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)

In recent years, several laboratories have suggested that chronic hepatitis C virus (HCV) infection is strongly associated with type II cryoglobulinemia (CG) and/or membranoproliferative glomerulonephritis (MPGN). We report here a case of MPGN due to type II CG probably associated with chronic HCV infection, and discuss the pathogenesis and treatment of such cases. A 60-year-old-female was referred to us from a local hospital because of progressive peripheral edema, purpura on the lower limbs, pleural effusion, ascites, hypertension, and renal failure. Laboratory findings indicated proteinuria, abnormal urinary sediments, normochromic normocytic anemia and azotemia. Other laboratory findings included positive rheumatoid factor, elevated serum IgM, hypocomplementemia and elevated circulating immune complexes. Cryoglobulin was detected and found to consist of a mixture of a monoclonal IgM kappa with polyclonal IgG. Renal biopsy showed MPGN. These observations suggested a close association between MPGN and type II CG. We did not find any causes of type II CG except for positive HCV antibody and HCV RNA. Therefore, we made the diagnosis of type II CG associated with chronic HCV infection. Symptoms related to CG was responsiveness to steroid, but development of liver dysfunction developed. Treatment with alfa-interferon (alpha IFN) was added and thereafter, the liver dysfunction improved. However, the serum Cryo level was not reproducibly lowered. While in this case it was unclear whether IFN therapy was beneficial, several reports in addition to the findings of this case suggest a close relation between HCV infection and type II CG and MPGN.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of membranoproliferative glomerulonephritis due to type II cryoglobulinemia probably associated with hepatitis C virus infection]. 819 26

This study evaluates the relationship between hemoglobin levels and diabetic retinopathy. Hemoglobin values measured in 1991 and 1992 were collected from 1691 subjects attending a diabetic clinic in Oulu, Finland, and the mean values for the two years were used in the analyses. A classification of retinopathy, based on non-mydriatic photographs taken in 1991 and 1992, was used as the outcome variable. Multiple logistic regression analyses, controlled for serum creatinine levels, proteinuria, and other prognostic factors associated with diabetes, showed that the odds ratio of having any retinopathy was 2.0 (95% confidence interval 1.2-3.3) among subjects with a hemoglobin level of less than 12 g/dl, as compared with those having a hemoglobin level > or = 12 g/dl. Among the retinopathic subjects with low hemoglobin levels, the relative odds of having a severe retinopathy rather than a mild one was 5.3 (2.3-12.6). We conclude that subjects with normocytic anemia tended to have an increased risk of retinopathy, especially of the severe form.
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PMID:The relationship between hemoglobin levels and diabetic retinopathy. 912 May 8

Arterial hypertension, which represents a common problem in patients with renal transplant, contributes to the cardiovascular morbidity and mortality of these patients. The most usual immunosuppressive drugs (cyclosporine and FK-506) collaborate on the development of hypertension. Calcium channel blockers are the most habitually used antihypertensive drugs in this population, although its long-term hemodimamycs effects could be deleterious especially in transplanted patients with chronic graft nephropathy. Losartan, a specific blocker of angiotensin II (AT1) receptors, has demonstrated a potent antihypertensive effect with a good safety and tolerance profile. The glomerular effects of losartan could be useful in transplanted patients. The present open, prospective and multicenter study evaluated the efficacy and safety of losartan in the treatment of hypertension in a group of patients with a renal transplant. Seventy-six patients with systolic blood pressure > or = 140 and/or diastolic blood pressure > or = 90 mm Hg, and/or patients on therapy with one antihypertensive drug and related side effects were included. After inclusion, therapy with losartan 50 mg/24 hr was started, discontinuing the previous antihypertensive therapy and/or therapy which caused the side effects. At four weeks, if blood pressure (BP) was not controlled, hydrochlorothiazide 25 mg or furosemide 40 mg/24 hr was added. At baseline and at weeks 2, 4, 8 and 12, the following parameters were monitored: BP, creatinine, hematocrit, hemoglobin, glucose, ions, uric acid, cholesterol, triglycerides, bilirubin, SGOT, SGPT, GGT, LDH, calcium, phosphate, alkaline phosphatase, proteinuria, and both cyclosporine and FK-506 levels in whole blood. Sixty-seven patients completed the 12-week study period. Mean blood pressure decreased from 113 +/- 10 to 102 +/- 9 mm Hg at the end of the study (P < 0.0001); 38 of the 67 patients (56.7%) who completed the study had a SBP lower than 140 mm Hg and a DBP lower than 90. These blood pressures were obtained in 30 patients on monotherapy with losartan (78.9%). Proteinuria decreased significantly at week 4 and was confirmed at week 12, especially in patients with proteinuria > or = 300 mg/24 hr. Nine patients were withdrawn during the study period for different reasons. Serum creatinine showed a slight, non-clinically significant increase at week 4, remaining stable until the end of the study. Two patients developed a mild normocytic anemia, and three others presented a mild impairment of pre-existent anemia. No interactions with cyclosporine or FK-506 were described. These results indicate that losartan is effective in reducing BP in hypertensive patients with a renal transplant. It has a good tolerance profile and does not interfere with immunosuppressive therapy.
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PMID:Efficacy and safety of losartan in the treatment of hypertension in renal transplant recipients. 983 98

