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)

Forty-five patients with uncomplicated rheumatoid arthritis and 45 control individuals were subjected to immunochemical investigation of the urinary excretion of renal tubular basement membrane antigen (TBM), renal tubular epithelial antigen (RTE), and beta-2-microglobulin. Tubular proteinuria occurred significantly more frequently in patients treated with gold salts than in those not treated (P less than 0.05). Large amounts of RTE and TBM were detected only in the urine of patients who received gold salt therapy. However, the amounts of these proteins in urine did no correlate with the total dose of gold. These results indicate that renal tubular damage frequently occurs in patients with rheumatoid arthritis who are treated with gold salts; the tests outlined are useful in detecting renal tubular disorders developing during gold salt therapy and have certain advantages over routine urinalysis.
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PMID:Renal tubular dysfunction as a complication of gold therapy in patients with rheumatoid arthritis. 703 44

Left (L) renal perfusion with an aminonucleoside of puromycin (PA), was used to produce unilateral proteinuria in 15 rats to examine the mechanisms responsible for renal salt retention in the nephrotic syndrome. Thirteen control rats underwent L renal perfusion with isotonic saline. Animals were studied 8 (group I) or 13 (group II) days after perfusion. Renal perfusion with saline per se did not change the glomerular filtration rate, renal plasma flow, or absolute and fractional excretion of sodium (Na) from the perfused kidney. PA animals showed a significant decrease in glomerular filtration rate from the perfused kidney and a proportional decrease in the absolute excretion of Na from the PA perfused kidney as compared to the right kidney. The fractional excretion of Na was equivalent in the L and R kidneys of the PA animals. The mean absolute Na excretion from the nonproteinuric R kidney of PA rats was almost twice that of the R kidney of the controls. The increased Na excretion by the nonproteinuric kidney of the PA animals compensated for the sodium retention by the proteinuric kidney.
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PMID:Renal function in rats with unilateral proteinuria produced by renal perfusion with aminonucleoside. 722 Jan 38

The drug puromycin aminonucleoside (PA), used to induce an experimental nephrosis in rats, inhibited the blastogenic response of normal rat spleen cells when cultured in vitro with autologous or heterologous serum. Only at final PA concentrations of less than 5 microgram/ml did PHA induce normal blastogenesis. When PA was unilaterally perfused through the rat kidney a nephrosis developed, characterized by massive proteinuria. Microscopically, the foot process fusion and mesangial cell increase were similar to that seen in human steroid-responsive nephrotic syndrome. Once proteinuria had developed, there was marked suppression of the lymphocyte blastogenic response of the nephrotic rat spleen cells when cultured in autologous sera. Neither proteinuria nor inhibited blastogenesis was found in animals perfused with a buffered salt solution. Animals which were perfused with PA, nephrectomized 2 days after perfusion, and did not show proteinuria, had suppressed lymphocyte blastogenesis after stimulation with PHA. However, the degree of stimulation by the spleen cells of these animals was similar to that from control perfused and nephrectomized animals. Therefore, the aberration in lymphocyte response was consistent with the development of the nephrosis and proteinuria.
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PMID:Experimental nephrosis: interassociation of proteinuria with impaired lymphocyte blastogenesis. 727 81

To elucidate the significance of hypertension associated with cerebrovascular lesions (CVL), renal perfusion pressure (RPP) was controlled by aortic clips of two different sizes in stroke-prone spontaneously hypertensive rats kept under normal or salt-loaded conditions. Tail and femoral arterial pressures (RPPs) in the mildly and severely clamped animals were reduced in proportion to the severity of the clamping. In contrast, carotid pressures in both clamped groups were significantly higher than that in the controls. Proteinuria and hyperreninemia accompanied by arteriolar changes in the renal cortex were observed in the controls prior to the onset of CVL. The renal changes were inhibited by both types of clamping. The onset of CVL was delayed by the mild clamping in salt-loaded animals, but accelerated by the severe clamping in both the normal and salt-loaded animals. Renal cortical blood flow was decreased only by the severe clamping. The results suggest that reduction in RPP and/or renal ischemia, which seems to be due to the hypertensive arteriolar changes in the renal cortex, may be related to the pathogenesis of CVL in the stroke-prone rats with or without hyperreninemia.
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PMID:Implication of renal perfusion pressure in stroke of spontaneously hypertensive rats. 736 76

