Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024141 (systemic lupus erythematosus)
 44,322 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

High plasma renin activity (PRA) was found in 16 of 42 randomly selected nonuremic systemic lupus erythematosus (SLE) patients. Mild hypertension was present in 3 of the 16.6 high-PRA and 10 normal-PRA patients were admitted to a metabolic ward. Salt restriction produced a disproportionate rise in both PRA and aldosterone, a decrease in glomerular filtration rate (GFR) and a slightly greater negative sodium balance in the group with high PRA. Potassium excretion was less than intake in both groups. Balance studies were performed in 6 additional high-PRA patients before and during indomethacin administration (150 mg/24 h). PRA and aldosterone were markedly suppressed by indomethacin. UnaV was significantly greater than in the control period despite of the 28% reduction in GFR. These results suggest that high PRA is secondary to impaired distal tubular sodium reabsorption. Such a defect could be responsible for the relatively low frequency of hypertension in lupus nephritis.
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PMID:Normotensive hyperreninemia in systemic lupus erythematosus. An indicator of tubular dysfunction. 74 33

Two patients with long-standing systemic lupus erythematosus were found to have persistent hyperkalemia. The hyperkalemia could not be explained by renal insufficiency, oliguria, diminished distal sodium delivery, acidemia, or hemolysis. After sodium depletion, urinary aldosterone excretion and plasma aldosterone concentration rose appropriately. No increase in urinary potassium excretion or decrease in serum potassium concentration was noted after fludrocortisone acetate, furosemide, or acetazolamide plus sodium bicarbonate. We conclude that these patients have a primary defect in renal tubular potassium secretion that may be related to an immune complex interstitial nephritis.
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PMID:Impaired renal tubular potassium secretion in systemic lupus erythematosus. 84 84

We report a case of 67-year-old woman with systemic lupus erythematosus presenting hyporeninemic hypoaldosteronism. She admitted because of anasarca in March, 1990. She manifested nephrotic syndrome, and hyperkalemia and hyperchloremic metabolic acidosis. The hyperkalemia was disproportionate to the degree of renal insufficiency. Basal levels of plasma renin activity and plasma aldosterone concentration were low. Renal tubular function studies revealed normal hydrogen ion secretion. Renal biopsy demonstrated diffuse proliferative lupus nephritis and prominent interstitial cell infiltration. There was no vasculitis of glomerular vascular poles. After treatment of lupus nephritis with prednisolone, levels of plasma renin activity and plasma aldosterone concentration were elevated. Hyperkalemia and metabolic acidosis were normalized and renal function improved. We conclude that the heperkalemia and metabolic acidosis could be attributed to hyporeninemic hypoaldosteronism.
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PMID:[A case of lupus nephritis with hyporeninemic hypoaldosteronism]. 177 Jun 40

Adverse effects of converting enzyme inhibitors are either substance-specific (neutropenia, proteinuria, skin rashes, taste disturbances) or due to the converting enzyme inhibition (hypotension, functional renal insufficiency, hyperkalemia, cough, angioedema). They are rare nowadays because of better knowledge of the pharmacokinetics and -dynamics of the converting enzyme inhibitors, resulting in lower dosage, and because of identifying patients at high risk. The dosage must be adjusted according to renal function, in order to prevent accumulation and toxicity. In addition to patients with renal insufficiency, patients at high risk are those with a stimulated renin-angiotensin-aldosterone system, i.e. patients with renovascular hypertension or heart failure. Patients with collagen vascular disease, for example, systemic lupus erythematosus or scleroderma, should not be considered for long-term therapy with converting enzyme inhibitors because of the increased risk of neutropenia. Life-threatening angioedema may develop, mainly during the first few hours after drug administration.
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PMID:[Angiotensin-converting enzyme inhibition: side effects and risks]. 285 Jun 87

We found that nearly 10% of 142 patients with systemic lupus erythematosus (SLE) had persistent, unexplained hyperkalemia. Renal mineralocorticoid resistance has been suggested to account for the hyperkalemia in SLE. We studied the renin-aldosterone response to intravenous furosemide (60 mg) and upright posture and the renin response to converting enzyme inhibition (captopril, 50 mg) and upright posture in five patients with SLE and hyperkalemia (group 1) and five normokalemic patients with SLE (group 2). Renal function was comparable. Plasma chloride level was higher and bicarbonate level slightly lower in group 1 than in group 2. Plasma cortisol level was normal in all patients. None of the patients was receiving nonsteroidal anti-inflammatory drugs or corticosteroids at the time of study. Basal plasma renin concentration and plasma aldosterone level were not significantly different between the two groups, although both tended to be higher in group 2. However, four of the five patients in group 1 had significantly blunted renin response to captopril compared with group 2. The same four patients also had blunted renin and aldosterone responses to furosemide. Thus, the majority of hyperkalemic patients with SLE had an impaired renin and aldosterone response to stimulation. We conclude that hyporeninemic hypoaldosteronism plays a key role in the pathogenesis of hyperkalemia in SLE.
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PMID:Mechanisms of hyperkalemia in systemic lupus erythematosus. 327 63

Hyperkalemia has been noted to occur spontaneously in patients with long-standing systemic lupus erythematosus who did not have advanced renal insufficiency. The patients previously described all had relatively normal renin-aldosterone systems, and the hyperkalemia was thus presumed to be secondary to a primary defect in renal tubular potassium secretion. We describe at 10-year-old girl with lupus nephritis, without significant renal insufficiency, who had hyperkalemia from hyporeninemic hypoaldosteronism postulated to be due to vasculitis involving the afferent/efferent arterioles and juxtaglomerular apparatus.
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PMID:Systemic lupus erythematosus presenting with hyporeninemic hypoaldosteronism in a 10-year-old girl. 353 7

