Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0033687 (proteinuria)
 24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The fawn-hooded rat (FH rat) develops hypertension accompanied with focal and segmental glomerulosclerosis and proteinuria, resulting in premature death. In a first experiment the relationship between renal lesions and blood pressure at various ages was investigated. In a second experiment blood pressure was measured weekly from 10 to 38 weeks of age in a number of male FH rats, followed by examination of renal tissues at 40 weeks of age. Plasma renin activity (PRA) had also been determined in individual FH rats. FH rats aged 4.5 weeks had no renal morphological abnormalities. The severity of the glomerulosclerosis increased with age and showed a positive relationship with blood pressure. The scores of the proteinaceous tubular casts also increased with age and they, too, showed a positive correlation with blood pressure. The severity of glomerulosclerosis and proteinaceous casts at 40 weeks of age was related positively to the course of blood pressure throughout life. The final blood pressure level showed a positive correlation with final PRA values. Only FH rats with malignant nephrosclerosis had high PRA values. The renal glomerular and vascular lesions in the FH rat, most likely caused by the hypertension, progressively deteriorate to malignant nephrosclerosis. At that stage PRA values are increased and may be contributing to the development of renal vascular lesions and acceleration of the hypertension.
 ...
PMID:Relationship between blood pressure level, renal histopathological lesions and plasma renin activity in fawn-hooded rats. 355 93

Fawn-hooded (FH) rats, primarily males, develop spontaneous low-renin hypertension associated with reduced urinary excretion of kallikrein as early as 2 months of age, followed by progressive glomerular sclerosis and proteinuria as early as 3 months of age. In the present study we determined the effects of early (5-7 weeks) or late (5 months) orchiectomy on the blood pressure and nephropathy of FH rats, compared to sham-operated (control) FH males. Early orchiectomy reduced significantly the progression of glomerular sclerosis and of proteinuria and ameliorated the hypertension but had no significant effect on excretion of urinary kallikrein. Late orchiectomy, in contrast, had no significant effect on the progression of glomerular sclerosis or proteinuria but did significantly reduce the blood pressure and marginally increase the excretion of urine kallikrein. These results suggest that (a) male sex hormones may play a role in the pathogenesis of hypertension and nephropathy in the FH rats and (b) renal disease in this strain progresses in spite of improvement in blood pressure.
 ...
PMID:Contrasting effects of early and late orchiectomy on hypertension and renal disease in fawn-hooded rats. 365 Jun 58

We describe an animal model of generalized sepsis, induced in the sheep by cecal perforation, which reproduces the high systemic flow and peripheral vasodilation seen in early human sepsis. Despite volume loading, animals demonstrate a fall in glomerular filtration rate, oliguria, low fractional sodium excretion, maintained urine osmolarity, and increased plasma renin activity. Histologically, kidneys show no consistent abnormality; overall the findings suggest volume contraction or hypoperfusion. This is contradicted, however, by maintained blood pressure and pulmonary capillary wedge pressure, increased cardiac output, and reduced peripheral resistance. Increased Fc lysozyme and low molecular weight proteinuria suggest tubular damage. These paradoxical observations are currently unexplained.
 ...
PMID:The renal response produced by nonhypotensive sepsis in a large animal model. 374 63

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).
 ...
PMID:[Prevalence of arterial hypertension in patients with radiologic signs of chronic pyelonephritis]. 377 67

