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)

In patients with hypertension and chronic renal parenchymal disease, BP should be controlled to 130/85 mmHg or lower (125/75 mmHg) in patients with proteinuria in excess of 1 g/day. Reducing dietary sodium (< 7 g/day) and protein (< 0.6-0.7 g/kg) helps control high BP and renal function in patients with renal insufficiency. As first antihypertensive drug, ACE inhibitors or long-acting Ca antagonists are recommended. In patients with renovascular hypertension, angioplasty is the first choice increasingly to be accompanied by stenting, and surgical revascularization is the next choice. As antihypertensive drugs, beta blockers, ACE inhibitors, and AII-receptor blockers are recommended. Hypertension accompanied by endocrine disease with adenoma or tumor is almost cured or improved by surgical removal. Spironolactone and Ca antagonists are used in patients with idiopathic aldosteronism (bilateral hyperplasia). Alpha and beta blockers are used in patients with pheochromocytoma during preoperative period.
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PMID:[Secondary hypertension]. 1139 95

Primary aldosteronism rarely complicates pregnancy. We present a woman with primary aldosteronism in pregnancy associated with severe preeclampsia. A 33-year-old Japanese woman with hypertension was referred to our hospital at 25 weeks of gestation. Her blood pressure was 180/100 mmHg, and laboratory tests identified a low serum potassium level and moderate proteinuria on urinalysis. The fetus was diagnosed with growth restriction. Plasma renin activity (PRA) value was 2.2 ng/mL/h and plasma aldosterone concentration (PAC) was elevated (260 pg/mL). The patient was treated medically. At 27 weeks of gestation, we noted persistent late fetal heart rate decelerations associated with uterine contractions. Therefore, elective caesarean section was performed and she was delivered of a 698-g female. After delivery, PRA declined and PAC remained elevated. Abdominal computerized tomography scan and I131-iodochoresterol scan revealed a tumor in the left adrenal gland. Laparoscopic adrenalectomy was performed and confirmed the clinical diagnosis.
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PMID:Diagnosis and management of primary aldosteronism in pregnancy: case report and review of the literature. 1185 94

Blockade of the renin-angiotensin-aldosterone system with angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor antagonists has resulted in beneficial effects in essential hypertensive patients. However, occurrence of cardiovascular events has not been appropriately controlled beyond a certain percentage. One reason could be the effects of aldosterone, the final component of the system. The aldosterone escape phenomenon could explain undesirable outcomes observed in hypertensive patients even under treatment with ACE inhibitors or angiotensin antagonists. Aldosterone has direct effects on the vasculature and has been associated with vascular smooth muscle cell hypertrophy, endothelial dysfunction, cardiac fibrosis, proteinuria, and renal vascular injury. Animal models and clinical trials have proven the benefit of aldosterone receptor antagonism. With increased recognition of the prevalence of hyperaldosteronism in patients thought to have "essential" hypertension, the use of drugs that block aldosterone action may become more widespread and protect the vasculature from the deleterious effects of aldosterone.
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PMID:Aldosterone: a risk factor for vascular disease. 1253 Sep 37

Based on two patients, we discuss the difficulties in diagnosing and managing primary aldosteronism in pregnancy, which derive from changes of the renin-angiotensin-aldosterone axis, from the uncertainty regarding blood pressure control along gestation and postpartum, and from the contraindication to the use of spironolactone. The first case is a 27 years old woman with a long standing refractory hypertension, a hemorrhagic stroke with left brachial hemiplegia and crural hemiparesia, two miscarriages, one stillbirth and one offspring with intrauterine growth retardation. Due to hypokalemia, a plasma aldosterone/renin activity ratio of 91, and a negative genetic screening for glucocorticoid remediable aldosteronism (GRA), a primary hyperaldosteronism with normal adrenals in CT scan was diagnosed, and good blood pressure control was attained with spironolactone. After two and a half years of normotension, a fifth pregnancy, managed with methyldopa evolved with satisfactory blood pressures, plasma potassium, fetal growth, uterine and umbilical arterial resistance indexes, and maternal endothelial function. At 37 1/2 weeks of pregnancy the patient delivered a healthy newborn weighing 2,960 g. Blood pressure rose during the 48 hours of postpartum in the absence of proteinuria and required i.v. hydralazine. The second patient is a 37 years old woman, with known refractory hypertension for 7 years, hypokalemia, plasma aldosterone/renin activity ratio greater than 40, normal adrenals in the CAT scan, and a negative genetic screening for GRA. She had normotensive pregnancies 5 and 3 years prior to the detection of hypertension, with hypertensive crisis in both postpartum periods, retrospectively considered as expressions of primary hyperaldosteronism.
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PMID:[Primary aldosteronism and pregnancy: report of 2 cases]. 1261 Dec 41

