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 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

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

A retrospective study of the prevalence of arterial hypertension in patients with radiological signs of chronic pyelonephritis was done. During six years i.v. urography has been performed in 936 patients, 297 (31.7%) of whom had hypertension, and 123 (13.1%) had radiological signs of chronic pyelonephritis. Out of the patients with chronic pyelonephritis 87 (70.7%) subjects (57 men, 30 women) had arterial hypertension. Bilateral chronic pyelonephritis was radiologically confirmed in 61 (70.1%) and unilateral parenchymal renal disease in 26 (29.9%) of the patients with hypertension. When the diagnosis has been postulated on the basis of radiologically evident changes of kidney parenchym (renal scarring) or the combined calyx-parenchymatous lesions, it could be shown that the frequency of hypertension in these patients was statistically higher (p less than 0.001) than in the group of patients that displayed only isolated calyx lesions. Moderate and pronounced hypertension were more common (52.5%) in patients with bilateral pyelonephritis scarring compared with hypertonic patients having the same, but unilateral changes. Patients with radiological signs of chronic pyelonephritis and hypertension had proteinuria and various degrees of renal failure significantly more often than these with normal blood pressure. On the basis of the presented results the authors concluded that the prevalence of arterial hypertension in patients with chronic pyelonephritis is much higher (70.1%) than in the average population (31.7%). Hypertension is more common and its complications are severe in the patients with chronic fibrose pyelonephritis. In these patients is also frequent chronic renal failure. The observed facts can be explained on the basis of recent knowledge about pathophysiological mechanisms in chronic pyelonephritis (the renin-angiotensin-aldosterone system, renal prostaglandins system and glomerulo-tubular balance).
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PMID:[Prevalence of arterial hypertension in patients with radiologic signs of chronic pyelonephritis]. 377 67

Hypertension accompanying diabetes mellitus may involve abnormalities in at least two major blood pressure-regulating systems: the body sodium-fluid volume state and cardiovascular reactivity. In metabolically stable nonazotemic diabetes, exchangeable sodium is increased by 10% on average, regardless of age, insulin dependence or nondependence, or the presence or absence of diabetic retinopathy or clinical nephropathy (proteinuria greater than or equal to 0.3 g/24 hr). Possible contributing mechanisms include renal sodium retention and an extravascular shift of fluid and sodium; intracellular accumulation is not excluded. Circulatory volume is normal or low and the total exchangeable sodium/blood volume ratio increased. In hypertensive diabetes, the latter abnormality is particularly pronounced; systolic pressure tended to correlate with exchangeable sodium (r = 0.47, p less than 0.001) and diastolic pressure with the plasma sodium/potassium ratio (r = 0.25, p less than 0.05). Plasma aldosterone, renin, epinephrine, and norepinephrine levels are generally normal or sometimes low in metabolically stable nonazotemic diabetic patients with normal or high blood pressure; the plasma clearance of norepinephrine also appears to be unaltered. The cardiovascular pressor responsiveness to norepinephrine is often exaggerated relative to concomitant plasma concentrations, regardless of age, type of antidiabetic treatment, or presence or absence of diabetic retinopathy, peripheral neuropathy, or high blood pressure. Pressor responsiveness to angiotensin II also may sometimes be increased relative to plasma renin levels. Sodium retention and diabetic vasculopathy of resistance vessels could be important complementary mechanisms of hyperreactivity. In diabetes with mild hypertension, diuretic treatment restored exchangeable sodium, norepinephrine pressor responsiveness, and blood pressure toward normal. Thus sodium retention and cardiovascular hyperreactivity tend to occur even at the normotensive, nonazotemic stage of diabetes and may concomitantly predispose for the frequent development of hypertension in the diabetic population.
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PMID:Pressor factors and responsiveness in hypertension accompanying diabetes mellitus. 390 20

The post-exercise urine samples from 122 long-distance runners showed evident abnormalities upon microscopic examination in 95% of all subjects. Proteinuria, alone or with microscopic hematuria, was frequently found. Macroscopic hematuria was a rare occurrence. The urine samples collected in 30 runners before, immediately after the race, and 6, 12, 24, 36, and 48 h later showed a significant post-race decrease in the osmolarity and a significant increase in gamma-glutamyl transferase and N-acetyl-beta-glucosaminidase enzyme activity. Plasma renin activity and plasma aldosterone, determined before and after the race in nine runners, showed a significant increase in the post-race samples. The abnormal urinary findings disappeared in all cases within 24-36 h. It can be concluded that urinary abnormalities are very common after exercise. These abnormalities are most often of a "renal" origin, probably due to a temporary hemodynamic impairment, partially of glomerular but principally of tubular function.
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PMID:Exercise-induced urinary abnormalities in long-distance runners. 615 14

The patients with severe and 10 with accelerated or malignant hypertension were treated with the angiotensin-converting enzyme inhibitor captopril. Captopril acutely reduced blood pressure in all patients except two who had suppressed plasma renin activity. Four patients with encephalopathy showed immediate improvement after the first dose. Two patients could be withdrawn from nitroprusside infusion upon administration of captopril. Nineteen of 20 patients have remained on captopril for 12-32 months. Blood pressure is controlled in 18 and improved in two. Eleven required addition of diuretic and one addition of clonidine. The maximal antihypertensive effect of captopril with or without diuretics was evident after 3 months of continuous therapy and was associated with elevated plasma renin levels, normal aldosterone excretion and preservation of renal function. Captopril was well-tolerated, but produced occasional rash, loss of taste and proteinuria. We conclude that captopril, alone or in combination with other drugs, is effective in both the acute and long-term management of severe and malignant hypertension.
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PMID:Acute and chronic treatment of severe and malignant hypertension with the oral angiotensin-converting enzyme inhibitor captopril. 616 12

