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)

AIDS-associated nephropathy (AAN) causing acute renal failure has been described in patients with AIDS. It is characterized by massive proteinuria and focal segmental glomerulosclerosis. From 1982 until 1987, 177 patients with AIDS were seen in our center. Most of them were homosexual or bisexual men. One patient was also an intravenous drug addict. One patient was a black female. None suffered from a nephrotic syndrome or needed hemodialysis during their illness. In 47 of the 110 patients who died an autopsy was performed. On microscopical examination of kidney tissue obtained at autopsy, no abnormalities were seen in 12 patients and slight abnormalities were found in 35 patients. Glomerular changes, mostly fibrous caps in Bowman's space, were present in 22 patients. Mesangial and intracapillary lesions were seen in only 5 patients. Tubular atrophy was found in 14 patients and sparse interstitial inflammation in 15 patients. A renal localisation of disseminated opportunistic infections was found in 11 patients: CMV (n = 4), tuberculosis (n = 2), Mycobacterium avium intracellulare (n = 1) and Cryptococcal infection (n = 4). In one patient a renal localisation of a Kaposi sarcoma and in another patient a renal localisation of a disseminated non-Hodgkin lymphoma was found. In conclusion the clinical picture of AAN with acute renal failure was not found in our center. As is the case with heroin associated nephropathy, AAN seems to be confined to certain areas in the USA, suggesting that racial or local co-factors, are important for the pathogenesis of AAN in AIDS.
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PMID:Glomerular lesions and opportunistic infections of the kidney in AIDS: an autopsy study of 47 cases. 278 96

Multicentric Castleman disease (MCD) is a heterogeneous lymphoproliferative disorder, characterized by systemic symptoms, generalized lymphadenopathy, hepatosplenomegaly, proteinuria, and rash. The clinical course is variable and may range from indolent to aggressive, fulminating in a rapidly fatal illness. Mortality is usually from infective complications and less commonly from malignancies, such as lymphoma or Kaposi sarcoma. The association of concurrent or preceding Castleman disease with Kaposi sarcoma is well documented. Castleman disease developed in a 51-year-old patient with AIDS about 10 months after diagnosis of Kaposi sarcoma. MCD was found to be associated with human herpesvirus 8/Kaposi sarcoma-associated herpesvirus.
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PMID:Castleman disease in an HIV-infected patient with Kaposi sarcoma. 1178 20

The frequency of membranous lupus nephritis recurrence (World Health Organization (WHO) class V) in the allograft after renal transplantation is unknown, but it appears uncommon (only two reported cases in the literature). Despite the increased incidence of sarcomas in organ transplant recipients (compared to the general population), non-Kaposi's sarcoma is an uncommon malignancy, and primary tumor involvement of a renal allograft is a rare occurrence. Our patient is a 28 year old female with end-stage renal disease (ESRD) secondary to membranous lupus nephritis who received a living related transplant from her mother. At 26 months post-transplant, she presented with proteinuria and a rise in creatinine (Cr). Allograft biopsy was consistent with recurrent membranous nephropathy. Five weeks later, she was found to have a high-grade leiomyosarcoma originating within the allograft. We reviewed the literature on recurrent post-transplant membranous nephropathy and the possible role of the Epstein-Barr virus (EBV) infection in smooth muscle tumors occurring in organ transplant recipients. We also considered the association of membranous nephropathy and malignancy.
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PMID:Recurrent membranous nephropathy and leiomyosarcoma in the renal allograft of a lupus patient. 1515 Dec 71

Sirolimus (SRL) is a new, potent immunosuppressive agent. More recently, proteinuria has been reported as a consequence of sirolimus therapy, although the mechanism has remained unclear. We retrospectively examined the records of 25 renal transplant patients, who developed or displayed increased proteinuria after SRL conversion. The patient cohort (14 men, 11 women) was treated with SRL as conversion therapy, due to chronic allograft nephropathy (CAN) (n = 15) neoplasia (n = 8); Kaposi's sarcoma, Four skin cancers, One intestinal tumors, One renal cell carsinom) or BK virus nephropathy (n = 2). SRL was started at a mean of 78 +/- 42 (15 to 163) months after transplantation. Mean follow-up on SRL therapy was 20 +/- 12 (6 to 43) months. Proteinuria increased from 0.445 (0 to 1.5) g/d before conversion to 3.2 g/dL (0.2 to 12) after conversion (P = 0.001). Before conversion 8 (32%) patients had no proteinuria, whereas afterwards all patients had proteinuria. In 28% of patients proteinuria remained unchanged, whereas it increased in 68% of patients. In 40% it increased by more than 100%. Twenty-eight percent of patients showed increased proteinuria to the nephrotic range. Biopsies performed in five patients revealed new pathological changes: One membranoproliferative glomerulopathy and interstitial nephritis. These patients showed persistently good graft function. Serum creatinine values did not change significantly: 1.98 +/- 0.8 mg/dL before SRL therapy and 2.53 +/- 1.9 mg/dL at last follow-up (P = .14). Five grafts were lost and the patients returned to dialysis. Five patients displayed CAN and Kaposi's sarcoma. Mean urinary protein of patients who returned to dialysis was 1.26 (0.5 to 3.5) g/d before and 4.7 (3 to 12) g/d after conversion (P = .01). Mean serum creatinine level before conversion was 2.21 mg/dL and thereafter, 4.93 mg/dL (P = .02). Heavy proteinuria was common after the use of SRL as rescue therapy for renal transplantation. Therefore, conversion should be considered for patients who have not developed advanced CAN and proteinuria. The possibility of de novo glomerular pathology under SRL treatment requires further investigation by renal biopsy.
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PMID:Proteinuria after conversion to sirolimus in renal transplant recipients. 1717 8

The aim of this study was to compare the clinical characteristics of recurrent and de novo membranous glomerulopathy (MG) among a cohort of 614 recipients transplanted between 1989 and 2006. Lupus nephritides were excluded. The diagnosis was established on protocol biopsies performed 1, 2, 4, or 8 years after transplantation or because of proteinuria/nephrotic syndrome and/or an increased serum creatinine level. HCV infection, cryoglobulinemia, monoclonal gammopathy, skin cancers, Kaposi sarcoma, diabetes mellitus, anti-HLA antibodies, and graft survival were not significantly different between the groups. Seventeen MG were diagnosed in 15 patients (2.45% of the whole group), including 6 recurrent MG (35%) and 11 de novo MG (75%). Recurrent MG occurred earlier than de novo MG (15.58 +/- 19.13 vs 49.27 +/- 32.71 months). Recipients with de novo MG were more frequently infected with HCV, which seemed to be the main etiologic factor for de novo MG, and may be linked to a Th2 polarization of the immune response.
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PMID:Recurent and de novo membranous glomerulopathy after kidney transplantation. 1932 52