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 rarely diagnosed nodular glomerulopathy is presented arising secondary to kappa light chain deposition and clinically characterized by hypertension, congestive heart failure, massive proteinuria and slowly progressive azotemia. Kappa light chains were detected in the urine, the glomerular nodules, and the basement membranes of both glomeruli and tubules. A malignant proliferation of plasma cells could not be detected. Two morphologic features were unusual: the presence of microaneurysms, and the deposition of immunoglobulin and complement in a similar pattern to the kappa light chains. Noteworthy clinical aspects included the elusiveness of the proper diagnosis, the massive proteinuria in the absence of amyloid deposits, and the remarkable improvement in renal function following intermittent chemotherapy.
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PMID:Kappa light chain nephropathy without evidence of myeloma cells. Response to chemotherapy with cessation of maintenance hemodialysis. 622 48

Antirheumatic drugs may cause a significant, although generally reversible, reduction of GFR, RPF, CNa and hyperkalemia in a wide range of extrarenal and renal disease states (severe liver disease, congestive heart failure, SLE, nephrotic syndrome, etc.); chronic ingestion has been associated with analgesic nephropathy. Recently cases have been reported of reversible acute renal failure with massive proteinuria and interstitial nephritis. The acute effects of a renal PG-inhibiting (ibuprofen) or a renal PG-sparing (sulindac) cyclo-oxygenase inhibitor on renal functional parameters (GFR, RPF, CNa, CK, urine volume) and proteinuria have been studied in 24 patients with clinically and biopsy proven chronic glomerular disease; in all patients ibuprofen significantly reduced GFR, RPF, CNa; these changes were fully reversible within a week of withdrawal of the drugs. A causal relationship exists between inhibited PG-synthesis and reduced renal function in these patients, since sulindac, which failed to reduce urinary PG excretion did not alter significantly the renal function. Moreover proteinuria is not reduced by ibuprofen at doses comparable, as far as concerns inhibition of PG-synthesis, to those of indomethacin.
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PMID:Clinical assessment of the renal toxicity of antirheumatic drugs. 633 23

In congestive heart failure, acute administration of the converting enzyme inhibitor captopril leads to a decrease in arterial pressure, systemic vascular resistance, left ventricular filling pressure, and the end-diastolic volumes of both ventricles, as well as to an increase in cardiac index, stroke volume index, right and left ventricular ejection fractions. The mechanism of action appears not only attributable to a decrease in angiotensin II but, possibly, may also be accounted for by central and peripheral sympathicolytic effects diminished degradation of bradykinin and an increase in synthesis of vasoactive prostaglandins. During continued treatment with captopril over three months a further decrease in left ventricular filling pressure and an increase in cardiac output can be observed. While the exercise tolerance is not meaningfully affected at the beginning of treatment, a significant increase may be seen during long-term use. After three months of therapy an increase in the acutely-lowered mean arterial pressure can be noted. As compared with placebo-treated control patients, a more favorable clinical course was seen in those receiving captopril. There does not appear to be a relationship, however, between the initial hemodynamic effects and the clinical response. On combined use of captopril and hydralazine, as compared to treatment with captopril only, there is a greater increase in cardiac output and stroke volume without marked additional fall in pulmonary capillary pressure and a further decrease in systemic arterial pressure, incurred without symptomatic hypotension in the majority of patients. The adverse effect is hypotension which precludes long-term treatment in about 10% of patients. Proteinuria, neutropenia and renal insufficiency occur only rarely, usually in patients who are maintained on daily dosages above 300 mg or who have preexisting renal disease. Skin rashes and taste alterations are more common but are frequently well-tolerated and, generally, do not warrant discontinuation of treatment.
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PMID:Converting-enzyme inhibitor therapy for chronic heart failure. 634 10

The appearance of proteinuria in an insulin-dependent diabetic patient is an ominous sign. Proteinuria heralds the presence of diabetic nephropathy and early death, or chronic renal failure requiring dialysis or transplantation, in 50% of patients. The pathogenesis of diabetic nephropathy is unknown. Adequate insulin administration is the most important preventive measure. Hypertension, if present, should be aggressively treated to delay progression of renal disease. Good nutrition, prompt treatment of urinary tract infections, and caution in the use of radiocontrast agents are other important preventive measures. Hemodialysis, peritoneal dialysis, and transplantation are options for patients with end-stage renal disease. No matter which is selected, the patient may still have multiple amputations, blindness, congestive heart failure, infections, and uncontrolled glycemia. Advancements are being made, however, that promise a better future for insulin-dependent diabetics.
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PMID:Diabetic nephropathy. Is end-stage renal disease inevitable? 635 91

