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)

The most serious complication of diabetes mellitus is clinical nephropathy. The development of persistent proteinuria (urinary excretion of more than 300 mg albumin/24 hours) implies an extremely high risk of early death. Renal failure is the most frequent cause of death but the mortality of cardiovascular diseases is also increased. Besides the link between albuminuria (nephropathy) and atherosclerosis in coronary arteries, albuminuria is also a predictor of microangiopathy in other organs than the kidneys. The annual incidence of proliferative retinopathy in early nephropathy is 10-15% compared to only 1% in patients without nephropathy. Also signs of cardiomyopathy have been demonstrated in early nephropathy. Further we have described markers of universal endothelial damage in these patients, and we hypothesize that albuminuria not only is a predictor of renal disease but also of widespread vascular disease. Long-term improvement of metabolic control by use of insulin infusion pumps and early antihypertensive treatment seem to stop the further progression of early diabetic nephropathy and to significantly improve the prognosis of clinical nephropathy.
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PMID:Diabetic retinopathy, nephropathy and neuropathy. Generalized vascular damage in insulin-dependent diabetic patients. 149 Jun 95

The association between proteinuria and congestive cardiac failure was investigated in patients with hypertensive heart disease, cardiomyopathy, rheumatic heart disease and cor pulmonale. In 33 such patients, proteinuria occurred before and after successful treatment of the cardiac failure. Overall there was a wide variation in the degree of proteinuria amongst the various groups and statistical analysis showed that the distribution of levels of proteinuria and the mean levels of proteinuria were statistically different between any two groups of patients, P = 0.05. Biopsy proven hypertensive nephrosclerosis was found to be a cause of heavy proteinuria which was in the nephrotic range in two such patients. Congestive cardiac failure due to hypertensive heart disease should be included in the differential diagnosis of massive proteinuria even in the absence of renal insufficiency.
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PMID:The pattern of proteinuria in congestive cardiac failure due to common heart diseases. 206 87

Literature data, reviewed by the author, are suggestive of the risk of acute and chronic intoxication for the humans exposed to cadmium. Cadmium poisoning can lead to rhinitis, nephropathy with typical proteinuria and osteomalacia. Investigators are specially interested in cadmium-related cardiomyopathy, symptomatic arterial hypertension, hepatic and prostatic disorders.
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PMID:[Cadmium-related pathology in man]. 306 52

Amyloidosis occurs in association with many diseases and can also be idiopathic. It is usually a systemic disease with variable presentations. The diagnosis should be suspected in patients with unexplained proteinuria, cardiomyopathy, congestive heart failure, peripheral neuropathy, carpal tunnel syndrome, macroglossia, or hepatosplenomegaly. Amyloidosis generally has a poor prognosis and responds poorly to therapy. Much needs to be learned about its pathogenesis and treatment possibilities.
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PMID:The many guises of amyloidosis. Clinical presentations and disease associations. 793 10

We undertook this study to determine the clinical, biologic, immunologic, and therapeutic factors associated with the prognoses of polyarteritis nodosa (PAN) and Churg-Strauss syndrome (CSS). Three hundred forty-two patients (260 with PAN, 82 with CSS) followed from 1980 to 1993 were included in a prospective study on prognostic factors. Two hundred eighty-eight of these patients were included in the prospective studies on PAN and CSS. Items to be considered for analysis were collected at the time of diagnosis, during the acute phase of the disease. A survival curve was plotted for each clinical and biologic symptom observed in PAN or CSS. Each treatment arm of the prospective therapeutic trials was also tested: 1) prednisone (CS) + oral cyclophosphamide (CYC) + plasma exchanges (PE) versus CS E, 2) CS + PE versus CS, 3) CS + oral CY versus CS + pulse CY, 4) CS + pulse CY + PE versus CS + pulse CY in severe PAN and CSS, and 5) PE + antiviral agents after short-term CS in hepatitis B virus-related PAN. Of the parameters thus evaluated, the following had significant prognostic value and were responsible for higher mortality: proteinuria > 1 g/d (p < 0.0001; relative risk [RR] 3.6), renal insufficiency with serum creatinine > 1.58 mg/DL (p < 0.02; RR 1.86), GI tract involvement (p < 0.008. RR 2.83 for surgery). Cardiomyopathy and CNS involvement were associated with a RR of mortality of 2.18 and 1.76, respectively; these were not statistically significant. Similar survival rates were obtained with the prospectively tested therapies. The five-factors score (FFS) we established considered the prognostic factors creatinemia, proteinuria, cardiomyopathy, GI tract involvement, and CNS signs. Multivariate analysis showed that proteinuria (due to vascular or glomerular disease) and GI tract involvement were independent prognostic factors. When FFS = 0 (none of the 5 prognostic factors present), mortality at 5 years was 11.9%; when FFS = 1 (1 of the 5 factors present), mortality was 25.9% (p < 0.005); when FFS > 2 (3 or more of the 5 factors present), mortality was 45.95% (p < 0.0001 between 0 and 2, p < 0.05 between 1 and 2). We conclude that an initial assessment of PAN or CSS severity enables outcome and mortality to be predicted. The FFS is a good predictor of death and can be used to help the clinician choose the most adequate treatment. Renal and GI signs are the most serious prognostic factors.
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PMID:Prognostic factors in polyarteritis nodosa and Churg-Strauss syndrome. A prospective study in 342 patients. 856 67