The unusual coincidence of Bartter syndrome and C1q nephropathy is described and the literature reviewed. An African-American girl presented at 4 years of age with acute hyponatremic dehydration and failure to thrive. Persistent hypokalemic alkalosis and secondary hyperaldosteronism were found. The case was atypical for Bartter syndrome in that proteinuria (0.19 g/day) was present. Renal biopsy showed juxtaglomerular hyperplasia and C1q nephropathy. Molecular analysis showed deletion of the renal chloride channel gene (CLCNKB) typical of autosomal recessive childhood Bartter syndrome. Chronic sodium and potassium chloride replacement therapy together with indomethacin normalized her metabolic status, and she experienced catch-up growth. Proteinuria persisted, however. This is the first documentation of C1q nephropathy, in mild form, complicating autosomal recessive Bartter syndrome. This case shows the importance of the renal biopsy and of molecular analysis in delineating the cause of atypical nephropathy associated with Bartter syndrome. These findings add to the evidence of a possible association between the congenital syndrome and acquired immune complex nephropathy.
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PMID:Bartter syndrome complicated by immune complex nephropathy. Case report and literature review. 1283 94

Edema of variable severity is an uncommon complication of insulin treatment. Increased sodium reabsorption, transient proteinuria and hypoalbuminemia are the most frequently reported laboratory disorders at the time of edema formation. This case report describes a 44-yr-old man with a 4-month history of anorexia, polyuria, polydipsia and weight loss of 25 kg who presented with diabetic ketoacidosis. On admission, there were no clinical or laboratory signs of volume depletion. Following insulin treatment he developed marked insulin edema and a cluster of abnormalities, including decreased sodium excretion, hypokalemia, hypouricemia, proteinuria, hypoalbuminemia and anemia. The diagnostic work-up showed the presence of high renin and aldosterone values despite the absence of evident hypovolemia and no evidence of gastrointestinal, cardiovascular, renal, thyroid, hepatic or other endocrine disorder. Complement values were normal; autonomic neuropathy and venoocclusive intraabdominal lesions were excluded and no other drugs except insulin were administered. Initiation of spironolactone was associated with prompt resolution of the edema and gradual correction of the laboratory abnormalities. Our findings show that hyperaldosteronism may occur in patients with insulin edema, even in the absence of volume depletion, contributing to the development of increased sodium reabsorption and of other laboratory disorders.
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PMID:A case of insulin edema with inappropriate hyperaldosteronism. 1576 45

Two siblings (brother and sister) with renal tubular hypokalemic alkalosis underwent clinical, biochemical and molecular investigations. Although the biochemical findings were similar (including hypokalemia, metabolic alkalosis, hyperreninemia, hyperaldosteronism and normal blood pressure), the clinical findings were different: the boy, who also presented syndromic signs, developed glomerular proteinuria and renal biopsy revealed focal segmental glomerular sclerosis; the girl showed the typical signs of classic Bartter syndrome. As described in a previous paper, a heterozygous mutation (frameshift 2534delT) was demonstrated in the gene encoding the thiazide-sensitive NaCl co-transporter (SLC12A3) of the distal convoluted tubule; the second molecular analysis revealed a compound heterozygous mutation (A61D/V149E) in the CLCNKB chloride channel gene in both subjects, inherited in trans from the parents. The children were finally diagnosed as having classic Bartter syndrome. These cases represent the first report of the simultaneous presence of heterozygous and compound heterozygous mutations in the SLC12A3 and CLCNKB genes, both of which are involved in renal salt losing tubulopathies, and confirm previous observations regarding classic Bartter syndrome phenotype variability in the same kindred.
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PMID:Simultaneous mutations in the CLCNKB and SLC12A3 genes in two siblings with phenotypic heterogeneity in classic Bartter syndrome. 1630 6

