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 whether the low serum C-reactive protein (S-CRP) level in patients with inflammatory arthritis and proteinuria was due to the loss of CRP into urine. In 19 patients with secondary amyloidosis (14 with rheumatoid arthritis and five with juvenile chronic arthritis), S-CRP was measured with both immunoturbidimetric and radioimmunoassays. The concentration of urinary CRP was measured with a double-antibody radioimmunoassay. One patient with the most extensive proteinuria (12 g/24 h) excreted CRP at 14 mg/24 h, while in 18 of 19 patients only negligible, if any, amounts of CRP were found in 24-h urine samples. Proteinuria of < 8 g/24 h did not reduce the S-CRP level. Proteinuria exceeding this level may result in increased excretion of CRP into urine and consequently may result in a reduced S-CRP level.
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PMID:Serum C-reactive protein is rarely lost into urine in patients with secondary amyloidosis and proteinuria. 969 59

Monoclonal gammapathies are detected because of clinical symptoms and biological tests confirm their presence. Wishing to investigate these diseases, we carried out a series of biochemical tests on 14 patients from October 1995 to July 1996: protein, cryoglobulin, electrophoresis of proteins, proteinuria of BENCE JONES, C-reactive protein, weight measuring of immunoglobulins (Ig), immunofixation of Ig, creatinine and calcium. The results we obtained confirmed the presence of 14 cases of myeloma with: -9 IgG myelomas with 6 kappa light chains and 3 lambda light chains -4 IgA myelomas with 2 kappa light chains and 2 lambda light chains -1 IgG kappa, Ig lambda biclonal gammapathy united to a cryoglobulin of class I. We observed a predominance of the IgG over the others Ig and the kappa over the alpha light chains. The proteinuria of BENCE JONES was present among 3 patients, hypercalcemia among 4 patients and hypercreatininemia in 1 patient with chronic renal failure.
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PMID:[Laboratory diagnosis of monoclonal gammopathies. Prospective study of 14 cases in Dakar, Senegal]. 977 1

Patients with anti-myeloperoxidase (MPO)-associated necrotizing crescentic glomerulonephritis (NCGN) may develop chronic renal failure (CRF) leading to end-stage renal disease despite an initially favorable response to treatment. The aim of this study was to determine the prognostic value of clinical, laboratory, and histopathologic features at the time of presentation and during follow-up for the development of CRF in 21 consecutive anti-MPO-positive patients with NCGN. Renal function did not recover in two of five patients who were dialysis-dependent at presentation. The remaining 19 patients all went into remission and were off dialysis at 3 mo after diagnosis. At long-term follow-up, nine of these patients had stable renal function and did not relapse (group A), five patients developed CRF without signs of relapse (group B), and five patients relapsed (group C). At diagnosis, serum creatinine, C-reactive protein, and anti-MPO levels did not differ between groups A, B, and C. Microscopic erythrocyturia resolved in all patients within 4 mo of treatment. BP at presentation and during follow-up did not differ between groups A, B, and C. Proteinuria at diagnosis and in the first 6 mo after diagnosis was higher in patients who developed CRF than in patients with a stable renal function. Anti-MPO levels at 3 mo had decreased compared with anti-MPO levels at diagnosis in groups A and C, whereas anti-MPO levels did not fall significantly in patients who developed CRF. The predictive value of a renal biopsy at diagnosis on long-term renal outcome was limited. In conclusion, a higher degree of proteinuria at diagnosis and during follow-up as well as persistently elevated anti-MPO levels after induction of remission are associated with the development of CRF and are predictive of poor renal outcome in anti-MPO-associated NCGN.
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PMID:Determinants of renal outcome in anti-myeloperoxidase-associated necrotizing crescentic glomerulonephritis. 977 93

