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 48-year-old male was referred to our university hospital for severe azotemia with muscle cramp. He had been taking Chinese herbs as a traditional medicine to reduce hyperuricemia for about 9 months. Urinalysis showed trace proteinuria and hematuria without any casts. Renal glucosuria was also observed. In addition to azotemia, hyperchloremic metabolic acidosis and severe anemia were revealed. Hemodialysis was conducted and his general condition improved. A renal biopsy specimen revealed severe interstitial fibrosis and tubular atrophy with cellular degeneration. No remarkable glomerular changes were observed except for wrinkling of the basement membrane in a few glomeruli. Aristolochic acid was detected in the Chinese herbs, leading to the diagnosis of aristolochic acid nephropathy (AAN). His renal dysfunction was considered to be irreversible and he underwent maintenance hemodialysis. In Japan, AAN or Chinese herbs nephropathy decreased after an outbreak from 1995 to 2000. The public should be warned again that Chinese herbs, which are not permitted by the Japanese government, may contain aristolochic acid.
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PMID:[Case of traditional herbal medicine-induced aristolochic acid nephropathy developing to end-stage renal failure]. 1597 92

Gestational hypertension is differentiated into higher and lower risk by the presence or absence of proteinuria. We asked if hyperuricemia, a common finding in pregnancy hypertension, might also be an indicator of increased risk. We examined fetal outcome data from 972 pregnancies collected from 1997 to 2002 in a nested case-control study. Participants were nulliparous with no known medical complications. The frequency of preterm birth, the duration of pregnancy, frequency of small-for-gestational-age infants, and birth weight centile were determined for pregnancies assigned to 8 categories by the presence or absence of combinations of hypertension, hyperuricemia, and proteinuria. In women with gestational hypertension, hyperuricemia was associated with shorter gestations and smaller birth weight centiles and increased risk of preterm birth and small-for-gestational-age infants. Hyperuricemia increased the risk of these outcomes in the presence or absence of proteinuria. Risk was also increased in a small group of women with hyperuricemia and proteinuria without hypertension. Women with only hypertension and hyperuricemia have similar or greater risk as women with only hypertension and proteinuria. Those with hypertension, proteinuria, and hyperuricemia have greater risk than those with hypertension and proteinuria alone. The risk of these outcomes increased with increasing uric acid. Hyperuricemia is at least as effective as proteinuria at identifying gestational hypertensive pregnancies at increased risk. Uric acid should be reexamined for clinical and research utility.
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PMID:Uric acid is as important as proteinuria in identifying fetal risk in women with gestational hypertension. 1624 74

Nephropathy is one of the frequent sequelae of hypertension. Arterial hypertension causes both arterial and capillary changes in the kidneys as well as development of interstitial fibrosis. Systemic or intraglomerular pressure increase leads to albuminuria and proteinuria, which in turn contributes to further damage of the kidneys. Impairment of the kidneys due to hypertension can ultimately result in terminal renal insufficiency necessitating dialysis. Metabolic factors such as hyperlipidemia, hyperuricemia, hyperhomocysteinemia, and insulin resistance can aggravate renal lesions. Effective lowering of blood pressure in conjunction with management of the metabolic risk factors is decisive for prevention of chronic kidney disease, which in turn must be considered a factor involved in exacerbation of the hypertension.
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PMID:[Sequelae of hypertenson: kidney disease]. 1647 Mar 57

A 12-year-old girl, who had been diagnosed as having Cockayne syndrome (CS), was admitted for emaciation and dehydration. On admission the patient had mild chronic renal failure (glomerular filtration rate: GFR 50 mL/min) and hyperuricemia. After rehydration, allopurinol was commenced for her hyperuricemia. Then, her renal function rapidly deteriorated (GFR 20 mL/min) with enhancement of proximal tubular dysfunction and hypertension. A renal biopsy showed that the patient had acute tubulointerstitial nephritis (ATIN). Based on this diagnosis, allopurinol was stopped and prednisolone was started (2 mg/kg per day), following which the renal tubular function improved. However, the proteinuria intensified to become nephrotic syndrome. After 1 month the patient developed a gastric ulcer. Famotidine was commenced but GFR deteriorated and renal proximal tubular dysfunction re-occurred. The renal pathology was evaluated by referring to the previous reports of renal pathology in CS. It is suggested that rapid deterioration of the renal function in CS patients might be the result of ATIN. In addition, the present nephrotic syndrome seemed to be accompanied by ATIN, as in other reports.
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PMID:Cockayne syndrome with recurrent acute tubulointerstitial nephritis. 1704 Feb 91

