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)

Antirheumatic drugs may cause a significant, although generally reversible, reduction of GFR, RPF, CNa and hyperkalemia in a wide range of extrarenal and renal disease states (severe liver disease, congestive heart failure, SLE, nephrotic syndrome, etc.); chronic ingestion has been associated with analgesic nephropathy. Recently cases have been reported of reversible acute renal failure with massive proteinuria and interstitial nephritis. The acute effects of a renal PG-inhibiting (ibuprofen) or a renal PG-sparing (sulindac) cyclo-oxygenase inhibitor on renal functional parameters (GFR, RPF, CNa, CK, urine volume) and proteinuria have been studied in 24 patients with clinically and biopsy proven chronic glomerular disease; in all patients ibuprofen significantly reduced GFR, RPF, CNa; these changes were fully reversible within a week of withdrawal of the drugs. A causal relationship exists between inhibited PG-synthesis and reduced renal function in these patients, since sulindac, which failed to reduce urinary PG excretion did not alter significantly the renal function. Moreover proteinuria is not reduced by ibuprofen at doses comparable, as far as concerns inhibition of PG-synthesis, to those of indomethacin.
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PMID:Clinical assessment of the renal toxicity of antirheumatic drugs. 633 23

The nature of circulating immune complexes (CIC) which appear in patients with type B hepatitis was investigated using a method of Raji cell fluorescent immunoassay. CIC were found in seventeen of thirty-five cases (48.6%) with HBs antigen (HBsAg)-positive liver diseases (4/8 cases with acute hepatitis, 9/18 cases with chronic hepatitis, and 4/9 cases with liver cirrhosis), whereas no CIC were detectable in sera of ten asymptomatic, healthy carriers with HB virus. Among the seventeen cases with CIC-positive liver diseases, HBs antigen-antibody immune complexes (HBsIC) were demonstrated in eleven (65%). A high incidence (54%) of proteinuria was observed in patients with CIC-positive liver disease compared to those without them (10%). Moreover, 83% of patients with HBsIC were associated with proteinuria. A case of fulminant type B hepatitis showed high titers of both CIC and HBsIC during the acute phase of the disease; in the recovery stage, the titers decreased to within normal ranges. These results demonstrate that HBsAg is a possible antigen in CIC during type B hepatitis. Determination of serum HBsIC is significant for the clinical evaluation of HB virus-related liver diseases.
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PMID:Significance of circulating HBs antigen-antibody immune complexes in patients with HBs antigen-positive liver disease. 711 81

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

Lecithin-cholesterol acyltransferase is responsible for the formation of most cholesteryl esters in plasma. Absence of this enzyme can result in a rare syndrome that includes diffuse corneal opacities, normocytic normochromic anemia, proteinuria, renal failure, and premature arteriosclerosis. The deficiency can be inherited in an autosomal recessive manner, or it can be acquired through liver disease. Diagnosis requires a high index of suspicion and documentation of impairment of enzyme mass or activity (or both). This article includes a case report of the first United States citizen known to have lecithin-cholesterol acyltransferase deficiency. The authors review the literature related to this disease.
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PMID:Lecithin-cholesterol acyltransferase deficiency: first report of case in a United States citizen. 802 2

A 46-yr-old multiparous cachetic woman presented with severe hypoalbuminemia in the absence of liver disease, proteinuria, and/or protracted starvation. The clinical presentation and work-up was indicative of protein-losing enteropathy. She developed an acute partial small bowel obstruction, and a presumptive diagnosis of lymphoma of the small intestine was entertained. Surgical resection of the terminal ileum revealed transmural involvement of the bowel by endometriosis. Her postoperative recovery was uneventful, with return of her serum albumin levels to normal.
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PMID:Endometriosis of the small intestine presenting as a protein-losing enteropathy. 842 Feb 54

A variety of renal diseases can be associated with end-stage liver diseases requiring orthotopic liver transplantation (OLT), including cirrhosis-associated glomerulonephritis (GN), and nephropathy unrelated to the liver disease. A retrospective survey showed that nine patients undergoing liver transplantation in our centre had histologically proven GN or interstitial nephritis with renal failure and/or nephrotic-range proteinuria, and experienced severe complications post-OLT since nephrotoxic immunosuppressive drugs (CsA and FK506) could not be adequately given. Four of the nine patients died. Therefore, combined liver-kidney transplantation has been suggested as first choice treatment in such patients. From January 1990 to February 1994, in patients with end-stage liver disease referred for OLT, and who presented with unexplained renal function impairment and/or significant proteinuria, severe nephropathy was confirmed by renal biopsy in nine: four mesangiocapillary GN with immune deposits, one membranous nephropathy, two diabetic glomerulosclerosis and two interstitial nephritis. All underwent liver transplantation immediately followed by kidney transplantation. The postoperative period was uneventful, and neither death nor renal failure were recorded. Combined transplantation resulted in all patients in the normalization of renal function, and in the disappearance of proteinuria within the first postoperative month. From 6 months to 4 years post-transplant, the renal function remained within normal ranges in all patients. Routine renal transplant biopsy was performed in two patients with pre-transplant cirrhosis-associated GN, and showed no evidence of recurrence of the original nephropathy. We conclude that combined liver-kidney transplantation is an adequate therapeutic option in patients with end-stage liver disease associated with advanced kidney disease.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Combined liver and kidney transplantation in patients with chronic nephritis associated with end-stage liver disease. 852 84

