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)

Carbetimer (carboxyimamidate) is a low molecular weight derivative of ethylene/maleic anhydride polymer. This compound has demonstrated antitumor activity against several animal models with a daily x 5 schedule appearing most effective. A phase I clinical study of the daily x 5 schedule repeated every 28 days was therefore performed. Forty-one evaluable patients received 66 evaluable cycles of Carbetimer at daily doses ranging from 100-11,000 mg/m2. Hypercalcemia was the dose limiting toxicity with both patients at the 11,000 mg/m2 daily dose level and one patient who received 6 cycles of drug at the 4200 mg/m2 dose level developing severe hypercalcemia not explained by the underlying malignancy. Mild nausea, concentration and rate dependent arm pain at the site of infusion, proteinuria, and coagulopathy were also seen. Calcium balance studies revealed hypercalciuria, suggesting increased mobilization of calcium rather than renal retention. In vitro coagulation studies revealed concentration dependent prolongation of the partial thromboplastin time and thrombin time. No complete or partial responses were seen. However mixed response or biochemical response (reduction in serum lactic dehydrogenase) were seen in 5 patients with melanoma or renal cancer. Due to unacceptable toxicity at the 11,000 mg/m2 daily dose level, Carbetimer 8500 mg/m2 is the recommended dose for a 5-day treatment schedule every 28 days. Special attention should be directed toward possible activity against melanoma and renal cancer.
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PMID:Phase I trial of a 5-day course of carbetimer. 238 16

Physical and social characteristics recorded at college physical examination and reported in subsequent questionnaires to alumni in 1962 or 1966 by 50,000 former students from Harvard University and the University of Pennsylvania were reviewed for their relationship to major site-specific cancer occurrence. The records of 1,359 subjects who died with a major site-specific cancer in a 16- to 50-year follow-up period and of 672 subjects who reported such a cancer by mail questionnaire in 1976 or 1977 were compared with those of 8,084 matched classmates who were known to be alive and free of cancer at the time subjects with cancer had died or had been diagnosed. Cigarette smoking, as reported both in student years and years as alumni, predicted increased risk for cancers of the respiratory tract, pancreas, and bladder. Student coffee consumption was associated with elevated risk for leukemia, but it was unrelated to cancers of the pancreas and bladder. Male students with a record of proteinuria at college physical examination experienced increased risk of kidney cancer, and those with a history of tonsillectomy experienced increased risk of prostate cancer. Students who at college entrance reported occasional vague abdominal pain were at elevated risk for pancreatic and colorectal cancers in later years. Increased body weight during college was associated with increased risks of kidney and bladder cancers, whereas for alumni this index was associated only with kidney cancer. Increased weight-for-height during college (but not in 1962 or 1966) predicted increased occurrence of female breast cancer. Jewish students experienced elevated risk for subsequent cancers of the female breast, colon, and combined colorectum. These and other findings are presented as clues deserving further exploration for any etiologic significance that they may hold for the cancer sites studied.
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PMID:Early precursors of site-specific cancers in college men and women. 385 86

Physical and social characteristics recorded at college physical examination or reported at subsequent alumni questionnaire in 1962 or 1966 by 47,271 male former students from Harvard University and the University of Pennsylvania were reviewed for their relationship to risk for cancers of the kidney, bladder, prostate and testis. The records of 213 subjects who died with 1 of these cancers in a 16-50 year followup period and of 280 subjects who reported such a cancer by mail questionnaire in 1976 or 1977 were compared with those of 1,972 matched classmates who were known to be alive and cancer-free at the time subjects with cancer had died or were diagnosed. Students with a record of proteinuria at college physical examination experienced increased risk of kidney cancer. Higher levels of body weight during college were associated with elevated risks of kidney and bladder cancers; however, increased weight in 1962/1966 related only to kidney cancer. A history of cigarette smoking as reported by questionnaire in 1962/1966 predicted increased occurrence of bladder cancer. Students with a history of tonsillectomy at college entrance experienced increased risk of prostate cancer, and those who reported cancer history in 1 or both parents were at increased risk for testicular cancer. These and other findings are presented as clues deserving further exploration for any etiological significance they may hold for the cancer sites studied.
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PMID:Early precursors of urogenital cancers in former college men. 650 30