To clarify the association between proteinuria and congestive heart failure (CHF), 24-hour urinary protein determinations were obtained from 27 patients with objectively documented CHF, before and after therapy of the CHF. The results demonstrate that modest proteinuria is a frequent feature of CHF and that this proteinuria reverses promptly with successful CHF therapy. Proteinuria exceeding 500 mg/day occurred only in patients with acute pulmonary edema. However, there was no other correlation between severity of proteinuria and type or chronicity of CHF. When proteinuria exceeds 1 g/24 h or when proteinuria does not reverse within 2 weeks of successful CHF therapy, intrinsic renal disease should be suspected.
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PMID:Proteinuria in congestive heart failure. 663 86

Captopril, a competitive antagonist of angiotensin converting enzyme, has been marketed in the United States for the treatment of resistant hypertension. Despite extensive study, its exact mechanism of action remains unclear; decreased renin-angiotensin-aldosterone and sympathoadrenal system activity as well as increased bradykinin and prostaglandin E and F activity have been postulated. The drug decreases peripheral vascular resistance. Controlled trials in resistant hypertension of various etiologies and chronic congestive heart failure have demonstrated sustained effectiveness and therapeutic benefits. Side effects include skin rash, loss of taste, proteinuria, and leukopenia; higher doses and concomitant renal dysfunction appear to be predisposing factors. The benefit-to-risk ratio for captopril clearly justifies its use in resistant cases of hypertension and congestive heart failure, but further experience is needed to evaluate its use in milder forms of these diseases.
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PMID:Captopril: clinical pharmacology and benefit-to-risk ratio in hypertension and congestive heart failure. 676 88

Since their initial description in 1957, the interferons (IFNs) have been increasingly used to treat a wide array of diseases. Acute adverse effects, i.e. 'flu-like' syndromes, hypo- or hypertension, tachycardia, headache, myalgias and gastrointestinal disorders, occur within the first hour or day after starting treatment. They are seldom treatment-limiting and are easily manageable. Sub-acute and chronic effects develop after several days, usually within 2 and 4 weeks of therapy. The most typical is neurological toxicity, including fatigue/asthenia, and behavioural and cognitive changes. Such symptoms may seriously impair quality of life and result in treatment discontinuation. Seizures have seldom been described. Other infrequent central nervous system adverse effects include vertigo, cramp and oculomotor nerve paralysis. Distal paraesthesias and peripheral neuropathy have been reported. IFN-associated autoimmunity is quite rare but a matter of concern. Biological or clinical manifestations usually require several months to become apparent. Autoantibodies have been shown to develop in most patients but have been inconsistently associated with clinical symptoms of systemic lupus erythematosus, rheumatoid-like arthritis and thyroiditis. Both hypo- and hyperthyroidism have been described but are usually reversible. Other infrequent autoimmune reactions include diabetes, pemphigus and worsening of multiple sclerosis. Although several patients present with a pre-existing autoimmune disorder, no predisposing factor has been clearly established. While hypotension and tachycardia are the most frequent acute cardiovascular complications, a few additional cases of cardiac arrhythmias and myocardial ischaemia have been reported after a short course or several weeks of treatment. These latter complications do not appear to be dose-dependent or age-related. Isolated cases of congestive heart failure have also been described. Mild proteinuria has been observed in 15 to 25% of patients, but acute renal toxicity is uncommon. A transient rise in serum aminotransferase levels is frequently noted during the first stage of therapy, especially in patients receiving the highest dosages. Direct hepatotoxicity is extremely rare. Autoimmune hepatitis, which is ill-diagnosed as chronic viral hepatitis, and de novo induction of autoimmune hepatitis, account for the majority of liver diseases. Haematotoxicity is relatively common but mild to moderate, and develops gradually during the first weeks of treatment. Neutropenia is the most common haematological toxicity, but is usually not dose-limiting and resolves rapidly upon drug discontinuation. Myelosuppression, autoimmune and immune allergic haemolytic anaemias and thrombocytopenias have seldom been described. Cutaneous adverse effects comprised nonspecific erythema and hair loss and, less frequently, vasculitis, local ulcerations at the site of injection and exacerbation of psoriasis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Clinical toxicity of the interferons. 751 63