To evaluate the biochemical and molecular mechanisms leading to glomerulosclerosis and the variable development of atherosclerosis in patients with familial lecithin cholesterol acyl transferase (LCAT) deficiency, we generated LCAT knockout (KO) mice and cross-bred them with apolipoprotein (apo) E KO, low density lipoprotein receptor (LDLr) KO, and cholesteryl ester transfer protein transgenic mice. LCAT-KO mice had normochromic normocytic anemia with increased reticulocyte and target cell counts as well as decreased red blood cell osmotic fragility. A subset of LCAT-KO mice accumulated lipoprotein X and developed proteinuria and glomerulosclerosis characterized by mesangial cell proliferation, sclerosis, lipid accumulation, and deposition of electron dense material throughout the glomeruli. LCAT deficiency reduced the plasma high density lipoprotein (HDL) cholesterol (-70 to -94%) and non-HDL cholesterol (-48 to -85%) levels in control, apoE-KO, LDLr-KO, and cholesteryl ester transfer protein-Tg mice. Transcriptome and Western blot analysis demonstrated up-regulation of hepatic LDLr and apoE expression in LCAT-KO mice. Despite decreased HDL, aortic atherosclerosis was significantly reduced (-35% to -99%) in all mouse models with LCAT deficiency. Our studies indicate (i) that the plasma levels of apoB containing lipoproteins rather than HDL may determine the atherogenic risk of patients with hypoalphalipoproteinemia due to LCAT deficiency and (ii) a potential etiological role for lipoproteins X in the development of glomerulosclerosis in LCAT deficiency. The availability of LCAT-KO mice characterized by lipid, hematologic, and renal abnormalities similar to familial LCAT deficiency patients will permit future evaluation of LCAT gene transfer as a possible treatment for glomerulosclerosis in LCAT-deficient states.
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PMID:Analysis of glomerulosclerosis and atherosclerosis in lecithin cholesterol acyltransferase-deficient mice. 1127 14

A 67-year-old female was admitted to our hospital with eruption and cervical lymphadenopathy which occurred one week after pneumococcal vaccination. Polyclonal hyperimmunoglobulinemia (IgG 6,620 mg/dl) and mild plasma cell proliferation (6.4%) in a bone marrow specimen were found, but a lymph node aspiration biopsy showed no specific findings. Normochromic and normocytic anemia with a positive direct Coombs test were also confirmed. Short-term intensive steroid therapy was given, but the systemic eruption and lymphadenopathy continued. About 4 months after vaccination, she suffered from edema in her face and legs and visual disturbance. When massive proteinuria (10.4 g/day) was found, she was admitted to our ward. A renal biopsy specimen showed a minor glomerular abnormality with mild interstitial plasmacytic infiltration. An abdominal CT scan showed hepatosplenomegaly and para-aortic lymphadenopathy. Uveitis was also found by ophthalmoscopy. These abnormalities completely disappeared after intensive steroid therapy including pulse therapy. On the basis of her clinical course and laboratory findings, it was suggested that minimal change nephrotic syndrome might be induced after vaccination, possibly due to hypersensitivity syndrome.
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PMID:Minimal change nephrotic syndrome, lymphadenopathy and hyperimmunoglobulinemia after immunization with a pneumococcal vaccine. 1214 10