PRA, active renin, and inactive renin (IR; activated by dialysis to pH 3.3 and 7.4) were measured in the plasma of 53 patients with diabetes mellitus and 32 normal volunteers (group 1). Proteinuria was present in 21 diabetics (group 3; nephropathy) and absent in 32 diabetics (group 2). The mean PRA was lower in group 3 than in groups 1 and 2. PRA less than 0.2 ng/ml . h occurred more frequently and at a younger age in uncomplicated diabetics than in normal controls. Despite very low PRA, plasma aldosterone was normal in most of the diabetics. IR was significantly higher than normal in the uncomplicated diabetics and was greatly increased in diabetics with nephropathy. Since the kidneys are a principal source of IR, and since patients with diabetic nephropathy have consistently elevated plasma IR, it is possible that increased plasma IR in patients without proteinuria or reduced renal function might be an early sign of renal involvement. However, as other explanations of increased plasma IR exist, the hypothesis must be tested by longitudinal studies of diabetic patients.
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PMID:Increased inactive renin in diabetes mellitus without evidence of nephropathy. 633 80

Functional and morphologic studies of the adrenal cortex and kidney have been carried out in pregnant sheep with spontaneous or dietary restriction-induced ovine toxaemia. It was found that proteinuria was an inconstant feature and no animal showed glomerular lesions analogous to those found in human preeclampsia; thus ovine toxaemia cannot be regarded as a precise experimental model for human toxaemia of pregnancy. The elevation of blood cortisol levels and the morphologic appearance of the adrenal zona fasciculata found in such animals suggest an adrenal response comparable to that caused by adrenocorticotrophic hormone. In addition, animals with severe disease showed evidence of stimulation of the renin-angiotensin-aldosterone system as reflected by elevated blood renin and aldosterone concentrations and raised renal juxtaglomerular indices. Ultrastructural changes in the adrenal zona glomerulosa and renal juxtaglomerular myoepithelioid cells in toxaemic animals resembled those described in non-pregnant sodium-depleted sheep. The finding of juxtaglomerular peripolar cell mitoses and granule exocytosis, the latter only being previously observed in sodium depleted sheep, together with the ultrastructural changes in the adrenal zona glomerulosa and juxtaglomerular myoepithelioid cells, suggest that sodium depletion may play a role in this disease.
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PMID:Functional and morphologic studies of the adrenal cortex and kidney in ovine toxaemia of pregnancy. 648 25

Exercise induces profound changes in the renal haemodynamics and in electrolyte and protein excretion. Effective renal plasma flow is reduced during exercise. The reduction is related to the intensity of exercise and renal blood flow may fall to 25% of the resting value when strenuous work is performed. The combination of sympathetic nervous activity and the release of catecholamine substances is involved in this process. The reduction of renal blood flow during exercise produces a concomitant effect on the glomerular filtration rate, though the latter decreases relatively less than the former during exertion. However, the degree of hydration has an important influence on the glomerular filtration rate. An antidiuretic effect is observed during intense exercise. Changes in urine flow are dependent on the plasma antidiuretic hormone levels which are increased by intense exercise. Heavy exercise has an inhibitory effect on most electrolytes (Na, Cl, Ca, P). With potassium, however, most studies report that potassium excretion is not consistently affected by moderate to heavy exercise. Increased aldosterone production helps the body to maintain sodium by increasing its reabsorption from the filtered tubular fluid. Recent studies suggest that sympathetic stimulation may be involved during exercise. Strenuous work leads to an increased excretion of erythrocytes and leucocytes in urine. Cylindruria has been regularly found in postexercise urine in different sports. Postexercise proteinuria is a common phenomenon in humans. It seems to be directly related to the intensity of exercise, rather than to its duration. This excretion of proteins in urine is a transient state with a half-time of approximately 1 hour. Postexercise proteinuria has a pattern different from normal physiological proteinuria. Immunochemical techniques demonstrate that postexercise proteinuria is of the mixed glomerular-tubular type, the former being predominant. The increased clearance of plasma proteins suggests an increased glomerular permeability and a partial inhibition of tubular reabsorption of macromolecules. Haemoglobinuria and myoglobinuria may be observed under special exercise conditions. The degree of hydration appears to be important to reduce these abnormalities.
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PMID:Exercise and renal function. 656 29

The participation of renal prostaglandins in the nephrotic syndrome has been investigated by the measurement of the urinary excretion of prostaglandin E2 (PGE2), renal function and the renin-angiotensin-aldosterone system before, during and after the administration of indomethacin in a group of patients diagnosed as having chronic idiopathic glomerulonephritis with and without nephrotic syndrome. Our results indicate increased renal production of PGE2 in nephrotic patients. This contributes to the maintenance of renal function, probably by counteracting an activated renin-angiotensin system and could be accompanied by a simultaneous and deleterious enhancement of the degree of proteinuria. Nevertheless, the participation of angiotensin II in this last even cannot be excluded.
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PMID:Participation of renal prostaglandins in the nephrotic syndrome. 657 32


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