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)

We report five patients who have taken inorganic germanium preparations over a prolonged period. In all cases, the renal function deteriorated with no proteinuria or hematuria. Histological examination of the kidneys showed widespread tubular degeneration and interstitial fibrosis with minor glomerular abnormalities. Most patients had gastrointestinal symptoms such as vomiting, anorexia and weight loss; one patient had peripheral neuropathy and myopathy. A considerable amount of germanium was detected in the hair or nails of these patients. These cases clearly show that abuse of inorganic germanium compounds can induce renal damage with various extrarenal manifestations.
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PMID:Germanium poisoning: clinical symptoms and renal damage caused by long-term intake of germanium. 165 Aug 57

Microscopic polyarteritis may involve medium-sized and small blood vessels as well as arterioles, venules and capillaries. We have compared the clinical and laboratory features in patients with microscopic polyarteritis and medium vessel involvement, with the features found in patients with polyarteritis nodosa affecting medium vessels alone. In a 9-year period, 21 patients presented to our hospital with a form of polyarteritis. Seven had microscopic polyarteritis demonstrated histologically (6/7, 86%) and associated with dysmorphic urinary red cells (7/7, 100%), as well as medium vessel vasculitis demonstrated histologically (7/7) or by angiography (1/7, 14%). Five patients had polyarteritis nodosa with medium vessel vasculitis demonstrated histologically (3/5, 60%) or by angiography (2/5, 40%); and no evidence of a glomerular vasculitis on biopsy (2/7, 29%) or in the urinary sediment (0/7, 0%). The remaining 9 patients had microscopic polyarteritis but medium vessel involvement was not excluded by angiography. All patients with microscopic polyarteritis and medium vessel involvement had glomerular hematuria (> 100,000 glomerular RBC/ml), proteinuria > 0.5 g/24 hours), and an elevated serum creatinine (0.166 to 0.811 mmol/l). Other symptoms included fever (6/7, 86%), night sweats (5/7, 71%), gastrointestinal bleeding (4/7, 57%), proximal myopathy (3/7, 43%) and peripheral neuropathy (3/7, 43%). One patient (1/7, 14%) had hypertension. Anemia (6/7, 86%), a raised ESR (6/7, 86%), thrombocytosis (6/7, 86%), hypoalbuminemia (6/7, 86%) and abnormal liver function tests (6/7, 86%) were common. Two patients (29%) had an eosinophilia. All 5 individuals who were tested for ANCA were positive (2cANCA, 2pANCA and one pattern not described). In contrast, in patients with polyarteritis nodosa and medium vessel involvement alone, an elevated ESR was common (4/5, 80%) but fever (1/5, 20%), night sweats (0/5, 0%), proximal myopathy (1/5, 20%) and peripheral neuropathy (1/5, 20%) were seen infrequently; hypertension (1/5, 20%) and eosinophilia (1/5, 20%) were also uncommon; and ANCA were not demonstrated (0/3, 0%). Medium-sized vessel involvement is common in patients with microscopic polyarteristis, and these patients are more likely to have renal involvement and systemic symptoms, and be ANCA-positive, than patients with polyarteritis nodosa alone. Gastrointestinal symptoms are often seen in both groups.
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PMID:Classical polyarteritis nodosa and microscopic polyarteritis with medium vessel involvement--a comparison of the clinical and laboratory features. 910 64