The ICR-derived glomerulonephritis (ICGN) mouse, a new inbred mouse strain with a hereditary nephrotic syndrome, is considered to be a good model of human idiopathic nephrotic syndrome and notably exhibits proteinuria and hypoproteinemia from the neonatal stage. In chronic renal disorder (CRD), anemia is a major subsequent symptom (renal anemia). The precise cause of renal anemia remains unclear, primarily owing to the lack of appropriate spontaneous animal models for CRD. To establish adequate animal models for anemia with CRD, we examined the hematological-biochemical properties and histopathological characteristics. With the deterioration of renal function, ICGN mice developed a normochromic and normocytic anemia, and exhibited normochromic and microcytic at the terminal stage. The expression of erythropoietin (EPO) mRNA both in the kidneys and liver and the EPO leak into the urine were observed in ICGN mice, indicating a disrupted metabolism of EPO in ICGN mice. In addition, a lack of iron induced by the hemolysis in the spleen and the leak of transferrin into urine as proteinuria aggravated the anemic condition. In conclusion, the ICGN mouse is a good model for anemia with CRD.
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PMID:Anemia with chronic renal disorder and disrupted metabolism of erythropoietin in ICR-derived glomerulonephritis (ICGN) mice. 1513 73

Pure red cell aplasia (PRCA) is a rare cause of anemia associated with SLE. We herein report a case presenting with SLE and PRCA. A 33-year-old woman, who had been suffering from photosensitivity, proteinuria, and pancytopenia, was diagnosed to have SLE. She showed normochromatic normocytic anemia. The serum level of haptoglobin was <10 mg/dl, and Direct Coombs' test was negative. Her reticulocyte count was 0.8%. Her clinical and laboratory features, except for anemia, had recovered in response to 50 mg/day of prednisolone. The serum level of haptoglobin had normalized, but the reticulocyte count remained low. The bone marrow findings revealed erythroid hypoplasia, and she was diagnosed to have PRCA complicated with SLE. No viral DNA of human parvovirus B19 in her bone marrow was detected. The anemia gradually improved following the further use of 50 mg/day prednisolone. In order to disclose the mechanism of PRCA in this patient, we examined the effects of her peripheral T lymphocytes on erythrogenesis, using erythroid colony-forming cells (ECFC) in her peripheral blood. When we co-cultured peripheral T cells and ECFC, her T cells inhibited erythroid colony formation in a dose dependent manner. Several reports have shown the presence of inhibitory factors in SLE patients' serum such as antibodies against erythroid progenitors or erythropoietin, while other reports have shown abnormal T cells that inhibit the growth of erythroid progenitors. Our study suggests that these inhibitory T cells may therefore have played an important role in the pathogenesis of this patient.
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PMID:[A case of systemic lupus erythematosus accompanied with pure red cell aplasia]. 1681 63

We describe the clinical case of 80 years, caucasian woman, with personal history of osteoporosis and chronic normochromic normocytic anemia (NN). She had a three month history of myalgias of the girdle, stiffness in the morning, exceeding 1 hour, associated with inflammatory arthralgia of the small joints of hands and feet. Complementary exams showed normocytic normochromic anemia with Hg 9.8 g/dL; ESR 44 mm/h; CRP 7 mg/dL. Given the profile suggestive of Polymyalgia Rheumatica started prednisolone 10 mg/day with favorable clinical response. Four months after treatment she started paresthesias of right hand and foot, polaquiuria, petequial lesions in lower limbs and inability to walk; there was worsening of anemia and elevation of the biological parameters of inflammation, beginning of renal insufficiency with creatinine clearance 22 ml/min, proteinuria and eritrocituria. Renal biopsy was compatible with Wegener's granulomatosis/microscopic poliangeite. Vasculitis is a rare disease of the elderly and its clinical presentation is varied. The arteritis of giant cells and Polymyalgia Rheumatica are more common in the elderly. It is not often Polymyalgia-like presentation in cases of Wegener's granulomatosis/microscopic polyangitis.
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PMID:[Myalgia of the girdle in the elderly: an uncommon etiology]. 2050 32

Familial lecithin-cholesterol acyltransferase (LCAT) deficiency (FLD) is a rare genetic disease characterized by corneal opacities, normocytic anemia, dyslipidemia, and proteinuria progressing to chronic renal failure. In all FLD cases, a mutation has been found in the coding sequence of the LCAT gene. FLD is clinically distinguished from an acquired form of LCAT deficiency by the presence of corneal opacities. Here we describe a 36-year-old woman presenting with clinical, pathological, and laboratory data compatible with FLD. Her mother and elder sister had corneal opacities. However, genetic analysis revealed there were no mutations in the LCAT coding sequences and no alterations in LCAT mRNA expression. Furthermore, we were unable to find any underlying conditions that may lead to LCAT deficiency. The present case therefore demonstrates that LCAT deficiency may be caused by factors other than mutations in the coding sequence and we suggest that a translational or posttranslational mechanism may be involved.
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PMID:Lecithin-cholesterol acyltransferase (LCAT) deficiency without mutations in the coding sequence: a case report and literature review. 2195 68