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)

A patient who was receiving rifampin treatment for tuberculosis developed heterogenous light-chain proteinuria and insidious renal failure after a period of fluid restriction. The renal damage was characterized pathologically by an interstitial nephritis with invasive tubular casts and an associated renal vein thrombosis. The possible role of the light-chain proteinuria in the pathogenesis of the renal failure is discussed.
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PMID:Insidious rifampin-associated renal failure with light-chain proteinuria. 40 68

Incidences of renal amyloidosis were studied in patients who were in various stages of pulmonary tuberculosis and a three year follow-up gave some opportunity to study the effectiveness of anti-tuberculosis treatment on the course of renal amyloidosis. It was concluded that 9 to 11 per cent of all patients with pulmonary tuberculosis will eventually develop proteinuria due to renal amyloidosis after a certain period of time. It has been postulated that once amyloidosis has extensively involved the kidneys, anti-tuberculous treatment will not cause any regression in the course of renal amyloidosis.
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PMID:Incidence of renal amyloidosis in pulmonary tuberculosis. 59 58

Light chain proteinuria was found in 9 of 17 tuberculosis patients treated with rifampin. Concomitant assay of cellular mediated immunity in these patients using skin test antigen and a lymphokine in vitro test provided results that were different. Response to Varidase skin test antigen was negative for all eight tuberculosis patients tested, but there occurred a hyper-responsiveness of the lymphocytes of these eight patients to phytomitogen (PHA-P). as well as of those of seven other tuberculous patients. This last finding may be related to time of testing and/or endogenous serum binding of rifampin which could have inhibited mitogen activity for the lymphocyte.
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PMID:Light chain proteinuria and cellular mediated immunity in rifampin treated patients with tuberculosis. 80 91

We have previously demonstrated the pathogenicity of the common anti-DNA idiotype designated 16/6 Id. Immunization of naive mice with the 16/6 Id induced SLE-like disease characterized by serological (e.g. anti-dsDNA and anti-Sm auto-antibodies), clinical (increased ESR, leucopenia and proteinuria), and pathological (16/6 Id deposition in kidneys) parameters. To elucidate further the role of the 16/6 Id in SLE induction the following studies were carried out: BALB/c mice were immunized with SA-1, a human anti-DNA monoclonal antibody carrying the 16/6 Id; TB-68, a mouse monoclonal anti-tuberculosis (TB) glycolipid, which binds dsDNA and carries the 16/6 Id; TB-72, a mouse monoclonal anti-TB glycolipid that binds DNA and does not harbour the 16/6 Id; and 4B4, a human anti-Sm antibody that carries the 16/6 Id. SLE was induced in BALB/c mice only when immunized with SA-1, TB-68, and 4B4, namely antibodies with diverse binding capacities albeit having the 16/6 Id. Our studies further support previous evidence on the pathogenic role attributed to the 16/6 Id in SLE, and suggest that SLE is most probably an idiotype-induced disease.
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PMID:The importance of the pathogenic 16/6 idiotype in the induction of SLE in naive mice. 240 76

There are indications that there is an increased risk of chronic renal failure (CRF) in the Negroid race, yet few studies have been carried out in the native 'black' environment. A clinico-pathological study of 100 consecutive Nigerian subjects with CRF, seen over a 3-year period, is presented. Primary chronic glomerulonephritis (CGN) accounted for 50, accelerated hypertension for 25, and various aetiological entities for a further nine; these included, chronic pyelonephritis (two), diabetic nephropathy (two), calculous nephropathy (one), toxaemia of pregnancy (one), renal dysplasia (one), tuberculosis (one) and polycystic disease in the ninth subject. In 16 cases, no definitive aetiological diagnosis could be made. Combinations of the following features, protracted hypertension, proteinuria, significant analgesic intake and gouty arthritis, were observed. CGN and accelerated hypertension still remain the leading causes of CRF, while diseases such as diabetes mellitus and chronic pyelonephritis do not contribute significantly to CRF in Nigerians. Recognition of the early features and the causes of CRF would considerably reduce the prevalence of this condition.
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PMID:Diseases causing chronic renal failure in Nigerians--a prospective study of 100 cases. 254 87

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

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

Electrolyte and renal hemodynamic imbalance, acute interstitial nephritis with nephrotic-range proteinuria, papillary necrosis, tubular necrosis, and vasculitis are complications after intake of nonsteroidal anti-inflammatory drugs (NSAID). We report on 2 cases of biopsy-proven granulomatous interstitial nephritis with rapidly progressing renal insufficiency. Patient 1 was on ketoprofen for 7 months and indomethacin for 10 weeks before admission to hospital. The medication was not discontinued and renal insufficiency progressed to end-stage renal failure. Renal function did not respond to steroid and tuberculostatic treatment. Patient 2 was on diclofenac for 6 months and indomethacin for 7 weeks before admission to hospital. These drugs were withdrawn at diagnosis and renal function rapidly improved. We conclude that granulomatous interstitial nephritis may be a complication of NSAID medication indicating a cell-mediated immunologic disorder. False diagnosis (sarcoidosis, tuberculosis) may lead to end-stage renal disease (case 1). Discontinuation of medication obviates further therapy (case 2).
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PMID:Granulomatous interstitial nephritis after nonsteroidal anti-inflammatory drugs. 307 Nov 48

Eleven patients with Wegener's granulomatosis were seen at this Institute over a period of 20 years. There were six men and five women. The average age of presentation was 38.3 years, and the mean duration of symptoms was 10.5 months. Constitutional symptoms (82%), cough (82%), ocular symptoms (64%), arthralgias (55%), rhinorrhoea (55%), haemoptysis (45%), nasal granuloma (45%), otorrhoea (36%), sinusitis (36%), skin lesions (27%), and renal failure (27%) were the clinical manifestations encountered. All patients had an elevated ESR, and 55% had leucocytosis. Proteinuria and haematuria were observed in 64% and 55% respectively. Chest radiographs were abnormal in 82%. In four patients the disease had a fulminant course and the patients died before adequate treatment was given. Two patients received corticosteroids alone and have since been lost to follow up. Five (45%) received adequate cytotoxic therapy and have done well for 8-46 months (mean, 24.8 months) after diagnosis. Wegener's granulomatosis in India is apparently similar to that seen elsewhere, but the high incidence of tuberculosis interferes with early diagnosis and treatment.
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PMID:Wegener's granulomatosis in north India. An analysis of eleven patients. 343 65

Thirteen cases of amyloidosis are reported from Vanuatu between 1983 and 1985. There appears to be a high incidence of the disease similar to that found in Papua New Guinea. The role of malaria as an aetiological agent is discussed although most cases had a history of past or active tuberculosis. Most patients presented as either nephrotic syndrome or a syndrome of abdominal pain, diarrhoea, weight loss and proteinuria.
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PMID:Amyloidosis in Vanuatu. 361 94


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