Cases reported "albuminuria"

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1/37. Treatment of protein-losing gastropathy with atropine.

    Protein loss from the gastric mucosa with hypertrophic gastric folds and hypoalbuminemia has been associated with low, normal and elevated gastric acid output. A case of protein-losing gastropathy with slightly elevated gastric acid output is described. Associated findings were hypertrophic gastric folds, hypoalbuminemia, hyperlipidemia, lymphadenopathy, edema, ascites and venous thrombosis. Oral administration of atropine resulted in a cessation of gastrointestinal protein loss and correction of hypoalbuminemia. ( info)

2/37. Bisalbuminuria in an adult with bisalbuminemia and nephrotic syndrome.

    Bisalbuminemia (or alloalbuminemia) is a relatively rare hereditary or acquired condition characterized by the presence of two distinct albumin bands, or, less commonly, a single widened albumin band, after agarose gel electrophoresis of serum. Bisalbumins are caused by point- or chain-mutations that occur with a population frequency of 1:10,000 to 1:1000. Although no adverse clinical effects have been attributed to bisalbumins, some albumin variants have altered affinity for steroid hormones, thyroxine, or drugs. We report a case of bisalbuminuria in a 25-year-old man with bisalbuminemia and nephrotic syndrome. ( info)

3/37. Case report: intestinal clearance of calcium and protein in Waldenstrom's macroglobulinemia.

    A 63-year-old man with Waldenstrom's macroglobulinemia had severe steatorrhea, marked protein-losing enteropathy, and excessive endogenous fecal calcium clearance. The malabsorption and protein loss resulted in weight loss and hypoalbuminemia. In contrast, the striking enteric calcium loss was completely compensated by an increase in calcium absorption resulting in a positive calcium balance. ( info)

4/37. urine free light chains in SLE: clonal markers of B-cell activity and potential link to in vivo secreted Ig.

    As a marker of in vivo B-cell activity, urine levels of free light chain (FLC) were measured twice weekly by radioimmunoassay (RIA) and correlated with disease activity over periods of 5-10 months in seven patients with systemic lupus erythematosus (SLE). In addition, RIA-measured urine albumin was used to track glomerular injury, and alpha1-microglobulin (alpha1-M) levels, 28- to 32-kDa protein, provided control measurements on excretion of low-molecular-weight proteins. As controls, urine FLC levels were obtained from healthy normals and in subjects with acute pharyngitis, sickle-cell anemia, and acute sepsis or pneumonia. The control results showed that with acute sepsis/pneumonia had marked increases in urine FLC, while pharyngitis and sickle-cell controls had normal FLC levels. In SLE, active patients receiving intravenous cyclophosphamide and high-dose steroids exhibited highly increased urine FLC that fluctuated widely during therapy and fell to normal range levels with disease remission. During active SLE, urine albumin often was increased, while alpha1-M levels remained in normal range. In contrast to the increased FLC of active disease, inactive patients on low-dose maintenance therapy had predominantly normal FLC levels throughout the collection period. These results support our hypothesis that longitudinal levels of urine FLC can be used to track disease-related B-cell activity in SLE. Furthermore, we suggest that the urine FLC of active SLE would share LC idiotype with the clonal associated in vivo secreted Ig, and thus permit the identification of these antibodies that are targeted to the culprit immunogen(s) responsible for the pathogenesis of SLE. ( info)

5/37. Microalbuminuria following anaphylaxis with general anaesthesia.

    Microalbuminuria is increasingly recognized as a marker of pathologies that cause acute systemic capillary leak. We report a case of an anaphylactic reaction to general anaesthesia involving cardiac arrest. In this case the urinary excretion of albumin following resuscitation suggests that severe anaphylaxis is another condition for which microalbuminuria is a sensitive monitor. ( info)

6/37. erythropoietin-dependent anaemia: a possible complication of diabetic neuropathy.

    We report the case of a 52-year-old woman with long-term type 1 diabetes mellitus, complicated with proliferative retinopathy, autonomic neuropathy and microalbuminuria and moderate renal failure. A normochromic, normocytic are generative anaemia had been diagnosed for three years. Clinical and biological investigations for the aetiology of anaemia remained normal or negative. Anaemia was associated with a concentration of erythropoietin (EPO) in the normal range, but inappropriately low regarding anaemia. Treatment with recombinant EPO induced a rapid increase in haemoglobin level and improved the patient's quality of life. The role of diabetic neuropathy in the genesis of anaemia, in conjunction with a modest renal impairment is discussed. ( info)

7/37. congenital hypothyroidism in a child with unsuspected familial dysalbuminemic hyperthyroxinemia caused by a mutation (R218H) in the human albumin gene.

