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)

Although IgA nephropathy (IgA N) is reportedly the most common form of primary glomerulonephritis worldwide, there is a very low incidence of IgA N in Black Americans, and IgA N in Black patients with renal allografts has not been reported. In this report, we present the case of a Black patient with endstage renal disease presumed secondary to hypertensive nephrosclerosis who developed nephrotic range proteinuria due to IgA N in a cadaveric renal allograft 2 years following transplantation. Biopsy of the allograft in the immediate post-transplantation period had revealed no evidence of IgA N. Chronic active hepatitis related to hepatitis C preceded the development of proteinuria by approximately 1 year, raising the possibility that IgA N in the renal allograft was secondary to the liver disease. The clinical and histological features of primary IgA N and IgA N secondary to liver diseases are discussed.
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PMID:Immunoglobulin A nephropathy in a renal allograft of a black transplant recipient. 141 57

A 54-year-old male patient with heterozygous Protein C deficiency associated with the nephrotic syndrome and deep femoral artery thrombosis is described. He was admitted to the hospital because of nephrotic syndrome. A few days later, severe pain appeared in his left leg and a diagnosis of deep femoral artery thrombosis was made. Thrombectomy was performed immediately. His proteinuria disappeared in response to corticosteroid. He was found to have Protein C deficiency, antigen: 44%, activity 31%, which was also present in his father and son. Digital subtraction angiography (DSA) revealed the obstruction of left internal iliac and deep femoral arteries at their origins. Renal and hepatic biopsy revealed minor glomerular abnormalities, and chronic active hepatitis. The presence of heterozygous Protein C deficiency, nephrotic syndrome and chronic active hepatitis seem to cause marked decrease in serum Protein C level and deep femoral artery thrombosis. He is now under successful control with warfarin (1.7 mg/day) and bucolome (300 mg/day). It was reported that Protein C might have a suppressive effect on hypercoagulability in nephrotic syndrome. Therefore, Protein C deficiency may not counteract the hypercoagulable state and promote thrombus formation in the case. The present report is the first of a case of Protein C deficiency associated with nephrotic syndrome and arterial thrombosis.
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PMID:[A case of heterozygous protein C deficiency associated with nephrotic syndrome and deep femoral artery thrombosis]. 206 19

Six patients with histologically proven HBsAg-negative chronic active hepatitis (CAH), who were initially treated successfully with prednisolone with or without azathioprine, developed unacceptable adverse effects due to prednisolone. In all six patients the liver disease relapsed on reduction of the prednisolone dose and they subsequently entered a trial of low dose D-penicillamine. Two of the patients required early withdrawal of D-penicillamine and a third patient, who had a good clinical and biochemical response initially, developed heavy proteinuria at 14 months. In the remainder, D-penicillamine was well tolerated and the liver disease satisfactorily controlled permitting reduction of the prednisolone dose to 2.5 mg daily. We conclude that in this subgroup of patients with HBsAg-negative CAH and major prednisolone-induced adverse effects, D-penicillamine is an effective alternative therapy although side effects are common.
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PMID:D-penicillamine therapy in patients with HBsAg-negative chronic active hepatitis and major prednisolone-induced adverse effects. 229 22

We report 6 cases with membranous glomerulonephritis associated with chronic hepatitis B virus infection, who came under our observation for microscopic haematuria in 2 cases, haematuria and proteinuria in 1 case, and nephrotic syndrome in the others. At the examination all 6 children were found to have hepatomegaly with raised serum transaminase activity. All the patients were positive in the serum for HBsAg and anti-HBc, 3 were HBeAg and anti-HBe negative. Liver biopsy showed features of chronic hepatitis with moderate signs of activity. Renal biopsy was consistent with membranous glomerulonephritis in all patients. With a fluorescent antibody technic HBeAg was found to be deposited in diffuse granular fashion, along glomerular capillary walls, together with IgG, in 2 out of 3 cases stained, but no deposition of HBsAg was detected in all the patients. Steroid therapy was started from 18 to 33 months. Urine analysis became negative in 4 cases and persisted normal in the follow-up. One patient with haematuria developed nephrotic syndrome and one died from miliary tuberculosis. Our findings suggest that the clinical outcome is favourable in children with membranous glomerulonephritis and chronic active hepatitis and that the pathogenesis probably is not unique.
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PMID:[Membranous nephropathy associated with chronic hepatitis caused by B virus]. 294 50

A patient with chronic active hepatitis and medically unmanageable ascites developed staphylococcal bacteremia after insertion of a peritoneovenous LeVeen shunt. The patient developed glomerulonephritis, manifested by moderate proteinuria, microscopic hematuria with red cell casts, azotemia, and evidence of complement activation. The protracted infection, urinary, and renal abnormalities subsided after removal of the LeVeen shunt and a 3-week course of antibiotics. The clinical course of this patient is typical of the immune-complex mediated glomerulonephritis that has been previously well described in hydrocephalic patients with chronically infected ventriculoatrial shunts.
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PMID:Nephritis associated with an infected peritoneovenous LeVeen shunt. 404 40

Baboons with long term, indwelling, intravascular catheters developed clinical signs of renal and hepatic impairment. These included proteinuria and hypoalbuminemia without edema, and albumin to globulin ratios were reversed. Serum IgM, IgG, rheumatoid factor, and liver enzyme concentrations were above normal. Immunofluorescent staining of renal glomerular capillary loops was positive for IgG, IgM, B1c, and C4. Major microscopic lesions were membranoproliferative glomerulonephritis, chronic active hepatitis, degenerative arthritis, and chronic sialoadenitis. Electron microscopy of renal glomeruli demonstrated dense deposits in a variety of locations, mesangial cell interpositioning, and foot process fusion. These alterations, found in conjunction with the isolation of Staphylococcus aureus from the blood of affected baboons as well as the intravascular catheters, suggested that chronic bacterial infection was important in the pathogenesis of this disease.
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PMID:Immune complex glomerulonephritis in baboons (Papio cynocephalus) with indwelling intravascular catheters. 645 37