The triad of severe pre-eclampsia is often described as a combination of hypertension, oedema and proteinuria. Hypertension alone arising in the second half of pregnancy however is not associated with any greater perinatal mortality or low birthweight than normotensive primigravidae and it is probable that this hypertension may be either physiological or a manifestation of essential hypertension or, in some cases, a mild form of pre-eclampsia. Oedema also does not necessarily signify abnormality. High weight gain, fluid retention or oedema is associated with a lower incidence of small babies, but with a higher incidence of pre-eclampsia. Considerable amounts of water retention can occur in normal pregnancy, either measured as an increase during pregnancy, or as a fall after delivery. The diuretics cyclopenthiazide, spironolactone and clopamide given prophylactically to high weight gain primigravidae did not prevent the onset of proteinuric pre-eclampsia, but caused the babies to be lighter in weight than those of controls. Sodium potassium and water content of leucocytes from primigravidae with proteinuric pre-eclampsia is the same as in mild pre-eclampsia and normal pregnancy. Although salt and water retention are common features of pre-eclampsia, they do not cause the condition and are not an essential part of it.
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PMID:The relevance of hypertension and oedema in pregnancy. 742 67

Many diabetic patients will develop a nephropathy that will eventually result in end-stage renal failure. The early stage ("incipient") of diabetic nephropathy generally appears after 5 to 20 years of diabetes and is characterized by microalbuminuria (30 to 300 mg/day), which is only detectable by sensitive radio-immuno-enzymatic methods. When a frank proteinuria develops (> 500 mg/day), the glomerular filtration rate inexorably declines, resulting in terminal renal failure after several years. The onset of microalbuminuria or the elevation of blood pressure (above 120-140/80 mmHg) are predictive of a poor evolution and require appropriate preventive therapeutic interventions. These include an optimal control of hyperglycaemia, dietary proteins and salt restriction, and prescription of anti-hypertensive drugs, with a particular benefit ascribed to angio-tension converting enzyme inhibitors (and maybe to certain calcium channel blockers). These interventions have been proven efficient to prevent or slow down the evolution of diabetic nephropathy.
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PMID:[Renal complications of diabetes]. 748 Dec 38

Endogenous nitric oxide plays an important role in modulation of renal hemodynamics and sodium handling, with increased nitric oxide production inducing renal vasodilation and natriuresis. In the normal rat, nitric oxide activity increases as an adaptive response to increased dietary salt intake, perhaps facilitating natriuresis and thus blood pressure homeostasis. We hypothesized that impaired nitric oxide synthetic ability would result in sensitivity to the pressor effects of high dietary salt intake. Four groups of normal Sprague-Dawley rats were observed for eight weeks: Control, 0.4% NaCl chow and tap water; Salt, 4% NaCl chow and tap water; NAME, 0.4% NaCl chow and water containing the nitric oxide synthase inhibitor, L-nitro-arginine-methylester; Salt+NAME, 4% NaCl chow and water containing L-nitro-arginine-methylester. Compared to Controls, Salt rats demonstrated a significant increase in urinary excretion rate of the stable nitric oxide metabolites, NO2 and NO3, and had no increase in blood pressure. Furthermore, Salt rats had no functional or structural evidence of renal injury. In contrast, Salt+NAME rats demonstrated a significantly higher blood pressure than NAME rats, and urinary NO2 and NO3 excretion rate did not increase despite high salt intake. After eight weeks, Salt+NAME rats had significantly impaired renal function and proteinuria. We conclude that adaptive changes in endogenous NO production play a critical role in sodium and blood pressure homeostasis. Furthermore, impaired nitric oxide synthase activity may be a pathogenetic factor in the development of salt-sensitive hypertension.
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PMID:Endogenous nitric oxide synthesis determines sensitivity to the pressor effect of salt. 752 54

