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)

Ten trauma patients and 13 burns patients were studied intensively for the first 36 h and subsequent 6 days post injury in order to investigate the mechanism of trauma and burn associated proteinuria. Burns patient's initial maximum proteinuria occurred between 4 and 8 h post injury, whilst trauma patients showed greatest proteinuria within 4 h. In both groups coexisting myoglobinuria or marked elevation of serum renin activity was not found during the first 36 h. Following admission serum lipid peroxides rose in burns patients reaching a maximum between 2 and 8 h following injury, after which levels fell rapidly; in contrast trauma patient's values were initially within normal limits, but rose sharply after 12 h with peaks occurring between 16 h and 7 days post injury. Some patients within both groups showed a recurrent protein leak 2 to 5 days post injury. The data suggest that myoglobinuria or raised renin levels do not play an important role in trauma associated proteinuria.
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PMID:Burn and trauma associated proteinuria: the role of lipid peroxidation, renin and myoglobin. 328 56

We evaluated a chronic renal injury in 37 cardiac transplant recipients treated for 12 to 24 months with cyclosporine (CsA). Twenty-four cardiac transplant recipients treated with azathioprine for more than 24 months served as controls. Despite equivalent cardiac performance, GFR in those treated with CsA was depressed, 47 +/- 3 versus 94 +/- 4 ml/min/1.73 m2 (P less than 0.001). CsA therapy was also associated with significant elevation of renal vascular resistance (RVR), proteinuria, arterial hypertension, and impaired intrarenal conversion of inactive prorenin to active renin. Histopathological changes associated with CsA included an obliterative arteriolopathy with deposition of proteinaceous material in necrotic arteriolar walls, and associated tubulointerstitial damage. A minority of glomeruli exhibited either ischemic collapse or sclerosis. Area perimeter analysis revealed enlargement of the remaining glomeruli with significant expansion of the mesangium. Longitudinal examination over a 48 month period (N = 15) during which CsA was reduced in dosage or withdrawn revealed persistent hypofiltration, increasingly elevated RVR and heavier proteinuria. Further histopathological deterioration was observed when renal tissue was sampled a second time in six patients, and three members of the experimental group developed end-stage renal disease. We conclude that continuous CsA therapy for more than 12 months causes a chronic injury to renal microvessels that is rarely reversible and potentially progressive.
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PMID:The long-term course of cyclosporine-associated chronic nephropathy. 328 2

In 35 initially normotensive patients with chronic glomerulonephritis and lupus nephritis (including 27 patients with nephrotic syndrome; NS), blood pressure (BP), urinary sodium excretion, plasma renin activity (PRA), plasma aldosterone level (PA), urinary aldosterone excretion (Au and blood volume were measured before and during prednisolone treatment. In 7 patients (all with NS) steroid-induced hypertension has developed. The patients prone to develop hypertension were hypervolemic nephrotics with initial depression of PRA, PA, Au, and severe sodium retention. In these patients prednisolone did not produce diuresis of natriuresis nor did it decrease proteinuria. In normo- and hypovolemic patients prednisolone produced significant diuresis and natriuresis and failed to induce hypertension. Thus, two types of response to prednisolone could be observed in patients with NS.
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PMID:Steroid-induced hypertension in patients with nephrotic syndrome. 328 84

This paper describes clinical features of high renin hypertension in the elderly. Peripheral plasma renin activity ranged from 0 to 20.1 ng/ml/hr in 59 hypertensive in-patients aged 70 to 86. The patients were divided into 2 groups: 9 cases with plasma renin activity greater than or equal to 3.0 ng/ml/hr (high renin group) and the remaining 50 with plasma renin activity less than 3.0 ng/ml/hr (control group). The development of hypertension differed between the 2 groups. Six of the high renin group (66.7%) had a history of acceleration of previously mild hypertension, while only 3 of the control group (6.0%) had this history (p less than 0.01). The frequencies of high diastolic blood pressure (greater than or equal to 120 mmHg), massive proteinuria (at least 3.0 g/day), hypokalemia (serum potassium less than or equal to 3.0 mEq/L) and high serum cholesterol (greater than or equal to 250 mg/100 ml) were significantly greater in the high renin group than in the control group (p less than 0.01, respectively). Renovascular hypertension was suspected in 6 patients from the high renin group (66.7%), as compared with 1 of the control group (2.0%) (p less than 0.001). There was massive proteinuria in 3 of 6 patients with renovascular hypertension in the high renin group and 2 showed nephrotic syndrome. Thus, two-thirds of the elderly patients with high renin hypertension had probable renovascular hypertension with a history of rapid progression of hypertension.
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PMID:High renin hypertension in the elderly. 329 10

We followed renal function through the natriuretic phase of 6 occasions of drug-induced recovery from minimal lesions nephrotic syndrome (MLNS). Protein excretion started to fall 1-3 days prior to the start of the natriuresis. The natriuresis was accompanied by a rise in glomerular filtration rate (GFR, inulin clearance). The filtration fraction, calculated from the GFR and the p-aminohippurate clearance, rose steadily in 5 subjects in whom it was low before therapy. Proximal and distal sodium reabsorption fractions, estimated from the changes in maximum free water clearance, fell, and fractional sodium, lithium, uric acid and free water clearance rose. At the time of these changes plasma protein had hardly risen, whereas renin activity was down. These results are in agreement with the notion that the sodium retention of MLNS is due to a renal defect. Repair of the glomerular filter, evident from the disappearance of proteinuria and the rise in filtration fraction, apparently normalizes the elevated tubular sodium reabsorption proximal to the macula densa, which leads to a fall in renin release.
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PMID:Renal function during recovery from minimal lesions nephrotic syndrome. 331 90