A 51-year-old woman, who had both aortitis syndrome (Takayasu arteritis) and IgA nephropathy, presented with hypertension, fever, a high erythrocyte sedimentation rate, high C-reactive protein and serum IgG levels, proteinuria, and renal dysfunction. Renal arteriography showed stenosis and poststenotic dilatation at the origin of the right renal artery, as well as tortuosity of the left renal artery branches and marked atrophy of the left kidney. Renal biopsy showed IgA nephropathy with deposits of IgA, C3, and fibrinogen in the glomeruli and arteriolosclerosis. The present patient had human leukocyte antigen (HLA)-B 52, which is reported to be related to the aortitis syndrome, as well as HLA-DR 4, which is possibly related to IgA nephropathy, suggesting that HLA status may be involved in the pathogenesis of both diseases.
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PMID:A case of aortitis syndrome and IgA nephropathy: possible role of human leukocyte antigens in both diseases. 1021 60

High lipoprotein(a) (Lp(a)) serum concentrations and the underlying apolipoprotein(a) (apo(a)) phenotypes are risk factors for cardiovascular disease in the general population as well as in patients with renal disease. Lp(a) concentrations are markedly elevated in patients with end-stage renal disease. However, nothing is known about the changes of Lp(a) depending on apo(a) size polymorphism in the earliest stages of renal impairment. In this study, GFR was measured by iohexol technique in 227 non-nephrotic patients with different degrees of renal impairment and was then correlated with Lp(a) serum concentrations stratified according to low (LMW) and high (HMW) molecular weight apo(a) phenotypes. Lp(a) increased significantly with decreasing GFR. Such an increase was dependent on apo(a) phenotype. Only renal patients with HMW apo(a) phenotypes expressed higher median Lp(a) concentrations, i.e., 6.2 mg/dl at GFR >90 ml/min per 1.73 m2, 14.2 at GFR 45 to 90 ml/min per 1.73 m2, and 18.0 mg/dl at GFR <45 ml/min per 1.73 m2. These values were markedly different when compared with apo(a) phenotype-matched control subjects who had a median level of 4.4 mg/dl (ANOVA, linear relationship, P < 0.001). In contrast, no significant differences were observed at different stages of renal function in patients with LMW apo(a) phenotypes when compared with phenotype-matched control subjects. The elevation of Lp(a) was independent of the type of primary renal disease and was not related to the concentration of C-reactive protein. Multiple linear regression analysis found that the apo(a) phenotype and GFR were significantly associated with Lp(a) levels. Non-nephrotic-range proteinuria modified the association between GFR and Lp(a) levels. In summary, an increase of Lp(a) concentrations, compared with apo(a) phenotype-matched control subjects, is seen in non-nephrotic patients with primary renal disease even in the earliest stage when GFR is not yet subnormal. This change is found only in subjects with HMW apo(a) phenotypes, however.
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PMID:Lipoprotein(a) serum concentrations and apolipoprotein(a) phenotypes in mild and moderate renal failure. 1061 46

A 75-year-old woman was admitted to our hospital because of high fever and appetite loss. A chest roentgenogram and computed tomographic scans revealed pleural effusion without obvious infitrative or interstitial shadows in both lung fields. Laboratory data showed microhematuria, proteinuria, and telescoped sediment with a moderate increase in C-reactive protein, suggestive of acute glomerulonephritis. Because infectious pleuritis, was initially suspected, the patient was treated with antibiotics. However, her general condition deteriorated, and the right pleural effusion increased. Levels of myeloperoxidase-specific anti-neutrophil cytoplasmic antibody (MPO-ANCA) in serum and pleural effusion were markedly elevated, yielding a conclusive diagnosis of MPO-ANCA-related vasculitis, especially microscopic polyangitis (MPA). The Patient was immediately treated treated with prednisolone, cyclophosphamide, and plasma exchange. Several weeks later, her general condition dramatically improved, and the level of MPO-ANCA in serum markedly decreased. In addition, the pleural effusion completely disappeared. Unfortunately, the patient eventually died of opportunistic infections (MRSA-pneumonia and Aspergillus-pneumonia) 6 months after admission. This was a unique case of MPA associated with pleuritis without interstitial pneumonia or alveolar hemorrhage.
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PMID:[Microscopic polyangitis with pleuritis as the only pulmonary complication]. 1084 5