Transarterial renal embolization has been used in the management of renal cancer. We report on 9 patients who underwent selective and superselective renal arterial embolization for nonmalignant renal lesions. Embolization was done in 5 patients for hemorrhage owing to renal angiomas, renal artery, pseudoaneurysm, percutaneous renal biopsy and adult polycystic kidney disease, and in 2 patients with end stage renal disease because of massive proteinuria. Another chronic renal failure patient with severe hypertension was treated successfully with bilateral renal embolization. A postoperative renal arteriovenous fistula was treated successfully by catheter vaso-occlusion. Renal embolization may be a suitable alternative to surgery in poor operative risk patients and for technically difficult benign lesions. Renal infection is a contraindication to embolization.
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PMID:Percutaneous vaso-occlusion for nonmalignant renal lesions. 684 8

We measured the thickness of the glomerular basement membrane (GBM) in 48 rheumatoid arthritis (RA) patients with proteinuria and/or hematuria and studied its relationship to clinical features of RA. Ten cases with minor glomerular abnormalities, renal cancer, donor of renal transplantation, were studied as controls. Secondary glomerular diseases and hereditary thin basement membrane disease (TBMD) were excluded. Mean GBM thickness was 289 +/- 74 nm (mean +/- SD) in RA patients, which was significantly thinner than that of control group (342 +/- 38 nm) (p < 0.01). Mean GBM thickness were 276 +/- 72 nm and 336 +/- 68 nm in RA patients with and without gold sodium thiomalate (GST) treatment, respectively (p < 0.05). Mean GBM thickness of RA patients without GST and controls were not different statistically, but RA patients with GST had significantly thinner GBM, compared with controls (p < 0.01). The mean thickness of GBM were also 274 +/- 69 nm and 344 +/- 72 nm in RA patients with and without hematuria, respectively (p < 0.01). According to these results, we suspect that the thinning of GBM in RA patients may be related to GST treatment.
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PMID:An ultrastructural study of glomerular basement membrane in rheumatoid arthritis patients with urinary abnormalities. 755 19

Obesity, which has reached epidemic proportions in the United States and other western countries, may be complicated by hypertension, an increased incidence of renal cancer or proteinuria. Patients with obesity-associated proteinuria show focal glomerulosclerosis and glomerulomegaly on biopsy, usually have minimal clinical edema and relatively normal levels of serum albumin, cholesterol and blood pressure, and can progress to end-stage renal disease. Severe obesity may also be an additive risk factor in patients with preexisting nephropathy or reduced renal mass. The pathophysiology of obesity-associated proteinuria is unclear but may include hyperfiltration, increased renal venous pressure, glomerular hypertrophy, hyperlipidemia and increased synthesis of vasoactive and fibrogenic substances, including angiotensin II, insulin, leptin and transforming growth factor-beta1. These substances may individually or interactively affect glomerular hyperfiltration, mesangial cell hypertrophy and matrix production, and the production of collagen, fibronectin, transforming growth factor-beta and other fibrogenic mediators of change. Although angiotensin-converting enzyme inhibition has proven to have an impact, perhaps temporarily, on obesity-associated proteinuria in humans, weight reduction early in the course of the disease would appear the most important therapeutic approach.
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PMID:Obesity and renal disease. 1198 Dec 64

Angiogenesis is important in the growth and progression of solid tumours. The main pro-angiogenic factor, namely vascular endothelial growth factor (VEGF), also known as vascular permeability factor, is a potent angiogenic cytokine that induces mitosis and also regulates the permeability of endothelial cells. The soluble isoform of VEGF is a dimeric glycoprotein of 36-46 kDa, induced by hypoxia and oncogenic mutation and it binds to two specific tyrosine-kinase receptors: VEGF-1 (flt-1) and VEGF-2 (KDR/flk1). An increase in VEGF expression in tumour tissue or some blood compartments (i.e. serum or plasma) has been found in solid and haematological malignancies of various origins and is associated with metastasis formation and poor prognosis. Bevacizumab, a recombinant humanised monoclonal antibody developed against VEGF, binds to soluble VEGF, preventing receptor binding and inhibiting endothelial cell proliferation and vessel formation. Pre-clinical and clinical studies have shown that bevacizumab alone or in combination with a cytotoxic agent decreases tumour growth and increases median survival time and time to tumour progression. Bevacizumab is the first anti-angiogenetic treatment approved by the American Food and Drug Administration in the first-line treatment of metastatic colorectal cancer. It has shown preliminary evidence of efficacy for breast, non-small-cell lung, pancreatic, prostate, head and neck and renal cancer as well as haematological malignancies. Common toxicities associated with bevacizumab include hypertension, proteinuria, bleeding episodes and thrombotic events. This review summarises the critical role of VEGF and discusses the data available on bevacizumab, from the humanisation of its parent murine monoclonal antibody (mAb) A.4.6.1 to its use in cancer clinical trials.
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PMID:Vascular endothelial growth factor (VEGF) as a target of bevacizumab in cancer: from the biology to the clinic. 1684 97