A point mutation in exon 6 of the alpha-galactosidase A gene (alpha-GAL A) was found in a Japanese hemizygous male without typical manifestations of Fabry disease other than renal involvement. This 45-year-old man developed moderate proteinuria and was diagnosed with Fabry disease on the basis of renal histologic findings and prominent decreases in alpha-GAL A activity in his plasma, urine, leukocytes, and skin fibroblasts. Determination of the cDNA sequence of his alpha-GAL A gene revealed substitution of a G to A in codon 301, resulting in a glutamine rather than an arginine residue. Our case is unique in that this patient only demonstrated renal manifestations while all other reported patients with atypical Fabry disease, including a case with the identical point mutation, present with a cardiomyopathy. Direct DNA sequencing of exon 6 and measurement of alpha-GAL A activity among the patient's family confirmed that the mutation was transmitted from his mother.
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PMID:Point mutation in the alpha-galactosidase A gene of atypical Fabry disease with only nephropathy. 873 59

Angiotensin I-converting enzyme (ACE) plays a pivotal role in cardiovascular homeostasis and by activating angiotensin I into angiotensin II and inactivating bradykinin. These two peptides play antagonistic roles on the cardiovascular system by regulating vascular tone and vascular smooth muscle cell proliferation. Identification of the ACE gene as a genetic marker for various forms of cardiovascular disease is a recent result of the progress made in molecular biology and genetics. The insertion/deletion (ID) polymorphism of the ACE gene defined by the presence or absence of the 287 base pair Alu sequence situated in intron 16 has been investigated as a possible genetic marker for a variety of cardiovascular disease including myocardial infarction, essential hypertension, cardiomyopathy, and diabetic vascular complications. This paper reviews prior reports and briefly describes our recent study on the association of the ACE I/D polymorphism and antiproteinuric effect of ACE inhibitors in patients with proteinuria.
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PMID:Angiotensin I-converting enzyme insertion/deletion polymorphism: potential significance in nephrology. 874 24

