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)

Adjustment of the mineralocorticoid activity under substitution therapy is of primary importance in Addison's disease. We report the clinical and biological conditions of 2 patients with Addison's disease who developed nephrotic proteinuria during their deficient mineralocorticoid state. Renal biopsy was performed and the specimens processed using conventional histochemistry, Congo red staining, and indirect immunofluorescence. The renal biopsy specimens showed focal segmental glomerular sclerosis and nodular deposits of IgM and C3. Negative for Congo red staining. Serum complement, circulating immune complexes, and anti-DNA and hepatitis B and C and human immunodeficiency virus antibodies were all normal or negative. Absence of vesicoureteral reflux was assessed by X-ray studies. Our observations suggest that deficiency in mineralocorticoid substitution therapy inducing a status of hyperreninemia could play a role in the development of focal segmental glomerulosclerosis in patients with Addison's disease.
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PMID:Focal segmental glomerular sclerosis in two patients with Addison's disease: any more than fortuitous development of glomerular disease? 1216 75

Human leucocyte antigen (HLA) associations have been reported in children with hepatitis B virus (HBV) associated membranous nephropathy (MN). In a previous study, we found an association with HLA DQB1*0603 in black children with HBVMN. To determine whether HLA DQB1*0603 predisposes to HBV carriage and development of abnormal proteinuria, we studied 70 family members of 14 children with HBVMN positive for HLA DQB1*0603. HBV was determined using third generation ELISA, slot-blot hybridisation, and nested polymerase chain reaction. HLA class I antigens were determined using a two-staged lymphocytotoxic test whereas class II antigen typing was done using sequence-specific primers. Abnormal proteinuria was defined by a protein/creatinine ratio > or =0.2. Associations of HLA DQB1*0603 with HBV carriage and abnormal proteinuria were determined using the mean probability ratio (LOD scores). Forty-seven (67%) family members were positive for HBV infection. Nineteen (27%) had abnormal range proteinuria. LOD scores in the study subjects with DQB1*0603 who were HBV negative versus those with DQB1*0603 who were HBV positive was not significant (anti-log sum =2.0559 and average 0.23). When a similar calculation was made for abnormal proteinuria, there were no significant findings (anti-log sum =3.8587 and average 0.43). This lack of association of HLA DQB1*0603 with either HBV carriage or abnormal proteinuria in family members suggests that additional factors may play a role in predisposing children to chronic HBV carriage and the development of MN. We therefore conclude that the main effect of HLA DQB1*0603 that distinguishes family members from HBVMN is the degree of proteinuria, which is a reflection of the severity of glomerular basement membrane damage in the latter.
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PMID:HLA associations with HBV carriage and proteinuria. 1221 25

Hepatitis B virus (HBV)-associated glomerulonephritides have been increasingly reported, and the association between HBV and glomerulopathy is striking, especially in children. In this study, we investigated clinical and immunohistological features of HBV-associated glomerulonephritis in 14 children aged from 2.5 to 16 years (mean 10 years). The nephrotic syndrome was present in 9 (64%) and the nephritic syndrome in 8 children (57%). Five children had both nephrotic and nephritic syndrome together (35%). Renal insufficiency was determined in 4 of 14 patients (28%). Surface antigen (HBsAg) was present in all, with no history of clinically apparent hepatitis. Investigation of all renal tissue samples with light and immunofluorescence microscopy confirmed the diagnosis of membranous glomerulonephritis (MGN) in 6, membranoproliferative glomerulonephritis (MPGN) in 7, and IgA nephropathy (IgAN) in 1 child. Renal tissue samples were studied by the immunoperoxidase method for HBsAg in all cases; only in 4 children was HBsAg detected in the glomeruli. Examination of liver tissue samples was available in 4 cases, revealing chronic hepatitis in all, with additional development of cirrhosis in 1 and the presence of HBsAg in hepatocytes in all. Of the patients, 8 received corticosteroid treatment; 1 of them achieved a complete remission, while 4 had a partial remission with persistent proteinuria and hematuria. Four patients who received no treatment had a spontaneous remission within 5 months to 10 years following the onset of the renal disease. Two patients died of renal failure, while 1 died of intercurrent sepsis. The patient with IgAN received interferon-alpha 2a and lamuvidine, which resulted in a remission and a marked decrease in HBV DNA titer. The remaining 2 were lost to follow-up. Although MGN has been reported as the nephropathy most commonly associated with HBsAg antigenemia in adults, our study revealed that MPGN could occur in children as well as MGN, without any clinical or historical evidence of hepatitis. The present study provides further evidence for a causal relationship between HBV hepatitis and HBs antigenemia-related glomerulonephritides in the pediatric age group. It also indicates the prognosis (71%) of the associated nephropathies with or without treatment is quite favorable in childhood.
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PMID:Hepatitis-B virus associated nephropathies: a clinicopathological study in 14 children. 1248 86