Endocrinology and obstetrics have one thing in common--diagnosis and treatment endocrine diseases in gravidity. These are modified by physiological changes in gravidity, often missing data and tests in normal condition and the influence of diagnosis and treatment on the pregnant female and fetus have also to be taken into consideration. If diagnosis of primary aldosteronism is suspected, suprimed plasmatic renin activity is determinant indicator (disregarding arterial hypertension, hypokaliaemia, hyperkaliuresis and proteinuria) as well as ultrasound diagnostics or adrenal gland diagnostics means magnetic resonance imaging. Aldosteron produced adenomas may by treated by adrenalectomy in the second trimester, late diagnosed adenoma and hyperplastic forms are treated by the administration of the respective medicaments.
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PMID:[Primary aldosteronism in gravidity]. 1706 1

Hydrochlorothiazide (HCTZ) is used to manage hypertension and heart failure; however, its side effects include mild hypokalemia, metabolic abnormalities, and volume depletion, which might have deleterious effects on renal and endothelial function. We studied whether HCTZ cause renal injury and/or altered vasoreactivity and if these changes are hypokalemia-dependent. Rats were given a normal diet or a diet moderately low in potassium K+ with or without HCTZ. Animals fed either a low K+ diet alone or HCTZ developed mild hypokalemia. There was no significant difference in systolic blood pressure in the different treatment groups. All three groups with hypokalemia had mild proteinuria; low K(+)-HCTZ rats had reduced creatinine clearance. HCTZ-treated rats displayed hypomagnesemia, hypertriglyceridemia, hyperglycemia, insulin resistance, and hyperaldosteronism. No renal injury was observed in the groups without HCTZ; however, increased kidney weight, glomerular ischemia, medullary injury, and cortical oxidative stress were seen with HCTZ treatment. Endothelium-dependent vasorelaxation was reduced in all hypokalemic groups and correlated with reduced serum K+, serum, and urine nitric oxide. Our results show that HCTZ is associated with greater renal injury for the same degree of hypokalemia as the low K+ diet, suggesting that factors such as chronic ischemia and hyperaldosteronism due to volume depletion may be responsible agents. We also found impaired endothelium-dependent vasorelaxation was linked to mild hypokalemia.
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PMID:Thiazide-induced subtle renal injury not observed in states of equivalent hypokalemia. 1875 9

Hyperaldosteronism is associated with hypertension, cardiovascular fibrosis, and electrolyte disturbances, including hypomagnesemia. Mechanisms underlying aldosterone-mediated Mg(2+) changes are unclear, but the novel Mg(2+) transporters TRPM6 and TRPM7 may be important. We examined whether aldosterone influences renal TRPM6/7 and the TRPM7 downstream target annexin-1 and tested the hypothesis that Mg(2+) administration ameliorates aldosterone-induced cardiovascular and renal injury and prevents aldosterone-associated hypertension. C57B6 mice were studied (12 weeks, n=8 to 9/group); (1) control group (0.2% dietary Mg(2+)), (2) Mg(2+) group (0.75% dietary Mg(2+)), (3) aldosterone group (Aldo, 400 microg/kg/min and 0.9% NaCl drinking water), and (4) Aldo+Mg(2+) group. Blood pressure was unaltered by aldosterone and was similar in all groups throughout the experiment. Serum Na(+) was increased and serum K(+) and Mg(2+) decreased in the Aldo group. Aldo mice had hypomagnesuria and proteinuria, and renal, cardiac, and aortic fibrosis, which were normalized by Mg(2+) supplementation. Renal and cardiovascular expression of interleukin-6, VCAM1 and COX2 was increased in the Aldo group. Magnesium attenuated renal and cardiac interleukin-6 content and decreased renal VCAM1 and cardiac COX2 expression (P<0.05). Aldosterone decreased expression of renal TRPM7 and the downstream target annexin-1 (P<0.05) without effect on TRPM6. Whereas Mg(2+) increased mRNA expression of TRPM6 and TRPM7, it had no effect on TRPM7 and annexin-1 protein content. Our data demonstrate that aldosterone mediates blood pressure-independent renal and cardiovascular fibrosis and inflammation through Mg(2+)-sensitive pathways. We suggest that altered Mg(2+) metabolism in hyperaldosteronism may relate to TRPM7 downregulation and that Mg(2+) protects against cardiovascular and renal damaging actions of aldosterone.
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PMID:Downregulation of renal TRPM7 and increased inflammation and fibrosis in aldosterone-infused mice: effects of magnesium. 1826 39


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