Cardiovascular disease is the leading cause of death following renal transplantation, accounting for 40% to 55% of all deaths. An analysis in our center showed a 15% mortality in a cohort of renal transplant recipients followed for an average of 10 years. Various contributing risk factors of cardiovascular diseases in transplant recipients such as tobacco use, hypertension, hyperlipidemia, hereditary risk, diabetes, physical inactivity, obesity, dialysis duration, hyperuricemia, proteinuria, hyperhomocysteinemia, hyperparathyroidism, anemia; C-reactive protein level, and immunosuppressive regimen as well as some rare risk factors, such as cytomegalovirus infection, were evaluated in a population of 1200 kidney transplant recipients. Also we introduced methods for early detection, monitoring, and follow-up of proven risk factors of cardiovascular disease.
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PMID:How to decrease cardiovascular mortality in renal transplant recipients. 1711 56

The aim of this project was to study the risk of developing hypertension over a 6-year follow-up in normotensive men with baseline hyperuricemia (serum uric acid >7.0 mg/dL) but without diabetes/glucose intolerance or metabolic syndrome. We analyzed the data on men without metabolic syndrome or hypertension at baseline from the Multiple Risk Factor Intervention Trial. These men (n=3073; age: 35 to 57 years) were followed for an average of 6 years by annual examinations. Follow-up blood pressure among those with baseline was consistently higher than among those with normal serum uric acid concentration. We used Cox regression models for adjustment for the effects of serum creatinine, body mass index, age, blood pressure, proteinuria, serum cholesterol and triglycerides, alcohol and tobacco use, risk factor interventions, and use of diuretics. In these models, normotensive men with baseline hyperuricemia had an 80% excess risk for incident hypertension (hazard ratio: 1.81; 95% CI: 1.59 to 2.07) compared with those who did not. Each unit increase in serum uric acid was associated with a 9% increase in the risk for incident hypertension (hazard ratio: 1.09; 95% CI: 1.02 to 1.17). We conclude that the hyperuricemia-hypertension risk relationship is present among normotensive middle-aged men without diabetes/glucose intolerance or metabolic syndrome.
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PMID:Hyperuricemia and incidence of hypertension among men without metabolic syndrome. 1719 Aug 77

Chronic lead nephropathy occurs as a result of years of lead exposure. Nowadays, with the induction of high standards for industrial hygiene, symptomatic lead intoxication has become extremely rare. We report a case of chronic lead nephropathy in a 59-year-old man who worked in a battery-recycling unit and was diagnosed with plumbism during a regular health screening few years ago. The diagnosis was suggested by the following findings: serum creatinine 160 microg/L, creatinine clearance 46 ml/min, daily urine protein excretion 0.1 g, uric acid 9.7 mg/dl, blood lead 9.2 microg/dl, and a urinary excretion of 850 microg lead/72 h after a mobilisation test by a Na2-Ca-EDTA chelating agent. Renal ultrasound showed bilateral borderline small kidneys. The kidney biopsy revealed moderate focal atrophy, loss of proximal tubules, and prominent interstitial fibrosis. The patient was prescribed angiotensin-converting-enzyme inhibitors to slow the progression of renal insufficiency and control the blood pressure. Hyperuricemia was also treated and controlled. During the regular follow-up, renal function remained stable with no proteinuria. A high index of suspicion for lead intoxication in chronic kidney disease patients should be practiced, especially in patients with hyperuricemia. Chelation of lead urinary excretion is helpful in the diagnosis of this disease.
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PMID:Chronic lead poisoning: a "forgotten" cause of renal disease. 1723 97