We investigated the role of the vasoconstrictors endothelin-1 (ET-1) and thromboxane in renal protection by the beta 1-selective adrenoceptor antagonist, bisoprolol, in Dahl salt-sensitive rats (Dahl S) and salt-resistant rats (Dahl R). Six-week bisoprolol treatment (20 mg/kg chow) reduced systolic blood pressure (SBP) by 14% in Dahl S rats fed a high-salt (4% NaCl) diet. This BP reduction was accompanied by a decrease in aortic wall thickness. ET-1 and thromboxane released from renal cortex was significantly decreased by 17 and 30% with bisoprolol, respectively. Other prostaglandin synthesis was unaffected. Renal function such as proteinuria, N-acetyl-beta-D-glucosaminidase (NAG) excretion, and glomerular filtration rate (GFR) was not influenced by bisoprolol. Morphologic investigation showed that bisoprolol significantly improved glomerular sclerosis by 29% and attenuated arterial damage by 71%, although tubular injury was not affected. The more severe the glomerulosclerotic lesions, the greater the generation of thromboxane and ET. The arterial lesions were positively correlated to thromboxane generation. These data indicate that long-term bisoprolol treatment reduces vasoconstrictive ET-1 and thromboxane generation and that these alterations may be partly responsible for the amelioration of glomerular and arterial injury in Dahl S rats.
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PMID:Vasoconstrictors and renal protection induced by beta 1-selective adrenoceptor antagonist bisoprolol. 752 81

Hypertensive renal injury is a major identifiable cause of end-stage renal disease in African-Americans. A complex nexus of sociologic, biologic, environmental, and sociocultural variables are involved in mediating this risk and interrelate with dietary salt consumption and salt sensitivity. It is likely that dietary salt intake and salt sensitivity are linked in influencing the risk of hypertensive renal injury, since it has been demonstrated that increasing dietary salt in salt-sensitive patients such as African-Americans results in an increase in glomerular filtration fraction and proteinuria. Dietary salt likely influences both carbohydrate metabolism and blood pressure, either directly or through its influence on other ions such as calcium or potassium. The interrelationship between salt and pharmacologic interventions is an important clinical issue, since the efficacy of these therapies is influenced by the amount of salt in the diet. It is also likely that the changes in blood pressure and carbohydrate metabolism induced by greater dietary salt intake may be more specifically corrected by some nonpharmacologic or pharmacologic interventions compared to others. Since dietary salt has identifiable influences on blood pressure, renal hemodynamics, and carbohydrate metabolism, its overall effect on cardiovascular risk, particularly in high-risk groups such as African-Americans, assumes increasing importance.
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PMID:Salt intake and hypertensive renal injury in African-Americans. A therapeutic perspective. 766 50

Previous studies have suggested that nitric oxide (NO) plays a role in regulation of renal vascular tone and sodium handling. We questioned whether the effects of NO synthase inhibition on renal function are direct or due to increased renal perfusion pressure (RPP) and whether stimulation of endogenous NO activity plays a role in adaptation to increased dietary salt intake. Intrarenal arterial infusion of the NO synthase inhibitor NG-monomethyl-L-arginine (L-NMMA) in control rats resulted in decreased glomerular filtration rate, renal vasoconstriction, natriuresis, and proteinuria. When RPP was held at basal levels with suprarenal aortic snare, L-NMMA had similar hemodynamic effects but decreased sodium excretion and did not induce proteinuria. Exposure of rats to high salt intake (1% NaCl drinking water) for 2 wk induced increased serum concentration and urinary excretion of the NO decomposition products, NO2 + NO3. Urinary NO2 + NO3 and sodium excretion were significantly correlated. Compared with controls, chronically salt-loaded rats also demonstrated enhanced renal hemodynamic responses to NO synthase inhibition. We conclude that the endogenous NO system directly modulates renal hemodynamics and sodium handling and participates in the renal adaptation to increased dietary salt intake. Enhanced NO synthesis in response to increased salt intake may facilitate sodium excretion and allow maintenance of normal blood pressure.
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PMID:Adaptation to increased dietary salt intake in the rat. Role of endogenous nitric oxide. 767 14


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