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)

To investigate the role of dietary components in immunoglobulin A mesangial nephropathy (IgAGN), this study focused on gliadin, based on the reported association between coeliac disease and IgAGN as well as the pilot observation that a gluten-free diet was able to reduce the levels of circulating IgA immune complexes (IgAIC). IgA mesangial deposits in mice were induced by oral immunization with gliadin and in rats by inducing alcoholic liver cirrhosis, which increased the levels of IgA against dietary antigens (Ag). Gliadin was able to bind to cultured mesangial cells by a lectinic bond, which was reversed by competitive sugars. Binding increased mesangial cell tumor necrosis factor synthesis and decreased prostaglandin E2 production. Several gluten lectinic fractions modulate leukocyte oxidative metabolism, cytotoxicity, and chemotaxis. In IgAGN patients, serum IgA to dietary Ag were sporadically positive and IgAIC containing IgA to dietary components were significantly increased. The affinity of serum IgA to various lectins was increased in some patients. Conversely, no substantial deposition in renal tissue of dietary Ags was observed by immunofluorescence. A gluten-free diet, given to IgAGN patients with high levels of circulating IgAIC and positive antigliadin IgA, was followed by a decrease in the mean levels of both IgAIC and IgA to various dietary Ag, parallel to a reduction in proteinuria. These data suggest that dietary components, such as Ag or lectins, may play a role in IgAGN by promoting IgAIC formation and perhaps favoring mesangial localization via lectinic interactions.
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PMID:Dietary antigens and primary immunoglobulin A nephropathy. 160 Jan 33

A 52-year-old man, who had been diagnosed as having alcoholic liver cirrhosis, presented a chronic nephritic syndrome due to hepatic glomerulosclerosis. Ten months before death, massive proteinuria exceeding 40 g/day was noted. A renal biopsy revealed diffuse mesangial sclerosis, associated with an IgA deposition consistent with hepatic glomerulosclerosis. Although the nephrotic syndrome subsided with immunosuppressive therapy, he died of hepatic failure. Postmortem examinations disclosed a diffuse, medium-size B-cell lymphoma, involving the peritoneal and retroperitoneal organs and an IgA-positive plasmacytosis. His massive proteinuria seems to have been caused by the paraneoplastic syndrome of a malignant lymphoma.
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PMID:[An autopsied case of a malignant lymphoma with a severe nephrotic syndrome overlapped by cirrhotic glomerulosclerosis]. 329 70

The incidence of mesangial IgA nephropathy (mIgAN) was investigated in a series of patients with alcoholic liver cirrhosis (ALC). Biologic parameters classically reported in IgAN were assessed in 98 patients, namely hematuria, proteinuria, and serum IgA. An immunohistologic study of the liver and kidney was performed in 33 patients who died during the study. Renal data were compared with those obtained in a matched necropsic series of controls. This study confirmed a global elevation of serum IgA levels in ALC. A possible hepatic origin of these immunoglobulins was supported by the observation of plasma cells in portal spaces in 68% of the patients. Biologic signs of renal disease consistent with mIgAN were observed in 16% of the patients; IgAN was diagnosed in 18% of patients with ALC and 10% of the controls. These data suggest that the incidence of mIgAN in ALC is not different than in the general population.
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PMID:IgA nephropathy and alcoholic liver cirrhosis. A prospective necropsy study. 1206 73

A 69-year-old female was admitted to our hospital because of leg edema, proteinuria (2.1 g/day), and gross hematuria. She had non-alcoholic liver cirrhosis of unknown etiology. Esophageal varices also were found. Examination of the renal biopsy specimen revealed mesangial proliferative glomerulonephritis with IgA deposits. Propranolol was administered orally to reduce portal hypertension, resulting in a progressive decrease in urinary microalbumin excretion. This case suggests that portal hypertension is involved in the pathogenesis of IgA nephropathy in liver cirrhosis.
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PMID:IgA nephropathy associated with portal hypertension in liver cirrhosis due to non-alcoholic and non-A, non-B, non-C hepatitis. 780 17

A 66-year-old man with erysipelas was admitted with complaints of oliguria and massive proteinuria/hematuria. He was diagnosed as having acute poststreptococcal glomerulonephritis(APSGN) due to erysipelas infected by group A streptococcus pyogenes. On admission, his white cell count increased to 31,000, and CRP was 27.3 mg/dl. Serum urea nitrogen and creatinine were increased to 90.1 mg/dl and 4.5 mg/dl, respectively. He had diabetes mellitus(HbA1c 7.9%) and liver dysfunction(total bilirubin 3.5 mg/dl, AST 76 IU, ALT 41 IU) caused by alcoholic liver cirrhosis. Hypocomplementemia was found in addition to ASO 216 U/ml and ASK 10,240 x. After antibiotics treatment was initiated, inflammation of the erysipelas began to improve. Disseminated intravascular coagulation syndrome, probably due to sepsis, occurred on the 5th hospital day. He died of gastrointestinal bleeding on the 18th hospital day. Renal autopsy revealed 37% formation of fibrocellular crescents, and marked mesangiolysis was noted by light microscopy. Granular deposition of C3 and IgG was seen along the capillary walls on immunofluorescence study. Intramembranous deposits were scattered on electron microscopy. This case illustrates a fulminant type of APSGN, which was in part attributed to the presence of diabetes and alcoholic liver cirrhosis. Histological findings of crescent formation and marked mesangiolysis may account for the fulminant clinical course.
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PMID:[A case of fulminant acute poststreptococcal glomerulonephritis showing mesangiolysis and crescent formation preceded by erysipelas]. 1247 94

It has been reported that glomerulosclerosis with IgA deposition is likely to be complicated with alcoholic liver cirrhosis. On the other hand, it is said that complications of nephrotic syndrome or rapidly progressive glomerulonephritis (RPGN) are relatively rare. We experienced two patients with alcoholic liver cirrhosis complicated with RPGN syndrome who had obtained favorable outcomes through the use of steroids and immune system suppressors. Case 1 was a 55-year-old male. He was being treated for alcoholic liver cirrhosis, but as bloody urine was noticed macroscopically, his renal function rapidly decreased. Specimens from a renal biopsy showed endocapillary proliferative lesions accompanying necrotic lesions. Granular deposition of IgA (IgA1) and C3 was seen along the capillary walls and in the mesangial areas. After the combined treatments of bilateral palatotonsillectomy, three courses of steroid semi-pulse therapy and post-therapy with steroids and mizoribin (MZR)were started, his hematuria and proteinuria disappeared and renal function improved markedly. Case 2 was a 37-year-old male with alcoholic liver cirrhosis complicated with hepatic encephalopathy. Although he was being treated at another hospital, nephritic syndrome occurred with rapidly worsening renal function and massive ascites. After continuous drainage of the ascites, we performed a renal biopsy. Mild proliferative lesions and notable wrinkling, thickening and doubling of the basal membrane were seen. Crescent formations were found in about half of the glomeruli. The fluorescent antibody technique showed positive pictures of IgA (IgA1) and C3. When three courses of steroid semi-pulse therapy and post therapy with steroids and MZR were combined, his proteinuria and serum Cre level decreased and stagnated ascites markedly decreased. The two cases were diagnosed as having secondary IgA nephropathy induced by the deposition of the IgA1 derived mainly from the intestinal tract, which had increased in the blood due to alcoholic liver cirrhosis. Active use of immune system suppressor therapy was effective.
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PMID:[Two cases of rapidly progressive nephritic syndrome complicated with alcoholic liver cirrhosis]. 2137 May 79