Autosomal dominant medullary cystic kidney disease type 2 (MCKD2) is a tubulo-in terstitial nephropathy that causes renal salt wasting, hyperuricemia, gout, and end-stage renal failure in the fifth decade of life. This disorder was described to have an age of onset between the age of 20-30 years or even later. Mutations in the Uromodulin (UMOD) gene were published in patients with familial juvenile hyperuricemic nephropathy (FJHN) and MCKD2. Clinical data and blood samples of 16 affected individuals from 11 different kindreds were collected. Mutational analysis of the UMOD gene was performed by exon polymerase chain reaction (PCR) and direct sequencing. We found the heterozygous C744G (Cys248Trp) mutation, which was originally published by our group, in an additional four kindreds from Europe and Turkey. Age of onset ranged from 3 years to 39 years. The phenotype showed a variety of symptoms such as urinary concentration defect, vesicoureteral reflux, urinary tract infections, hyperuricemia, hypertension, proteinuria, and renal hypoplasia. Haplotype analysis showed cosegragation with the phenotype in all eight affected individuals indicating that the C744G mutation may be due to a founder effect. Moreover, we describe a novel T229G (Cys77Gly) mutation in two affecteds of one kindred. Three of the affected individuals were younger than 10 years at the onset of MCKD2/FJHN. Symptoms include recurrent urinary tract infections compatible with the published phenotype of the Umod knockout mouse model. This emphasizes that MCKD2 is not just a disease of the young adult but is also relevant for children.
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PMID:The Uromodulin C744G mutation causes MCKD2 and FJHN in children and adults and may be due to a possible founder effect. 1724 95

Here, we report on a boy with acute tubulointerstitial nephritis (ATIN), who developed it following ingestion of Chlorella tablets as a food supplement. He was incidentally detected to have glucosuria, proteinuria, and leukocyturia during school mass screening. He had had a history of ingestion of Chlorella tablets for 3 months. Laboratory studies showed anemia, increased levels of creatinine, decreased glomerular filtration rate (GFR), hypokalemia, hypo-uricemia, hypophosphatemia, hypergammaglobulinemia, proteinuria, leukocyturia, and glucosuria. ATIN was diagnosed by renal biopsy. The patient's renal function improved after initiation of corticosteroid therapy and discontinuation of Chlorella for 6 months. Chlorella may be a causative allergen inducing tubulointerstitial injury in kidney.
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PMID:Acute tubulointerstitial nephritis following ingestion of Chlorella tablets. 1727 60

Hyperuricemia in hypertensive subjects has been considered one of risk factors of cardiovascular diseases. We investigated the status of uric acid management in 799 hypertensive subjects (432 females and 367 males; mean age 70.9 years) managed by 43 doctors (19 cardiologists and 24 noncardiologists; 25 private practice doctors and 18 hospital doctors). The serum uric acid level was available in 85.7% of the patients. This availability was equivalent regardless of facility size, and more cardiologists than noncardiologists monitored this information. The prevalence of hyperuricemia was 17.5% and was higher in men and in patients with high triglyceridemia, left ventricular hypertrophy, renal dysfunction, proteinuria, and smokers, but was not higher in subjects with chronic heart failure, diabetes mellitus, and those with prescriptions for diuretics and beta-blockers. The average serum uric acid level was higher in men and patients with chronic heart failure, renal dysfunction, high triglyceridemia, low high-density cholesterolemia, smokers, and subjects prescribed beta-blockers. Fifty percent of hyperuricemic patients were medicated, and 48.6% of them cleared the uric acid target level (6 mg/dL). No differences were observed in the treatment rate or the achievement rate of the target between genders, concurrent diseases, and physician specialties. Although doctors, especially cardiologists, have a high concern for the serum uric acid level, they do not intervene intensively, and specific treatment for individual patterns is not routinely given. Thus, more attention to uric acid management is necessary in hypertensive subjects to prevent cardiovascular diseases.
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PMID:Status of uric acid management in hypertensive subjects. 1766 59


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