Proteinuria is occasionally detected on "routine" examination (not done for a suspected renal or urinary tract problem) and often presents a diagnostic problem. Even mild proteinuria is abnormal and needs an explanation. Its degree and persistence should be ascertained and associated hematuria looked for. Nonpathological (including orthostatic) proteinuria and renal tubular disorders should be excluded. Persistent proteinuria is mostly due to a primary or secondary (eg hepatitis B) glomerular condition, which requires expert evaluation of renal biopsy. Aggressive therapy may be needed in some cases. The intensity of proteinuria can be decreased with ACE inhibitors. Long-term observation is essential.
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PMID:Isolated asymptomatic proteinuria. 1255 59

A 6 year old boy presenting with a five month history of fever, lethargy, and anorexia, was found to have hepatitis B associated membranous glomerulonephropathy and nephrotic syndrome. After two months treatment with oral lamivudine, his proteinuria cleared and serum albumin and aminotransferases normalised, associated with disappearance of hepatitis B e antigen (HBeAg) and appearance of anti-HBeAg antibodies. After 12 months, without side effects, lamivudine was discontinued. He remains well 11 months off treatment.
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PMID:HBV associated nephrotic syndrome: resolution with oral lamivudine. 1271 31

From January 1985 to July 2000, a retrospective study of 53 patients in Taiwan was performed in order to evaluate the underlying diseases causing heavy proteinuria and the clinical outcome in children under 2 years of age (33 boys and 20 girls). Renal biopsy or autopsy was performed in 26 of the children. Renal pathology revealed 2 patients with congenital nephrosis (CNS) (7.7%), 4 with diffuse mesangial sclerosis (DMS) (15.4%), 4 with minimal change nephrotic syndrome (MCNS) (15.4%), 5 with focal segmental glomerulosclerosis (FSGS) (19.2%), 9 with IgM nephropathy in (34.6%), and 2 with hepatitis B virus-associated membranous glomerulonephritis (7.7%). Based on available histology and family history of heavy proteinuria progressing to end-stage renal disease (ESRD), patients were divided into two groups. Group I comprised 10 patients, including CNS (2 cases), DMS (4 cases), and 4 children with a familial history of heavy proteinuria progressing to ESRD. All patients in group I were initially steroid resistant. After methylprednisolone pulse therapy plus cyclosporin A treatment, no patients with CNS or DMS responded, but the other 4 patients experienced a remission. Group II comprised 43 patients; 19 patients (44.2%) were initially steroid resistant. Of these steroid-resistant patients, all experienced remission after methylprednisolone pulse therapy plus cyclosporin A, except 3 children with FSGS. One experienced a thromboembolic event during his clinical course. In conclusion, steroid-resistant nephrotic syndrome (NS) was more common than steroid-sensitive NS in Chinese patients under 2 years of age. Patients with CNS, DMS, or a family history of heavy proteinuria progressing to ESRD had a poor prognosis. Methylprednisolone pulse therapy plus cyclosporin A treatment achieved remission in some children who were initially steroid resistant. This study indicates that children with conditions associated with poor steroid responsiveness (e.g., CNS, DMS) do not respond to immunosuppressive therapy, but other children under 2 years of age, including those with a family history of progression to ESRD, may benefit from aggressive immunosuppressive therapy.
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PMID:Long-term outcome of heavy proteinuria in patients under 2 years of age. 1289 78

The authors report the first case of immunotactoid glomerulopathy (ITG) in a human immunodeficiency virus (HIV)-positive, hepatitis B- and C-negative African-American man who presented with hematuria and proteinuria. His initial presentation was compatible with HIV associated nephropathy, but on renal biopsy he was found to have ITG. He has been treated with highly active antiretroviral therapy and an angiotensin-converting enzyme inhibitor, but his proteinuria has not responded after 4 months of treatment. This case emphasizes the diverse glomerular lesions seen in HIV-positive patients and supports the use of renal biopsy to establish a diagnosis.
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PMID:Immunotactoid glomerulopathy in an HIV-positive African-American man. 1465 25