The incidence of vascular complications in 224 patients with aldosterone-producing adenoma (APA) which was proven on adrenal surgery, was compared to that in 224 sex- and age-matched patients with essential hypertension (EHT). The incidence of cerebral hemorrhage was significantly higher (p < 0.05) in the patients with APA when compared to the EHT group. On the other hand, the incidence of myocardial infarction and/or congestive heart failure in the APA group was lower, although this difference did not reach statistical significance. Diastolic blood pressure in the APA group was significantly higher (p < 0.001) in the EHT group. However, a significant difference in diastolic blood pressure was not detected between the APA groups with and without vascular complications, whereas in the EHT group diastolic blood pressure was significantly higher (p < 0.001) in cases with vascular complications as compared to those without complications. As a possible factor contributing to the higher incidence of cerebral hemorrhage in the APA group, proteinuria was suggested. It was recommended that patients with primary aldosteronism should undergo operation when localization of the APA is established.
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PMID:Vascular complications in patients with aldosterone producing adenoma in Japan: comparative study with essential hypertension. The Research Committee of Disorders of Adrenal Hormones in Japan. 759 26

Angiotensin II (Ang II) is the primary mediator of the renin-angiotensin system (RAS). Inappropriate control of the RAS is critically involved in the development and maintenance of hypertension and congestive heart failure. The actions of Ang II are thought to be mediated by specific surface receptors on the various target organs. At present, two receptors for Ang II have been firmly established in mammals, including man. According to current nomenclature, losartan represents the prototype antagonist of the Ang II type 1 (AT1) receptor and does not possess significant affinity for the so-called AT2 receptor. Losartan is the first of a new class of orally active, nonpeptide Ang II receptor antagonists able to very specifically and selectively inhibit the RAS while lacking the agonistic effects of the peptide receptor antagonists, e.g. sarlasin, or the bradykinin potentiating effects of the angiotensin converting enzyme (ACE) inhibitors. Virtually all of the known actions of Ang II, e.g. those defined by Ang II itself, saralasin, ACE or renin-inhibitors are blocked by losartan, emphasizing the major role of this distinct Ang II receptor subtype in mediating the responses of Ang II. The functional correlate of the AT2 receptor remains poorly understood. In several models of experimental and genetic hypertension, AT1 receptor antagonists are effective antihypertensive agents with similar efficacy to that of ACE and renin-inhibitors. In animal models of renal disease, AT1 receptor antagonists significantly decrease proteinuria, protect against diabetic glomerulopathy and increase survival in stroke-prone spontaneously hypertensive rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A new class of therapeutic agents: the angiotensin II receptor antagonists. 763 3

A 34-year-old female patient was admitted to our hospital with a 1-year history of chronic congestive heart failure, massive proteinuria and tibial edema. On admission, she presented with hemolytic anemia, hepatomegaly, splenomegaly and renal impairment. Furthermore, the skin of her face, hand, forearm, lower extremities showed crust and bulla. Laboratory examination revealed a large amount of protoporphyrin in her blood and feces, but no increase in urine. Light microscopy of renal biopsy showed moderate chronic tubulointerstitinal disease and mild proliferation of mesangial cells. The prophyians are a group of compounds associated with involving the disturbance of various biosynthetic heme pathwas. Until now, the regulation of porphyrin and heme metabolism in the kidney have received relatively little attention as compared with those in liver and erythropoietic tissue. However, some recent reports have confirmed that proximal tubular cells may contribute to heme biosynthesis. It was strongly suggested that chronic tubulointerstitinal injury in this case might be directly induced by the disturbance of the biosynthetic heme pathway in the tubules.
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PMID:[A case of erythropoietic protoporphyria associated with tubulointerstitial disease and dilated cardiomyopathy]. 773 Nov 9


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