Food intake increases glomerular filtration and proteinuria in adult rats. That this postprandial hyperfiltration could be age dependent was investigated in 3-, 10-, 20-, and 30-mo-old rats. Glomerular filtration rate and protein excretion were measured in fed or 24 h fasted conscious animals. In the 3-mo-old rats food ingestion increased renal filtration by 45% from 1.17 +/- 0.08 to 1.73 +/- 0.11 ml.min-1.g kidney wt-1 (n = 6). As the animals became older, the differences between fed and fasted periods became smaller: in 30-mo-old rats glomerular filtration rate was 0.85 +/- 0.03 and 1.01 +/- 0.06 ml.min-1.g kidney wt-1 (n = 6) in fasted and fed conditions, respectively. Proteinuria, which was mainly albuminuria, increased slightly with age and was more markedly reduced by acute food restriction in the 30-mo-old than in the 3-mo-old rats. Because the renin-angiotensin system activity decreases with age, its role in postprandial hyperfiltration was assessed by measuring glomerular filtration in 3-mo-old animals whose angiotensin II converting-enzyme activity was chronically inhibited by daily administration of perindopril. In such experimental conditions there was no longer a difference in renal filtration between fed and fasted rats. These data indicate that 1) postprandial increase in glomerular filtration is to some extent related to the renin-angiotensin system activity; 2) short-term reduction of food intake reduces proteinuria even in senescent rats, although the feeding dependence of the glomerular filtration is blunted with age.
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PMID:Effect of feeding on glomerular filtration rate and proteinuria in conscious aging rats. 340 83

Seven salt depleted patients with the idiopathic nephrotic syndrome were treated with various non-steroidal anti-inflammatory drugs. Indomethacin, diclofenac-sodium and flurbiprofen decreased proteinuria, glomerular filtration rate, plasma renin activity and renal prostaglandin E2 excretion by 59%, 19%, 55% and 68% respectively. Sulindac induced no major changes in proteinuria, glomerular filtration rate, plasma renin activity and renal prostaglandin E2 excretion. The relative change in proteinuria and glomerular filtration rate during non-steroidal anti-inflammatory drug treatment correlated strongly with that of the renal prostaglandin E2 excretion (r = 0.89 and r = 0.70, respectively p less than 0.05). It is likely that the anti-proteinuric effect of non-steroidal anti-inflammatory drugs is dependent on their potency to inhibit renal prostaglandin synthesis and it is suggested that this effect is mediated by lowering transcapillary glomerular hydraulic pressure.
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PMID:Reduction of urinary protein and prostaglandin E2 excretion in the nephrotic syndrome by non-steroidal anti-inflammatory drugs. 351 75

Nephrotic range proteinuria occurred in a 42-year-old woman with renal arterial occlusion and hyperreninemia. The administration of captopril, an angiotensin converting enzyme inhibitor, led to an amelioration of the proteinuria and the decrease of blood pressure, without surgical treatment. From the present observation, it is highly probably that the increased activity of the renin-angiotensin system plays an important role in massive proteinuria. Conservative treatment for renovascular hypertension with nephrotic syndrome was effective in this patient.
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PMID:A case of renovascular hypertension with the nephrotic syndrome. 353 95

We have previously reported on a high prevalence of high renin essential hypertension in psoriasis. Since angiotensin-converting enzyme (ACE) was also reported to be increased in some psoriatics, we found it rational to treat 10 patients with hypertension and diffuse psoriasis with captopril at a dose of 25 mg t.i.d. Five patients had high PRA levels and in 1 of them serum ACE was also increased. Serum creatinine, BUN and urinalysis were normal in all of them. SPB fell from 163 +/- 3 to 138 +/- 3 and DBP from 107 +/- 3 to 86 +/- 2 mm Hg after 1 month of captopril treatment. A surprising clinical improvement of the cutaneous lesions occurred in 3 patients previously resistant to every local or systemic treatment. Unfortunately, however, 3 patients developed heavy proteinuria (greater than 2 g/day) which disappeared after captopril discontinuation. The unexpected incidence of reversible proteinuria induced by low doses of captopril in our patients recommends a careful monitoring of the renal function every time this drug is employed in the treatment of hypertension in a psoriatic.
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PMID:Captopril-induced proteinuria in hypertensive psoriatic patients. 354 Jun 94

Except for infections (pyelonephritis, abscess of the kidney), which cause symptoms such as pyuria, pain and fever, most diseases of the renal parenchyma were unknown in Greek and Roman antiquity. Even in the Renaissance they were not yet properly identified. Edema was generally thought to be related to liver disease. Proteinuria was discovered at the end of the 18th century. In 1827 Bright provided the first, almost complete clinical description of the various forms of acute and chronic glomerulonephritis and showed that they were accompanied by macroscopic changes in the kidneys. Between 1850 and 1885, Frerichs, Klebs and Langhans described the primary glomerular lesions. The amount of new knowledge acquired during the 20th century has been tremendous, and covers the mechanism of urine formation, the role of sodium retention in edematous states, the physiology and physiopathology of the renin-angiotensin-aldosterone system, the glomerular origin of the nephrotic syndrome, new methods of investigation, progress in histology and immunology, the discovery of many tubular syndromes, the introduction of antibiotics and antihypertensive drugs, and the development of dialysis and transplantation.
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PMID:[On the history of kidney disease]. 355 Oct 58


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