Rosuvastatin (Crestor), an HMG-CoA reductase inhibitor (statin), has a favorable pharmacologic profile, including its selective uptake by hepatic cells, hydrophilic nature, and lack of metabolism by cytochrome p450 (CYP) 3A4 isoenzyme. This last property means that the potential for CYP3A4-mediated drug interactions and, as a consequence, adverse events is low in those requiring concomitant therapy with a statin and agents metabolized by CYP3A4. In a broad spectrum of adult patients with dyslipidemias, oral rosuvastatin 5-40 mg once daily effectively and rapidly improved lipid profiles in several large, randomized, mainly double-blind, multicenter trials of up to 52 weeks' duration. After 12 weeks' treatment, rosuvastatin was significantly (all p < 0.05) more effective at milligram equivalent dosages than atorvastatin, pravastatin, and simvastatin in improving the overall lipid profiles of patients with hypercholesterolemia (intent-to-treat analyses). Moreover, overall a significantly (all p < 0.001) higher proportion of patients achieved National Cholesterol Education Program (NCEP) Adult Treatment Panel (ATP) III low-density lipoprotein-cholesterol (LDL-C) goals with rosuvastatin 10 mg/day than with therapeutic starting dosages of these other statins after 12 weeks' treatment in pooled analyses. Rosuvastatin treatment for up to 52 weeks was generally well tolerated in patients with dyslipidemias in clinical trials. The most commonly reported treatment-related adverse events were myalgia, constipation, asthenia, abdominal pain, and nausea; these were mostly transient and mild. The incidence of proteinuria or microscopic hematuria with rosuvastatin 10 or 20 mg/day was <1% versus <1.5% with rosuvastatin 40 mg/day; these events were mostly transient and not associated with acute or progressive deterioration in renal function at recommended dosages. Importantly, very few patients experienced elevations in serum creatine phosphokinase (CPK) levels of over [corrected] 10-fold the upper limit of normal (0.2-0.4% of patients) or treatment-related myopathy (<or=0.1%) [i.e. muscle aches or weakness plus the same elevated serum CPK levels] at dosages of 5-40 mg/day. In conclusion, rosuvastatin treatment effectively and rapidly improves the lipid profile in patients with a broad spectrum of dyslipidemias. In those with hypercholesterolemia (including high-risk patients), rosuvastatin was more efficacious than and generally as well tolerated as atorvastatin, simvastatin, and pravastatin, with significantly more rosuvastatin recipients achieving their NCEP ATP III target LDL-C levels. Thus, rosuvastatin has emerged as a valuable choice for first-line treatment in the management of low- to high-risk patients requiring lipid-lowering drug therapy.
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PMID:Rosuvastatin: a review of its use in the management of dyslipidemia. 1504 23

The safety and tolerability of rosuvastatin were assessed (as of August 2003) using data from 12,400 patients who received 5 to 40 mg of rosuvastatin in a multinational phase II/III program, which represented 12,212 patient-years of continuous exposure to rosuvastatin. An integrated database was used to examine adverse events and laboratory data. In placebo-controlled trials, adverse events, irrespective of causality assessment, occurred in 57.4% of patients who received 5 to 40 mg of rosuvastatin (n = 744) and 56.8% of patients who received placebo (n = 382). In fixed-dose trials with comparator statins, 5 to 40 mg of rosuvastatin showed an adverse event profile similar to those for 10 to 80 mg of atorvastatin, 10 to 80 mg of simvastatin, and 10 to 40 mg of pravastatin. Clinically significant elevations in alanine aminotransferase (>3 times the upper limit of normal) and creatine kinase (>10 times the upper limit of normal) were uncommon (<or=0.2%) in the groups that received rosuvastatin and comparator statins. Myopathy (creatine kinase >10 times the upper limit of normal with muscle symptoms) that was possibly related to treatment occurred in <or=0.03% of patients who took rosuvastatin at doses <or=40 mg. A positive finding of proteinuria with dipstick testing at rosuvastatin doses <or=40 mg was comparable to that seen with other statins, and the development of proteinuria was not predictive of acute or progressive renal disease. No deaths in the program were attributed to rosuvastatin, and no rhabdomyolysis occurred in patients who received 5 to 40 mg of rosuvastatin. Rosuvastatin was well tolerated by a broad range of patients who had dyslipidemia, and its safety profile was similar to those of the comparator statins investigated in this extensive clinical program.
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PMID:Safety of rosuvastatin. 1546 70