A fifteen-year-old boy was admitted to our hospital because of lower abdominal pain, watery diarrhea and mucobloody stool. Two years before admission, he was diagnosed to have Still's disease presenting with polyarthritis, sore throat, remittent fever and typical skin rash. He had been treated with non-steroidal anti-inflammatory agents, oral prednisolone and low-dose methotrexate. Although he was almost free of symptoms during the next two years, serum C-reactive protein (CRP) levels continued to be elevated moderately. He began to complain of lower abdominal pain and loose stool in May 1997 and came down with mucous-bloody diarrhea in June. Laboratory data on admission showed an elevated level of serum CRP (13.9 mg/dl). The biopsy of the stomach, ileum, sigmoid colon and rectum revealed the deposition of amyloid protein of AA type, which confirmed the diagnosis of secondary amyloidosis. The dose of prednisolone was increased and dimethyl sulfoxide per os or rectum was instituted, which improved his gastro-intestinal symptoms to some extent. However, fever, arthritis and diarrhea recurred along with tapered prednisolone dosage. In addition to gastro-intestinal symptoms, arrhythmia and proteinuria appeared. These symptoms were considered to reflect general deposition of amyloid in his body. He is now on immunosuppressive agent and high-dose prednisolone. Several studies report the higher frequency of gamma-allele of SAA 1 gene in the cases of rheumatoid arthritis with AA-amyloidosis than in those without. In the patient presented here, molecular biological analysis revealed that his SAA 1 gene was composed of beta- and gamma-allele. The presence of gamma-allele in his SAA 1 gene might be one of the factors that predisposed him for generalized deposition of amyloid protein in such a short period of time.
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PMID:[Rapidly progressed secondary amyloidosis in a patient with Still's disease with gamma-allele in his SAA 1 gene]. 1092 Jun 89

The urinary loss of transferrin is sufficient to reduce plasma transferrin concentrations in the nephrotic syndrome. Hypotransferrinemia may lead to iron loss and microcytic anemia. The mechanism responsible for the hypotransferrinemia in the nephrotic syndrome is, however, unknown. In the present study, synthesis rate of transferrin was measured in vivo in nephrotic patients (n = 7) compared with control subjects (n = 6) using L-[1-(13)C]-valine. Plasma transferrin and iron concentration in the patients were significantly lower than in control subjects (transferrin, 1.39 +/- 0.08 versus 2.57 +/- 0.11 g/L, P < 0.0001; iron, 10.2 +/- 0.8 versus 21.1 +/- 4.5 micromol/L, P = 0.02). Furthermore, albuminuria correlated with transferrinuria (r(2) = 0.901, P = 0.001). The absolute synthesis rate of transferrin was increased in the patients (10.0 +/- 1.1 versus 7.4 +/- 0.7 mg/kg per d, P = 0.07), although this value failed to achieve significance. C-reactive protein, plasma iron, and proteinuria did not correlate with transferrin synthesis. In contrast, transferrin synthesis correlated with albumin synthesis (r(2) = 0.648, P = 0.03; n = 7). The present study indicates that increased transferrin synthesis occurs in nephrotic patients but is insufficient to compensate for urinary losses. Because, overall, no significant relationship was found between transferrin synthesis and either C-reactive protein or iron, it is unlikely that inflammation suppresses or that iron deficiency stimulates increased transferrin synthesis in these patients. The correlation between transferrin synthesis and albumin synthesis suggests that transferrin synthesis is a component of a general response in hepatic protein synthesis in the nephrotic syndrome. This suggests that a therapeutic approach to maximize plasma transferrin concentrations in nephrotic patients should be aimed primarily at reducing urinary protein excretion.
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PMID:Transferrin synthesis is increased in nephrotic patients insufficiently to replace urinary losses. 1131 61

