

The commonest clinical presentation of both immunoalergic interstitial nephritis (IIN) and atheroembolic renal disease (ATD) is an acute renal failure accompanied by skin lesions and eosinophilia. As a consequence, differential diagnosis between both entities is often very difficult. We have performed a comparative retrospective study of those patients diagnosed as having IIN or ATD in our Hospital in the period 1980-2000. A total of 42 patients have been diagnosed of IIN and 16 of ATD. Demographic data, as well as clinical and laboratory parameters and outcomes of every studied patient were analysed. We found a significantly higher prevalence of male sex (100% vs 57%, p < 0.01), previous history of hypertension (100% vs 55%, p < 0.01), chronic renal insufficiency (56% vs 17%, p < 0.01), ischemic heart disease (56% vs 14%, p < 0.001), peripheral ischemic disease, endovascular procedures (87% vs 7%, p < 0.001) and anticoagulant treatments (25% vs 5%, p < 0.001) among patients with ATD as compared with IIN, respectively. On the contrary, previous infections (45% vs 12%, p < 0.01) and exposure to new drugs (100% vs 40%, p < 0.001) were significantly more frequent among IIN patients in compare with ATD. ATD patients showed skin lesions consisting of livedo reticularis and digital infarcts (63% vs 31%, p < 0.05) accompanied by blood pressure increase (100% vs 24%, p < 0.001), whereas IIN patients showed fever (41% vs 19%, p < 0.05) and cutaneous rash as significant clinical manifestations, respectively. The number of ATD patients with proteinuria > 1 g/24 h was significantly higher, but no differences between both groups in the prevalence of urinary sediment abnormalities were observed. The prevalence of absolute eosinophilia was high in both groups (88% among ATD patients, 64% among IIN patients; pNS). Prognosis of both entities was clearly different: Almost all patients with ATD died (69%) or evolved to end-stage renal failure, whereas most patients with IIN showed a recovery of renal function after withdrawal of responsible drugs and steroid treatment. In summary, the analysis of clinical and laboratory data allows an initial differential diagnosis in patients suspected as having IIN or ATD.
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PMID:[Immunoallergic interstitial nephritis vs. cholesterol atheroembolism. Differentiating characteristics]. 1277 76

In 2002, a 38-year-old woman was referred to the department of dermatological sciences for the evaluation of erythematous-infiltrated lesions with prominent purpuric and erosive components distributed on her face, upper chest, and extensor surfaces of the limbs, which developed over a 3-month period. In 1997 the patient suffered from polyarthralgia (proximal interphalangeal,knee, wrist, and metacarpophalangeal joints) associated with morning stiffness. In 1999 she was admitted to a psychiatric unit for depression with episodes of lipothymia. In the same year, since she developed diffuse and persistent urticarial manifestations with angioedema and livedo reticularis of the limbs in association with anticardiolipin antibodies, vasculitis was proposed. Upon examination, erythematous-infiltrated and erosive lesions in association with serohemorrhagic crusts were present on the face,neck, chest, upper trunk, and extensor surfaces of the upper limbs and thighs (Figures 1-3). Telangiectasias were especially evident on the cheeks, where prominent edema conferred her face a moon-like appearance (Figure 1). Laboratory investigations disclosed microcytic anemia, elevated erythrocyte sedimentation rate, proteinuria (30 mg/dL), positive antinuclear antibodies (1:80) with diffuse fluorescence pattern, lowered complement levels (C3: 31 mg/dL, C4: 3 mg/dL), circulating immunocomplexes binding Clq, and high titers of anti-TSH receptor antibodies. Indirect immunofluorescence was negative for the detection of anti-basement membrane zone antibodies. Histological examination of the lesional skin of the shoulder documented epidermal atrophy, marked vacuolar degeneration of the basal cell layer, colloid bodies, and a perivascular lymphohistiocytic infiltration of the upper and deep dermis (Figure 4). Direct immunofluorescence performed on affected skin showed junctional granular deposition of IgG, C3,and Clq in association with perivascular C3 and Clq deposits in the upper dermis; direct immunofluorescence on sun-protected,non-lesional skin showed similar immunological deposition both at the basement membrane zone and in the perivascular dermis.Based upon the clinical, histologic, and immunopathologic findings, we proposed the diagnosis of systemic lupus erythematosus with maculopapular and erosive skin lesions. The patient was treated with methylprednisolone IV (pulse therapy, 250 mg) tapered over 10 days and later continued p.o. After a few weeks, significant improvement of cutaneous manifestations was noted.
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PMID:Systemic lupus erythematosus with unusual maculopapular and erosive cutaneous lesions. 1536 71

Antiphospholipid syndrome spans many medical disciplines. Classic criteria include the presence of anticardiolipin antibody or lupus anticoagulant with typical complications of thrombosis or pregnancy loss. Other common associated manifestations include livedo reticularis, thrombocytopenia, valvular heart disease, and nephropathy with renal insufficiency, hypertension, and proteinuria. Treatment of serious complications with anticoagulation is standard; generally warfarin for thrombosis and aspirin/heparin for pregnancy prophylaxis. Detailed recommendations regarding precise intensity and duration of anticoagulation are still a subject of debate.
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PMID:Antiphospholipid syndrome: review. 1600 69


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