Cardiovascular disease is the leading cause of death in the US and other industrialised societies. Rosuvastatin, a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor, is the most efficacious lipid-lowering agent of the statin class. New guidelines and recent evidence-based studies confirm the benefit of intensive reduction of low-density lipoprotein cholesterol in terms of cardiovascular risk reduction. Both naturally occurring and synthetic statins have demonstrated significant lowering of low-density lipoprotein cholesterol, the primary target of cholesterol-lowering therapy. Rosuvastatin, specifically, is a synthetic statin shown to lower low-density lipoprotein cholesterol, total cholesterol, apolipoprotein B, non-high-density lipoprotein cholesterol and triglycerides, in addition to increasing high-density lipoprotein cholesterol. Compared with other statins, there is a similar low risk of serious muscle damage (myopathy and rhabdomyolysis), and no consistent pattern of renal failure or renal injury, despite mild transient tubular proteinuria, as seen with all statins. Therefore, rosuvastatin offers an effective alternative in the clinical management of hyperlipidaemia, while awaiting the results of ongoing cardiovascular risk reduction trials.
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PMID:Rosuvastatin: a risk-benefit assessment for intensive lipid lowering. 1614 9

Safety has become a central issue in the management of dyslipidemia with statins. A review of New Drug Applications (NDAs) and the US Food and Drug Administration (FDA) Web site was conducted for all 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, or statins, with a major focus on cerivastatin and rosuvastatin. The findings provide insight into the incidence of adverse events for this class of drugs and support the significant benefits of statins relative to associated risks. These data delineate the nature of statin associated liver, muscle, and renal adverse events. Although transaminase levels increase in a dose-related fashion with statins, a definitive correlation between statin therapy and hepatotoxicity is not supported by statin NDA data. Statin-induced myopathy is a relatively rare event (1 in 1,000) and rhabdomyolysis is even rarer (1 in 10,000). The cerivastatin NDA, along with its supplementary NDA, was the first to demonstrate a clear statin dose-response relation with myopathy and a threshold effect above which myotoxicity increases significantly. Proteinuria was identified as a consequence of statin therapy with data from the rosuvastatin NDA, and subsequent analysis suggests a class effect that is dose related but transient. Studies in cell culture suggest the mechanism is a pharmacologic effect on the proximal renal tubule. The available evidence suggests no clear renal toxicity with currently approved statins, because no declines in renal function or glomerular filtration rate have been documented over time. Overall, currently marketed statins have a very favorable benefit-to-risk relation with respect to liver, muscle, and renal issues.
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PMID:Statin safety: lessons from new drug applications for marketed statins. 1658 28

A systematic review of cohort studies, randomized trials, voluntary notifications to national regulatory authorities, and published case reports was undertaken to assess the incidence and characteristics of adverse effects in patients treated with 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, or statins. For statins other than cerivastatin, the incidence of rhabdomyolysis in 2 cohort studies was 3.4 (1.6 to 6.5) per 100,000 person-years, an estimate supported by data from 20 randomized controlled trials. Case fatality was 10%. Incidence was about 10 times greater when gemfibrozil was used in combination with statins. Incidence was higher (4.2 per 100,000 person-years) with lovastatin, simvastatin, or atorvastatin (which are oxidized by cytochrome P450 3A4 [CYP3A4], which is inhibited by many drugs) than pravastatin or fluvastatin (which are not oxidized by CYP3A4). In persons taking simvastatin, lovastatin, or atorvastatin, 60% of cases involved drugs known to inhibit CYP3A4 (especially erythromycin and azole antifungals), and 19% involved fibrates, principally gemfibrozil. The incidence of myopathy in patients treated with statins, estimated from cohort studies supported by randomized trials, was 11 per 100,000 person-years. For liver disease, randomized trials reported fewer hepatobiliary disorders in patients allocated statins than in those allocated placebo. The notification rate of liver failure to regulatory authorities was about 1 per million person-years of statin use. Randomized trials show no excess of renal disease or proteinuria in statin-allocated participants, and the decline in glomerular filtration rate was smaller with statins than with placebo. Evidence from 4 cohort studies and case reports suggests that statins cause peripheral neuropathy, but the attributable risk is small (12 per 100,000 person-years). No change in cognitive function was found in randomized trials of statins in elderly patients.
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PMID:Statin safety: a systematic review. 1658 29

