Cases reported "Proteinuria"

Filter by keywords:

Retrieving documents. Please wait...

1/582. alpha-Interferon therapy for HBV-related glomerulonephritis.

    We report a case of a patient with hepatitis b virus (HBV)-related membranous glomerulonephritis (MGN) who showed improvement after interferon-alpha (IFN-alpha) therapy. A 35-year-old man with nephrotic syndrome and HBV antigens received a 24-week course of IFN-alpha. At the end of therapy there was an elevation in the level of plasma aminotransferase and an increase in proteinuria, which were followed by antigen/antibody seroconversion. This "flare-up" before seroconversion suggests an increase in disease activity in the liver and kidney, demonstrating in vivo HBV involvement in MGN. ( info)

2/582. Possible induction of renal dysfunction in patients with lecithin:cholesterol acyltransferase deficiency by oxidized phosphatidylcholine in glomeruli.

    To clarify the causes of renal dysfunction in familial lecithin:cholesterol acyltransferase (LCAT) deficiency, kidney samples from 4 patients with LCAT deficiency (3 homozygotes and 1 heterozygote) were examined immunohistochemically. All of the patients exhibited corneal opacities, anemia, renal dysfunction, deficiencies in plasma high density lipoprotein and LCAT activity and mass, and an increase in the ratio of plasma unesterified cholesterol to esterified cholesterol. Renal lesions began with the deposition of lipidlike structures in the glomerular basement membrane, and these structures accumulated in the mesangium and capillary subendothelium. By electron microscopy, 2 types of distinctive structure were found in glomerular lesions: vacuole structures and cross-striated, membranelike structures. The plasma oxidized phosphatidylcholine (oxPC) -modified low density lipoprotein (LDL) levels in LCAT-deficient subjects were significantly (P<0.01) higher than those in controls (1.30 /-0.82 versus 0.42 /-0.32 ng/5 microg LDL, respectively), and a significant (P<0.01) difference was observed even after adjustment for confounding factors by an analysis of covariance. The patient with the highest plasma oxPC-modified LDL had the most membranelike structures in the glomeruli and showed the greatest renal deterioration from a young age. In glomerular lesions, although there was an abundance of apoB and apoE, oil red O-positive lipids, macrophages, apoA1, and malondialdehyde were scarce. OxPC was found extracellularly in glomerular lesions, and although its distribution differed from that of apolipoproteins, it was quite similar to that of phospholipids. In conclusion, these results indicate that oxPC in plasma and glomeruli is distinctive for patients with LCAT deficiency. Therefore, oxPC may be a factor in the deterioration of kidneys in patients with familial LCAT deficiency. ( info)

3/582. "Idiopathic" Bence-Jones proteinuria.

    During a prospective screening for proteinuria in diabetic patients, isolated Bence-Jones proteinuria was detected in 2 cases. The first patient, a 52-year-old black female, was seen for evaluation of a slow but progressive weight loss which was attributed to poor adjustment of insulin therapy. The patient gained weight after an increase of the daily insulin administration. She had plasmocytosis in a bone marrow aspirate, but no other evidence of myelomatosis. The second patient, a 59-year-old black male who was seen for routine evaluation of his diabetes, had no clinical or laboratory evidence of myelomatosis. Although precise definition of these cases as "benign" or "idiopathic" Bence-Jones proteinuria is impossible without prolonged follow-up, at the time of presentation they appeared to fit this classification. This observation is one further example that isolated Bence-Jones proteinuria may be seen without any evidence of malignant B-cell dyscrasia. ( info)

4/582. Chronic granulocytic leukemia, neutrophilic type, with paraproteinemia (IgA type K).

    A patient with chronic granulocytic leukemia, neutrophilic type, was followed for 28 months. A paraproteinemia, IgA type K, and Bence Jones proteinuria (K) appeared without prior chemotherapy with alkylating agents. ( info)

5/582. Effect of camostat mesilate on urinary protein excretion in three patients with advanced diabetic nephropathy.

    Effective treatment has not yet been established for patients with persistent proteinuria and hypoproteinemia related to advanced diabetic nephropathy. We report three patients with diabetic nephropathy presented with the nephrotic syndrome who showed a marked decrease in proteinuria following the administration of camostat mesilate, a protease inhibitor. Each patient was resistant to treatment with an angiotensin-converting enzyme (ACE) inhibitor and a platelet-aggregation inhibitor. Camostat mesilate, 600 mg/day, orally, caused a marked decrease in urinary protein excretion after the 7th consecutive day of drug administration. There were no serious adverse effects. Its mechanism of action in this respect is not known. Camostat mesilate thus merits clinical trials in the treatment of nephrotic syndrome related to diabetic nephropathy. ( info)

6/582. Imerslund-Grasbeck syndrome in an African patient.