There have been anecdotal reports describing patients with systemic lupus erythematosus (SLE) and inappropriately elevated secretion of antidiuretic hormone (ADH), but no systematic studies of ADH and its metabolism in SLE have been performed. We measured plasma ADH levels in 36 stable SLE patients with normal renal function and examined the relationship of the circulating ADH concentration to clinical disease activity and effective extracellular fluid volume as reflected by peripheral plasma renin activity (PRA) and plasma aldosterone concentration. The mean ADH level was elevated, 11.4 +/- 1.0 microU/ml (normal 0.4-1.4 microU/ml), while mean PRA and aldosterone were 5.4 +/- 0.6 ng/ml/h and 10.6 +/- 1.6 ng/100 ml, respectively. When patients were divided into two groups according to disease duration, those with SLE for 2 years or more had significantly higher plasma ADH levels (13.9 +/- 1.4 vs. 7.7 +/- 0.9 microU/ml; p less than 0.001 and urinary osmolality (697 +/- 63 vs. 445 +/- 49 mosm/kg; p less than 0.02) compared to those with SLE of less than 2 years duration. No differences in serum Na+, K+, PRA, plasma aldosterone concentration, C3, or 24-hour urinary protein excretion were noted between these two groups. Six patients with SLE for less than 2 years underwent a standard water load (20 ml/kg); in 3/6 there was a paradoxical increase in the plasma ADH concentration. These findings indicate that SLE is associated with elevated plasma ADH levels that increase with prolonged disease duration. This abnormality is unrelated to the usual serologic indices of SLE activity, effective extracellular fluid volume status, or any apparent renal unresponsiveness to ADH.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Abnormal antidiuretic hormone secretion in patients with systemic lupus erythematosus. 360 Sep 13

In 30 resting normal persons, 5 ambulant normal persons and 3 patients with disorders of the pituitary-adrenal-system before and 30 minutes after intravenous injection of 0,25 mg synthetic adrenocorticotrophin (tetracosactid, Synacthen) plasma cortisol and aldosterone levels were evaluated. The evaluation of the corticoids was continued over 240 minutes in intervals of 30 minutes. The basal cortisol and aldosterone levels of the resting normal persons and ambulant persons ordinarily doubled 30 minutes after ACTH application. The plasma cortisol level of a steroid-treated patient with lupus erythematodes disseminatus rose subnormally but his aldosterone level increased normally. 2 patients with untreated hypopituitarism had subnormal plasma cortisol and normal aldosterone responses after ACTH administration. In contrast with patients with primary adrenal insufficiency, whose plasma aldosterone levels fail to rise, patients with secondary adrenal insufficiency had normal corticotrophin-stimulated aldosterone increments. Thus the extended ACTH test can be useful in differential diagnosis of primary and secondary adrenal insufficiency.
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PMID:[Extended ACTH rapid test for differentiation of primary and secondary adrenal insufficiency]. 625 78

Two patients with systemic lupus erythematosus (SLE) and hyperkalemia were studied. The hyperkalemia was disproportionate to the degree of renal excretory impairment. The usual causes of hyperkalemia were excluded. Basal levels of plasma renin activity (PRA) and plasma aldosterone (PAC) were low. The responses of PRA and plasma aldosterone to the combined stimulus of ambulation and furosemide were blunted. Plasma levels of 18-hydroxycorticosterone (18-OH-B) were normal. The hyperkalemia in both patients could be attributed to hyporeninemic hypoaldosteronism (HH). In one patient, the hyperkalemia was corrected by the administration of fludrocortisone. In the second patient, treatment of lupus nephritis with azathioprine, prednisone, and plasmapheresis normalized both the serum creatinine and the serum potassium.
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PMID:Hyporeninemic hypoaldosteronism in two patients with systemic lupus erythematosus. 637 83

The renin-angiotensin-aldosterone system (RAAS) has been considered one of the probable pathophysiologic mechanisms involved in disease progression. Genetic polymorphism of the RAAS has been associated with the clinical course of renal disease. One of the genetic polymorphisms is a deletion or insertion of a 287 base pair fragment in intron 16 of the angiotensin-converting enzyme (ACE) gene. It is known that ACE gene polymorphism is present in humans and that it is associated with an increased risk of cardiovascular diseases, renal disease progression and sarcoidosis. In this study, the potential significance of ACE gene polymorphism in patients with systemic lupus erythematosus (SLE) was investigated. ACE gene polymorphism was determined in 18 patients with SLE and in 21 healthy volunteers as a control group. The mean age of patients was 38.5 years. All patients had a mean follow-up of 30.7 +/- 20.2 months (range 5-95 months). ACE genotypes were determined by the method of polymerase chain reaction. Proteinuria and creatinine were also followed. The frequency of DD, ID and II genotypes was 50%, 28% and 22% in SLE patients and 25%, 50% and 25% in healthy controls, respectively. DD genotype was more common in SLE patients than in the control group. The patients with II genotype had lower proteinuria and creatinine level than those with DD genotype (p < 0.05). The time to disease remission was shorter in patients with II genotype (p < 0.05). Study results indicated an increased frequency of D allele in SLE patients. The increased ACE activity in these patients pointed to the need of further studies of ACE gene polymorphism in SLE.
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PMID:Angiotensin-converting enzyme gene polymorphism in patients with systemic lupus. 1150 31


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