Strenuous exercise can lead to the occurrence of various abnormalities in the urine. Hematuria and proteinuria are those most frequently described. Other less common possibilities are pigmenturia like hemoglobinuria and myoglobinuria. These urine abnormalities are found not only in sportsmen/women or soldiers, but also in percussionists. Other possible causes are hereditary metabolic myopathy and the use of drugs or medication. Exertion-related urine abnormalities occur frequently and are usually benign. Any abnormalities should disappear after a period of 24-72 h of rest. Exertional rhabdomyolysis only appears 24-48 h after exercise. This condition rarely leads to acute renal failure and the need for (temporary) renal replacement therapy. When exertion-related urine abnormalities do not disappear spontaneously following a period of rest, further investigation as to the cause, e.g. renal or urological disease, should be started. Prevention of exertion-related urine abnormalities is possible by ensuring an adequate fluid intake during and following exertion.
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PMID:[Exertion-related abnormalities in the urine]. 1676 89

Statins are the most frequently used lipid-lowering drugs in all cardiovascular disease. It has been postulated that also patients with renal failure and end-stage renal disease (ESRD) may benefit from statin therapy. Moreover, statins may exhibit additional inhibitory effects on the atherogenesis, such as a modulation of the immune system as triggered by oxidatively modified LDL and a reduction of the inflammatory marker C-reactive protein (CRP). Statins reduce inflammation, cell proliferation, which leads to a reduction in cellular damage. Those effects are probably independent of cholesterol levels. Limited data suggest that HMG-CoA reductase inhibitors (statins) may slow loss of renal function in individuals with chronic renal insufficiency. It is concluded on the basis of the CARE trial that pravastatin may slow renal function loss in individuals with moderate to severe kidney disease, especially those with proteinuria. Similar data were obtained from recently published HPS trial with simvastatin. These findings require confirmation by a large randomized trial conducted specifically in people with chronic renal insufficiency. Statins vary in their pharmacological profiles, leading to distinct levels of systemic exposure and capacities to penetrate skeletal myocytes. Pharmacokinetic interactions with certain agents increase the likelihood of statin-induced myopathy and, in exceedingly rare instances, potentially fatal rhabdomyolysis with myoglobinuria and renal failure, therefore two statins have been suggested for renal failure patients. These are the ones that are not metabolised by the cytochrome P450 3A4 system--fluvastatin and pravastatin. The article summarizes the current therapeutic status of statin use in renal failure patients.
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PMID:[Statins in patients with renal failure--the current therapeutic status]. 1662 20

Cardiac ankyrin-repeated protein (CARP) was originally identified as a protein specifically expressed in cardiomyocytes, but has recently been found to be upregulated in some muscle diseases including muscular dystrophy and myopathy, suggesting that CARP may be induced in some pathologic conditions. In this study, we immunohistochemically analyzed 69 renal biopsy samples from patients with glomerular diseases and 2 individuals with normal kidney. We found that CARP was expressed in renal podocytes at a high level in 10 of 13 cases of crescentic glomerulonephritis, 7 of 19 cases of diabetic nephropathy, and 12 of 20 cases of lupus nephritis, although it was not expressed in endocapillary glomerulonephritis, minimal change disease, thin basement membrane disease, membranous glomerulonephritis, and normal kidney. Interestingly, in lupus nephritis, CARP expression tended to be induced in cases exhibiting nephrotic syndrome, but less so in cases without nephrotic syndrome, suggesting that CARP expression is correlated with the severity of proteinuria. Furthermore, we found that CARP was not expressed in membranous glomerulonephritis but evidently expressed in most cases of membranous lupus nephritis. Although membranous glomerulonephritis and membranous lupus nephritis are sometimes morphologically indistinguishable, it is suggested that their pathologic mechanisms differ. Therefore, we propose that examination of CARP expression is useful for precise differential diagnosis of membranous glomerulonephritis and membranous lupus nephritis.
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PMID:Upregulated expression of cardiac ankyrin-repeated protein in renal podocytes is associated with proteinuria severity in lupus nephritis. 1723 33


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