A direct causal association between hepatitis B virus (HBV) infection and the development of nephropathy remains controversial. Epidemiological studies have shown that chronic carriage of HBV in some individuals (particularly children) leads to the development of nephrotic syndrome with a strong male predominance, the commonest histological type being membranous nephropathy (MN). Spontaneous clearance of HBV antigens (particularly the HBeAg) leads to abrogation of proteinuria. The isolation of immune complexes in the kidney suggests that the pathogenesis of the disease may have an immune-complex basis. Recent studies showing expression of HBV viral antigens in kidney tissue suggest direct viral-induced pathological alterations and chronic immunologic injury. Biosocial studies have detected no correlation between HBV carriage and proteinuria using both quantitative and qualitative urinary protein analysis. Genetic studies of HLA class I and II genes showed a predisposition to MN but no similar correlation in those with milder degrees of proteinuria. These findings suggest that milder proteinuria is unrelated to HBV carriage or genetic factors but the development of nephropathy, particularly MN, in patients with chronic HBV carriage (HBsAg and/or HBV DNA positive) is based on an interaction of virus and host factors. Although the natural history of the disease tends to remission with preservation of renal function, there is considerable morbidity and a small but significant mortality. Use of naturally occurring cytokines (such as interferon-alpha2b) and other candidate therapies accelerates clearance of the virus and proteinuria. The most effective tool in reducing the incidence of the disease is the use of HBV vaccines.
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PMID:Hepatitis B virus-associated nephropathy. 1498 43

Chronic renal failure represents a major problem of public health. Incidence for patients arrived at the terminal stage of the disease is in France 126.4/million inhabitants and the cost of medical care reaches 2 % of the expenses of the National Health Insurance. The progression of the disease is divided into 5 stages that are defined by the level of creatinine clearance from the stage of renal diseases with a normal renal function (clearance>90 ml/min) to the terminal stage (clearance <15 ml/min). Prevalence of patients at this ultimate stage is around 50,000. Prevalence for the totality of patients with a renal disease is evaluated between 2 and 3 millions. Renal diseases must be screened because they are silent and because an early pre-dialysis nephrological care allows renal replacement therapy to be delayed and the number of cardiovascular accidents to be diminished. Screening must be performed in the high-risk populations, essentially patients with diabetes, hypertension, coronary ischemia, renal tract diseases and all subjects treated with drugs toxic for the kidneys. Screening in the total population seems inadequate because of a high cost to benefit ratio. Screening is based on testing for the presence of proteinuria, quantifying the number of formed elements and plasma creatinine determination, the latter allowing, together with age and weight, glomerular filtration rate to be evaluated according to Cockcroft's formula. Prevention of renal diseases in the whole population necessitates the same life style as that recommended for prevention of cardiac and metabolic diseases. In the high-risk populations, one must control glycemia, blood pressure and cholesterol plasma level. In patients that have been already screened, renal function decay has to be slowed down by blocking the renin angiotensin system with converting enzyme inhibitors, controlling plasma cholesterol with statins and diminishing dietary proteins. In the light of these various data, the National Academy of medicine recommends: 1 - in the field of public health, to extend to the whole country the registries containing data on patients with terminal chronic renal failure, to support the creation of medical networks for the screening of renal diseases, to vaccine the patients against hepatitis B, flue and pneumococcal infections and to verify whether a low birth weight is associated with a greater risk of renal diseases in adulthood; 2 - in the field of teaching and research, to stop the decrease in the number of nephrologists, to promote research in genetics, to evaluate the efficacy of antifibrosis drugs and the possible renal toxicity of all new drugs.
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PMID:[Prevention and screening of chronic renal failure]. 1591 71

We present a case of chronic hepatitis B with membranous nephropathy, that was improved by lamivudine treatment. A 37-year-old man was admitted to our hospital for the evaluation of proteinuria. He was diagnosed as having chronic glomerulonephritis associated with chronic hepatitis B. Histopathological findings of the renal biopsy specimen indicated membranous nephropathy. He suffered from nephrotic syndrome associated with leg edema, which was parallel to the exacerbation of hepatitis. Lamivudine was started for the treatment of hepatitis, which caused the disappearance of serum hepatitis B virus DNA and the normalization of ALT level in 4 weeks. Additionally, proteinuria disappeared 120 weeks after the treatment was started. Lamivudine treatment may remit HBV-associated nephropathy.
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PMID:Successful treatment of hepatitis B virus-associated membranous nephropathy with lamivudine. 1642 43


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