The aim of this study was to examine the incidence of different renal lesions in rheumatoid arthritis (RA) and to determine their relationships with the type of previous drug therapy and with the specific features of immune disorders. Ninety four patients, 84 (89.9%) females and 10 (10.6%) males) with RA whose mean age was 45.2 +/- 11.9 years and duration of the disease 7.5 +/- 6.5 years were examined. Most of them had degrees 2 and 3 PA (62.7 and 24.4%, respectively). Systemic manifestations were encountered in 60 (63.8%) patients. Eighty one patients took nonsteroidal antiinflammatory drugs (NSAID) continuously: 18 patients for a year, 32 for 5 years, 14 for 6 to 10 years, and 17 for over 10 years. All the patients underwent clinical, laboratory, and instrumental study of partial functions of the kidney. Immunological study involved solid-phase immunoassay of IgA and IgM rheumatoid factor, von Willebrand factor antigens (WF:Ag), C-reactive protein. The serum concentrations were measured by the Mancini method. Changes in urinalysis and/or signs of decreased glomerular and tubular functions were found in 69 (73.%) patients, 25 (26.6%) had arterial hypertension. Tubular dysfunctions were more common [31 (32.9%) patients]. Signs of early renal failure were detected in 20 (21.2%) patients. There were no cases of acute renal failure. Amyloidosis, glomerulonephritis, pyelonephritis were diagnosed in 5 (5.3%), 16 (17%), and 13 (13.8%) patients, respectively. The above renal lesions were concurrent in some patients. Renal lesion correlated with the progression and severity of RA, the presence of systemic manifestations, and age. There was no relationship of both 5- and 10-year use of NSAID to the symptoms of renal disease. The use of these drugs for over 10 years was concurrent with the signs of chronic renal failure and arterial hypertension. Analyzing immunological disorders showed an association of increased erythrocytic sedimentation rates and WF:Ag with amyloidosis, that of higher IgA concentrations with proteinuria and tubular dysfunctions. It is concluded that renal lesion is common in RA, there is a predominance of tubular interstitial changes. In rare cases nephropathy is characterized by a benign course and fails to result in uremia. The symptoms of renal diseases are largely associated with RA progression and severity and the patients' age. Prolonged continuous use of NSAID may contribute to the development of renal failure. Different immune mechanisms are involved in the pathogenesis of glomerular and tubular nephropathy in RA.
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PMID:[Clinico-immunological aspects of renal lesions in rheumatoid arthritis]. 1152 52

Hantaviruses cause two severe human diseases: hemorrhagic fever with renal syndrome (HFRS) and hantavirus pulmonary syndrome (HPS). Approximately 200,000 cases are reported annually, and there is to date no specific treatment available. A major obstacle in studying the medical aspects of HFRS and HPS has been the lack of an adequate animal model. Here we show that infection of cynomolgus macaques by wild-type Puumala hantavirus resulted in typical signs of HFRS including lethargy, anorexia, proteinuria, and/or hematuria, in addition to cytokine (interleukin 6 [IL-6], IL-10, and tumor necrosis factor alpha), C-reactive protein, creatinine, and nitric oxide responses. Viral RNA was detected in plasma from days 3 to 7 postinoculation until days 24 to 28 postinoculation, infectious virus was recovered, and the virus-specific immune responses (immunoglobulin M [IgM], IgG, and neutralizing antibodies) mimicked those seen in humans. The results indicated that the monkey model will provide a valuable tool for studies of pathogenesis, candidate vaccines, and antivirals for hantavirus disease.
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PMID:Wild-type Puumala hantavirus infection induces cytokines, C-reactive protein, creatinine, and nitric oxide in cynomolgus macaques. 1173 12


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