    We found familial dysalbuminemic hyperthyroxinemia (FDH) in a 5-month-old boy with congenital hypothyroidism (CH) who had a blood thyrotropin (TSH) level of 479 mU/L but normal total serum thyroxine (T4) and higher than normal total triiodothyronine (T3) levels. Thyroid hormone substitution began at 5 weeks of age when T4 and T3 concentrations were below normal. Until the age of 5 months, treatment with levothyroxine was suboptimal on the basis of high serum TSH levels despite above-normal T4 levels. FDH was confirmed by isoelectric focusing and testing of other family members. dna analysis of the patient revealed R218H, a mutation in the serum albumin gene associated with FDH, which was also present in the patient's euthyroid father and brother. Thyroid scans, serum thyroglobulin measurements, and free T4 measurements using equilibrium dialysis or 2-step immunoassay methods can identify thyroid hormone-binding protein defects and simplify the diagnosis and treatment of infants with CH. ( info)

8/37. Acute presentation of undiagnosed end-stage renal disease in a young active duty male soldier.

    Chronic renal insufficiency is a condition involving the deterioration of renal function over a period of months to years. This differs from acute renal failure, which is a sudden decrease in renal function that occurs over a period of hours to days. patients with chronic renal insufficiency are often clinically asymptomatic until nearing end-stage renal disease, at which time their signs and symptoms reflect subtle changes in metabolic and volume control. In contrast, acute renal failure patients often present with overt symptoms caused by sudden metabolic abnormalities and volume overload. We describe a patient who's clinical presentation suggested acute renal failure but was actually caused by end-stage renal disease from a chronic renal process. ( info)

9/37. Can glomerular mRNAs in human type 1 diabetes be used to predict transition from normoalbuminuria to microalbuminuria?

    BACKGROUND: mRNAs of pathogenetic importance in the development of diabetic nephropathy were measured in subjects with type 1 diabetes to determine whether these might be used to predict progression from normoalbuminuria to microalbuminuria. We proposed that conversion from normoalbuminuria to microalbuminuria would be most likely in subjects whose connective tissue growth factor (CTGF) and collagen mRNAs were above the 95% confidence interval (CI) for live renal donors and within the 95% CI for subjects with abnormal albuminuria. methods: Glomerular CTGF, collagen alpha2(IV), and control glyceraldehyde-3-phosphate dehydrogenase (GAPDH) mRNAs were measured in microdissected glomeruli from living renal donors (n = 10), and subjects with normoalbuminuria (n = 12), microalbuminuria (n = 5), and overt proteinuria (n = 6). RESULTS: After 44 /- 2 months of follow-up, one subject converted from normoalbuminuria to microalbuminuria. Although the data are limited, progression from normoalbuminuria to microalbuminuria occurred in the only normoalbuminuric subject whose mRNA levels were above the live renal donors' 95% CI for CTGF and collagen alpha2(IV) and within the 95% CI of subjects with abnormal albuminuria. No clinical or histopathologic finding distinguished the progressor from the nonprogressors at the time of biopsy. CONCLUSION: This case report provides proof-of-principle that a panel of glomerular mRNA markers chosen because of their pathogenetic relevance may be useful adjuncts to albuminuria and histology in predicting clinical stability or clinical progression in diabetic nephropathy. ( info)

10/37. Atypical presentation of churg-strauss syndrome: another "forme fruste" of the disease?

    vasculitis is a clinicopathologic process characterized by inflammation and damage to blood vessels. A broad and heterogenous group of syndromes may result from this process, because any type, size, and location of blood vessel may be involved. The cause of these conditions remains unclear, but an autoimmune inflammatory process, characterized by involvement of both neutrophils and endothelial cells, seems to play an important role. In 1951, Churg and Strauss described a clinical syndrome of severe asthma, hypereosinophilia with eosinophilic infiltrates, eosinophilic vasculitis, and granulomata in various organs. asthma may precede this vasculitis by many years. We report a case of anti-neutrophil cytoplasmic antibody-positive, pauci-immune, crescentic, necrotizing glomerulonephritis with peripheral and interstitial eosinophilia but without asthma. This is very unusual in churg-strauss syndrome. ( info)
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