Sirolimus is a novel immunosuppressant with potent antiproliferative actions through its ability to inhibit the raptor-containing mammalian target of rapamycin protein kinase. Sirolimus represents a major therapeutic advance in the prevention of acute renal allograft rejection and chronic allograft nephropathy. Its role in the therapy of glomerulonephritis, autoimmunity, cystic renal diseases and renal cancer is under investigation. Because sirolimus does not share the vasomotor renal adverse effects exhibited by calcineurin inhibitors, it has been designated a 'non-nephrotoxic drug'. However, clinical reports suggest that, under some circumstances, sirolimus is associated with proteinuria and acute renal dysfunction. A common risk factor appears to be presence of pre-existing chronic renal damage. The mechanisms of sirolimus-associated proteinuria are multifactorial and may be due to an increase in glomerular capillary pressure following calcineurin inhibitor withdrawal. It has also been suggested that sirolimus directly causes increased glomerular permeability/injury, but evidence for this mechanism is currently inconclusive. The acute renal dysfunction associated with sirolimus (such as in delayed graft function) may be due to suppression of compensatory renal cell proliferation and survival/repair processes. Although these adverse effects occur in some patients, their occurrence could be minimised by knowledge of the molecular effects of sirolimus on the kidney, the use of sirolimus in appropriate patient populations, close monitoring of proteinuria and renal function, use of angiotensin-converting enzyme inhibitors or angiotensin II receptor blockers if proteinuria occurs and withdrawal if needed. Further long-term analysis of renal allograft studies using sirolimus as de novo immunosuppression along with clinical and laboratory studies will refine these issues in the future.
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PMID:Sirolimus-associated proteinuria and renal dysfunction. 1714 61

A 32 year-old man presented with sinusitis, proteinuria, mononeuritis multiplex, very increased acute phase proteins. Anti-PR3 ANCA were detected and Wegener's granulomatosis (WG) was diagnosed. As abdominal tomodensitometry detected a tumoral process of the left kidney, a paraneoplastic vasculitis associated with a renal cancer was suspected. Biopsy of the mass showed fibrosis, inflammatory infiltrates and necrotizing granulomas. No malignant cells were detected. The outcome was favourable after administration of methylprednisolone and cyclophosphamide. Characteristics of the nine previously reported renal inflammatory pseudotumors associated with WG are discussed.
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PMID:Wegener's granulomatosis masquerading as a renal cancer: a case report and review of the literature. 1718 31

MicroRNAs (miRNAs) are noncoding, single-stranded RNA molecules that have important roles in a number of physiological and pathological processes. Previous studies have proved that miRNAs targeting ZEB1 and ZEB2 may repress epithelial-to-mesenchymal transition. In this work, we studied the intrarenal expression of miR-200 family, miR-205 and miR-192 in patients with immunoglobulin A (IgA) nephropathy. We studied 43 patients with biopsy-proven IgA nephropathy (IgA group). The intrarenal expression of miRNAs was quantified and compared with that of 15 patients with noninflammatory glomerulosclerosis (GS group) and 20 patients with nephrectomy for kidney cancer as controls (CTL group). The level of intrarenal miR-200c was downregulated, whereas the levels of intrarenal miR-141, miR-205 and miR-192 were upregulated in IgA but not GS group. Proteinuria significantly correlated with the intrarenal expression of miR-200c (r=-0.324, P=0.011) and glomerular filtration rate (GFR) significantly correlated with the intrarenal expression of miR-205 (r=-0.280, P=0.030). The degree of tubulointerstitial scarring correlated with miR-205 expression (r=0.389, P=0.021), whereas glomerulosclerosis correlated with miR-192 expression (r=-0.311, P=0.045). The rate of GFR decline significantly correlated with the intrarenal expression of miR-192 (r=0.373, P=0.015). The intrarenal expression of E-cadherin significantly correlated with the intrarenal expression of miR-200c (r=0.392, P=0.002). The results show that intrarenal expression of miR-200c, miR-141, miR-205 and miR-192 was diversely regulated and correlated with disease severity and progression in patients with IgA nephropathy. These miRNA species may be important in the pathogenesis and progression of IgA nephropathy.
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PMID:Intrarenal expression of microRNAs in patients with IgA nephropathy. 1990 13


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