The incidence, causes, and consequences of hypoalbuminemia after renal transplantation are not well defined. We examined clinical correlates of serum albumin measured at 3 months, 6 months, 1 year, and annually thereafter in 706 renal transplant recipients who survived at least 6 months with a functioning allograft. Follow-up was 7.0 +/- 4.2 years. Hypoalbuminemia (< or = 3.5 g/dL) was most common at 3 months (31%, n = 692), least common at 1 year (12%, n = 656), and then became increasingly common among survivors, for example, 14% (n = 466) at 4 years, 20% (n = 204) at 8 years, and 29% (n = 77) at 12 years after transplantation. By multiple linear regression, variables that correlated (P < 0.05) with lower serum albumin at 3, 6, 12, and 24 months included age, diabetes, proteinuria, and cytomegalovirus infection. Other independent correlates on at least one of these occasions included renal function and chronic disease (malignancy, liver disease, and cardiovascular disease). Serum albumin, as a time-averaged and time-dependent covariate, was a strong independent risk factor for death using Cox proportional hazards analysis (relative risk for each g/dL increment, 0.26; 95% confidence interval, 0.16 to 0.44 [1.00 = no risk]). The effects of albumin on mortality were independent of age, diabetes, serum lipids, renal function, chronic liver disease, malignancies, and cardiovascular disease. The effects of albumin on mortality were evident even when the analysis was restricted to patients dying several years after albumin was measured. Thus, hypoalbuminemia is common and serum albumin is a strong independent risk factor for all-cause mortality after renal transplantation.
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PMID:Serum albumin and mortality after renal transplantation. 854 25

Indian childhood cirrhosis (ICC) is an almost uniformly fatal disease whose outcome may be modified with penicillamine if given at a sufficiently early stage. Twenty nine children with ICC seen in Pune, India, in 1980-7, who had survived at least five years from onset of penicillamine treatment, were reviewed aged 6.3 to 13 years. They were assessed clinically, biochemically, histologically, and by duplex Doppler ultrasound examination. None had symptoms suggestive of liver disease. There were no toxic effects of penicillamine other than asymptomatic proteinuria. Hepatosplenomegaly reduced significantly and liver function tests returned to normal in all. In four children, significant hepatosplenomegaly was associated with an abnormal duplex Doppler hepatic vein flow pattern and micronodular cirrhosis on biopsy. Clinical findings, growth and development, and ultrasound examination were normal in the remainder. Review of serial liver biopsy specimens showed a sequence of recovery from ICC through inactive micronodular cirrhosis to virtually normal histological appearances. The four children who still have micronodular cirrhosis beyond four years from onset remain on penicillamine treatment. In the others penicillamine was stopped after 1-7 (mean 3.5) years without relapse, strong evidence that ICC is not due to an inborn error of copper metabolism.
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PMID:Long term survival in Indian childhood cirrhosis treated with D-penicillamine. 866 42

Glomerular abnormalities are frequent in patients undergoing liver transplantation; however, renal dysfunction following transplantation is mainly attributed to cyclosporine toxicity. Membranoproliferative glomerulonephritis (MPGN) is seen in patients infected with hepatitis C virus (HCV), the virus responsible for 30% of the end-stage liver disease leading to liver transplantation. To determine the incidence of renal abnormalities in liver transplant recipients and the association with HCV, we undertook a longitudinal study in HCV-positive (n=91) and HCV-negative (n=106) liver transplant recipients. Mean creatinine clearance before transplantation was 94 ml/min/1.73 m2 in HCV+ patients and 88 ml/min/1.73 m2 in HCV- patients. By 3 months after transplantation, the mean creatinine clearance decreased by approximately one third in both groups. A greater proportion of HCV+ patients excreted >2 g protein/day after transplantation (P=0.05) and had renal biopsies showing MPGN than did HCV- recipients (4/10 HCV+ patients vs. 0/7 HCV- patients; P=0.1). In the HCV+ group, proteinuria was not associated with recurrent HCV hepatitis, DQ matching, posttransplant diabetes, or hypertension. Treatment of HCV-related MPGN with interferon-alpha2b appeared to stabilize proteinuria and renal function but did not reverse renal dysfunction nor cause liver allograft rejection. After transplantation, HCV+ patients had similar renal function over 3 years after transplantation, compared with HCV- patients, but they had an increased risk of proteinuria and occurrence of MPGN that was only partially responsive to interferon.
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PMID:Renal disease in hepatitis C-positive liver transplant recipients. 915 23


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