The clinical course of 40 patients with significant quantities of mixed cryoglobulins, but without lymphoproliferative, collagen-vascular or chronic infectious diseases, is presented. These cases comprise 51.3 percent of all mixed and 31.7 percent of all types of cryoglobulins evaluated by us over the period 1960--1978. A characteristic clinical syndrome, consisting of recurrent palpable purpura (100 percent), polyarthralgias (72.5 percent) and renal disease (55 percent), was seen. Biopsy specimens of skin lesions showed cutaneous vasculitis, and half had immune reactants in vessel walls. Seventy percent of patients had evidence of hepatic dysfunction, often subclinical, and more than 60 percent of those tested had serologic evidence of prior infection with hepatitis B virus. Hepatic lesions ranged from minimal triaditis to chronic active hepatitis and/or cirrhosis. All 22 patients in whom clinical renal disease developed had significant proteinuria; 63.6 percent had diastolic hypertension, 77.3 percent edema, 45.5 percent renal failure and 22.7 percent were nephrotic. Glomerular disease associated with deposition of immunoglobulin G, immunoglobulin M and complement, often with coexistent renal arteritis, was confirmed pathologically in 15 cases. All cryoglobulins had rheumatoid factor activity and consisted of IgM and polyclonal IgG; five also contained IgA. Thirteen had a monoclonal IgM kappa component. Serum protein electrophoresis was unremarkable or showed diffuse hyperglobulinemia. Striking depression of early complement components was noted but did not correlate well with the cryoprotein concentration, renal involvement or clinical course. Follow-up for periods up to 21 years from onset of symptoms revealed that renal involvement has a deleterious effect on prognosis. Postmorten examinations of nine patients demonstrated widespread vasculitis in addition to renal involvement. Preterminal infection was found in eight.
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PMID:Mixed cryoglobulinemia: clinical aspects and long-term follow-up of 40 patients. 699 82

A case of chronic active hepatitis associated with monoclonal gammopathy (MG) is reported. In addition, the patient had Bence-Jones proteinuria, which is said to be an unusual finding in benign MG. Although a polyclonal increase in immunoglobulins is not uncommon in patients with liver disease, MG is relatively rare. No evidence of malignant disease was found in our patient, but it should be noted that numerous malignant disorders occur with increased frequency in patients with benign MG. A further reason for careful follow-up in these patients is that the paraproteinaemia itself may become malignant with time.
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PMID:Monoclonal gammopathy in a patient with chronic active hepatitis. A case report. 722 98

Hepatitis C virus (HCV) infection may present as a primary glomerular disease. We report 34 adult patients who presented with proteinuria and had circulating anti-HCV antibodies. Primary risk factors included a history of intravenous drug abuse (56%) or blood transfusion (18%). Patients presented with nephrotic syndrome (71%) or with non-nephrotic proteinuria (29%) and had membranoproliferative or acute proliferative glomerulonephritis on renal biopsy. Signs of clinical liver disease were infrequent (18%), though elevated liver function tests were common (66%) and liver biopsy in 16 of 18 patients showed chronic active hepatitis. Cryoglobulinemia was frequent (59%), but only 44% had extrarenal manifestations. In 100% of cases tested, HCV RNA could be found in the serum or cryoprecipitates. Fourteen patients received interferon alpha for 6 to 12 months with a significant reduction in proteinuria but no improvement in renal function. A good clinical response correlated with disappearance of HCV RNA from the serum during treatment; however, relapse of viremia and renal disease was common after completing therapy. Evidence for HCV infection should be sought in all patients with primary glomerular disease. The optimal treatment strategy, however, remains to be defined.
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PMID:Hepatitis C virus-associated glomerulonephritis. Effect of alpha-interferon therapy. 753 69

Although the occasional occurrence of glomerulonephritis associated with hepatitis C virus (HCV) infection has been reported recently in the literature, the type described has been mainly membranoproliferative glomerulonephritis (MPGN); membranous glomerulonephritis (MGN) is very rare. In this paper, two cases of MGN associated with HCV infection are reported. Case 1 was a 56-year-old male who had positive HCV Ab and HCV RNA. The diagnosis of chronic active hepatitis was verified by liver biopsy. Laboratory data showed proteinuria (5g per day), hematuria and hypocomplementemia by hemolytic assay. Renal biopsy led to the diagnosis of MGN in stage II. The patient was treated with interferon alpha for 6 months, resulting in improvement of hypocomplementemia, transient reduction of GOT and GPT during the course of treatment. The GOT and GPT were aggravated again after the completion of therapy. No improvement was seen in proteinuria and hematuria, and HCV Ab remained positive. Case 2 was a 69-year-old male who had positive HCV Ab and HCV RNA, and had normal liver function. Subsequently, his GOT value was slightly elevated. Proteinuria (2g per day) was demonstrated. The diagnosis of MGN in stage II was made on the basis of renal biopsy. The clinical characteristics of these two cases suggest that MGN is a type of glomerulonephritis associated with HCV infection.
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PMID:[Two cases of membranous glomerulonephritis associated with hepatitis C virus infection]. 781 54


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