The morbidity and lethality of AL amyloidosis is caused by the deposition of lg light chains as fibrillar amyloid protein in vital organs, disrupting their function, and not by the generally low burden of clonal plasma cells that produce the paraproteins. Survival of patients with AL amyloidosis is no more than 1 to 2 years from the time of diagnosis with current management approaches. Clearly, more effective therapies are needed for this rapidly lethal disease. Five patients were treated with dose-intensive melphalan and blood stem cell support and followed for a period of 1 year. Patients were diagnosed with AL amyloidosis by tissue biopsy and categorized by performance status and organ involvement. Their plasma cell dyscrasias were evaluated with immunofixation electrophoresis of serum and urine specimens, quantitative serum lgs, and immunohistochemical staining of bone marrow biopsy specimens. After treatment with dose-intensive intravenous melphalan followed by infusion of autologous growth-factor-mobilized blood stem cells, clinical evaluations and plasma cell studies were repeated at 3 and 12 months. Three men and 2 women aged 38 to 53 years were treated. Median performance status (SWOG) was 2 (1 to 3), and clinical presentations included nephrotic syndrome (n = 1), symptomatic cardiomyopathy (n = 1), gastrointestinal involvement with polyneuropathy (n = 2), and hepatomegaly (n = 1). With a median follow-up of 13 months (12 to 17 months), all five patients are well and have shown stable or improved performance status and clinical remission of organ-related dysfunction, including a 50% reduction in daily proteinuria with no change in creatinine, reversal of symptoms of cardiomyopathy and reductions of posterior wall and septal thickening, reversal of polyneuropathy and gastric atony, and resolution of hepatomegaly by computed tomographic scan. In 3 of the 5 patients (60%) at 12 months after treatment, plasma cell dyscrasias could not be detected. Dose-intensive chemotherapy with intravenous melphalan and growth-factor-mobilized blood stem cell support is feasible therapy for patients with AL amyloidosis, even when there is clinical evidence of cardiac involvement. At least some patients with AL amyloidosis achieve complete remission of their plasma cell dyscrasia, improvement in performance status, and clinical remission of organ-specific disease after this form of treatment.
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PMID:Dose-intensive melphalan with blood stem cell support for the treatment of AL amyloidosis: one-year follow-up in five patients. 883 79

We have studied 46 patients, 30 men and 16 women, with type 2 (non-insulin-dependent) diabetes in a follow-up period of 6-52 months (mean 30 months). The patients were consecutively entered in the study from the out-patient diabetic clinic. None had urinary tract infections nor proteinuria at entry. Investigations were done every 3 months during the first year and after that every 6 months. At entry 16 patients (35%) had microalbuminuria and a further 16 patients developed microalbuminuria and 16 proteinuria. The systolic blood pressure was higher in men with microalbuminuria compared to men without microalbuminuria. The glomerular filtration rate decreased with time for patients with microalbuminuria without change in plasma creatinine. The C-peptide concentration was higher in the hypertensive patients compared to non-hypertensive and the same was found for the triglyceride concentration. During the observation period the various complications increased in frequency (retinopathy, cardiomyopathy, neuropathy, angiopathy and hypertension) without significant relation to the presence of microalbuminuria or proteinuria. During the observation period nine patients died mainly due to cardiovascular events.
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PMID:Microalbuminuria in type 2 diabetic patients: a prospective follow-up study. 954 19

In autumn 1999 results of two well-controlled studies were published that are consistent with a frequent association between Helicobacter pylori seropositivity and coronary heart disease (CHD). Concerning the therapy of CHD, attention is mainly focused on new thrombolytic agents, bypass grafting (CABG) and balloon angioplasty (PTCA). In patients with intractable angina where aggressive medical therapy was exhausted and who were no longer candidates for CABG or PTCA, transmural laser revascularisation (TMLR), enhanced external counterpulsation (EECP) and spinal cord stimulation can be considered. TMLR was shown to improve symptoms but not myocardial perfusion; the preoperative mortality accounts for 10-20%. In hypertrophic obstructive cardiomyopathy, alcohol-induced transmural septal myocardial ablation (PTSMA) reduces both the symptoms and the left ventricular outflow tract gradient. Although the prevalence of hypertension emergencies has dramatically diminished, the number of hypertensive patients with heart failure and end-stage renal disease is increasing. It is important to detect and treat mild hypertensives in early stages, especially diabetics and younger women with additional risk factors and/or proteinuria. The choice and dosage of drugs is to be individualised. In chronic heart failure (CHF), the protective effect of ACE inhibitors, metoprolol and carvedilol has been repeatedly shown in CHF stage NYHA II and III. The merit of ACE inhibitor and beta-blockers in high doses remains questionable in old patients and those with severe CHF (NYHA IV). In the latter indication, spirolactone was successfully reintroduced. Eplerenone (epoxymexrenone) is a new aldosterone antagonist with little affinity to other steroid receptors and has therefore less undesirable effects than spirolactone. The body of knowledge in therapeutic and technical progress in medicine of the 20th century are summarised and their positive and negative consequences briefly discussed.
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PMID:[Cardiology at the end of the 20th century]. 1104 3


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