    Imerslund-Grasbeck syndrome (IGS) is a rare cause of megaloblastic anaemia in young children. We wish to report the first case described from africa. The diagnosis of IGS was made on the findings of a low vitamin B12 level, mild proteinuria, and a vitamin B12 absorption test unaffected by the intrinsic factor. The patient responded well to treatment with intramuscular vitamin B12. ( info)

7/582. Discordant evolution of asymptomatic proteinuria in identical twins.

    We describe a pair of 17-year-old identical twin brothers with asymptomatic proteinuria, one of whom showed focal segmental glomerulosclerosis (FSGS) while the other showed immunoglobulin m (IgM) nephropathy. For each twin, audiological examination was normal. There was no family history of renal failure, deafness, or hematuria. HLA typing revealed an identical phenotype consisting of A25, A33, B44, B54, Cw1, Cw7, DR7 and DRB1. There is still controversy about whether minimal change disease, IgM nephropathy, and FSGS are discrete entities or different aspects of the same disease. The coexistence of IgM nephropathy and FSGS in identical twins suggests that the same genetic factors may be involved in the development of both diseases. However, although the brothers are identical twins, they had different eating habits and body weight. The twin who preferred to eat a protein-rich diet and who was heavier developed early proteinuria and manifested FSGS on renal biopsy. The discordant evolution of asymptomatic proteinuria in identical twins may provide a clue for the existence of environmental factors on the progression from IgM nephropathy to FSGS. Therefore, this report provides indirect support for the hypothesis that IgM nephropathy and FSGS represent different aspects in the spectrum of a single disease. ( info)

8/582. nephrotic syndrome at 5 months: no definitive treatment or complications for 12 years.

    We describe a patient who developed nephrotic syndrome at 5 months, with extensive glomerular and tubular damage on biopsy. The patient was treated with diuretics and was asymptomatic for a decade despite unremitting proteinuria. A repeat biopsy at 13 years of age showed remarkable healing with histopathological features consistent with "minimal change" nephrotic syndrome. This patient illustrates a favorable clinical outcome, without specific treatment, of nephrotic syndrome of long duration. ( info)

9/582. gold nephropathy in juvenile rheumatoid arthritis.

    A 2-year-old girl was treated with gold salts for juvenile rheumatoid arthritis. Treatment had to be discontinued when persistent proteinuria was detected. As this case report indicates, close monitoring of the urine is mandatory during treatment with gold salts to detect early signs of toxicity: hematuria followed by casts and then proteinuria as therapy is continued. Histologic examination with electron microscopy will help to differentiate the different forms of gold toxicity. When the findings are consistent with gold-induced renal involvement, therapy should be discontinued. The gold nephropathy usually resolves in time, with no permanent renal damage. ( info)

10/582. Crossroads of the effects of cyclophosphamide pulse therapy for lupus nephritis--experience of 11 cases.

    In this study time for initial assessment of monthly intravenous cyclophosphamide (CP) pulse therapy is discussed for a better outcome with less complications. Eleven patients with lupus nephritis (LN) resistant to conventional therapy (serum creatinine level < or = 2.7 mg/dl) were given 500 mg/m2 of CP 7-9 times with an interval of one month. Urinary protein (Up) decreased in all patients after 3 courses of CP pulse therapy and kept similar levels thereafter. In one group of patients (n = 7), Up decreased to < 2 g/day after 3 courses, while in the other group (n = 4), it did not decrease to < 4 g/day. creatinine clearance increased by 0-100% in the former group, while it decreased by 5-20% in the latter group after 6-9 courses. Renal function of the patients with insufficient response after 3 courses tended to show no further improvement or worsened thereafter, although Up decreased during CP pulse therapy. A relatively small dose of CP (500 mg/m2) pulse therapy was useful in most LN patients regardless of the renal histology and it was thought important to assess its effects after 3 courses for a prediction of the clinical course. Modification of the protocol at that time might be necessary in regard to dose or interval of CP administration especially for patients with insufficient outcome. ( info)
| Next ->

Leave a message about 'Proteinuria'

We do not evaluate or guarantee the accuracy of any content in this site. Click here for the full disclaimer.