A case of renal hypertension after pyelolithotomy cured by segmental nephrectomy is reported. The patient, a 39-year-old man had had pyelolithotomy performed by the lumbodorsal approach at another hospital. Two months after operation he started to complain of headache and palpitation. The blood pressure was markedly high when he visited our hospital and peripheral plasma renin activity was also elevated. Urinalysis was normal except for slight proteinuria. The excretory urogram demonstrated cortical scarring in the lower portion of the left kidney. The renal scintigram demonstrated low uptake in this area, suggesting renal infarction. Renal arteriogram showed decreased vascularity in this area. Plasma renin activity was measured on the blood drawn from the renal vein of both sides and the ratio was about 2.4, and renin activity of the segmental renal vein from the left lower portion was elevated. Segmental nephrectomy of the lower pole was performed. The blood pressure three weeks after lower pole resection was estimated to be normal and renin activity returned to an almost normal level. Discussion was made on the cause of renal hypertension after renal surgery. In this case, it was suggested that renal hypertension is caused by subinfraction due to lesions of the dorsal renal artery in surgery for renal calculus.
 ...
PMID:[A case of renal hypertension after pyelolithotomy cured by segmental nephrectomy]. 383 24

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.
 ...
PMID:Pressor factors and responsiveness in hypertension accompanying diabetes mellitus. 390 20

We studied the functional effects of intraperitoneal sepsis on systemic hemodynamics in general, and on renal function in particular, in sheep in whom bacterial peritonitis was induced by cecal perforation. In the first group of seven sheep (group 1) fluid was administered throughout the period of sepsis to maintain pulmonary capillary wedge pressure as close to presepsis values as possible. These sheep exhibited hemodynamic changes known to be associated with sepsis in man: increased cardiac output and decreased systemic vascular resistance. In a second group of seven sheep (group 2) fluid intake was restricted; compared with group 1, these sheep demonstrated a smaller increase in cardiac output that did not persist and that was associated with an increase in the systemic vascular resistance during the septic period. Plasma renin levels increased fivefold in group 2 but were unchanged in group 1. Serial renal biopsies during the septic period revealed that all sheep had evidence of tubular cell damage on electron microscopy: cell swelling, loss of the microvillous brush border, and cell necrosis. Both groups of sheep also demonstrated marked tubular proteinuria similar to that found in humans with generalized sepsis. Despite this, sheep in group 1 exhibited no functional renal changes: creatinine clearance levels rose slightly from control values, urine concentrating ability was unimpaired, and fractional excretion of sodium increased appropriately in response to a sodium load. In contrast, group 2 sheep exhibited a fall in creatinine clearance levels but fractional sodium excretion did not fall as would have been expected were renal function entirely normal. The results suggest that generalized "hyperdynamic" sepsis induces tubular cell damage and tubular proteinuria by an unknown mechanism. However, this does not necessarily produce renal impairment since the glomerular filtration rate does not fall unless volume contraction is also allowed to occur.
 ...
PMID:Renal and cardiovascular response to nonhypotensive sepsis in a large animal model with peritonitis. 396 24

Altered glomerular metabolism of arachidonic acid (AA) has already been demonstrated in experimental nephrotoxic nephritis. The enhanced synthesis of thromboxane A2 (TxA2) in isolated glomeruli that has been found may mediate changes in renal hemodynamics. The objectives of this investigation were: to check whether glomerular AA metabolism is also altered in a model of glomerulopathy in which no leukocyte infiltration or platelet deposition could be demonstrated; to establish a correlation between the altered AA metabolism and proteinuria; and to explore whether the alteration of the prostaglandin (PG) pathway found in isolated glomeruli is an in vitro artifact or reflects a modification in vivo. We used a model of glomerular damage characterized by heavy and persistent proteinuria, which was induced in the rat by a single intravenous injection of adriamycin. At light microscopy, minimal glomerular abnormalities were found in this model. Electron microscopy showed profound alterations of glomerular epithelial cells with extensive fusion of foot processes and signs of epithelial cell activation. Electron microscopy of numerous glomeruli showed no platelet deposition or macrophage and leukocyte infiltration in this model. Isolated glomeruli from nephrotic rats studied 14 or 30 d after a single intravenous injection of adriamycin (7.5 mg/kg) when animals were heavily proteinuric generated significantly more TxB2, the stable breakdown product of TxA2, than normal glomeruli. No significant changes were found in the other major AA metabolites formed through cyclooxygenase. Urinary excretion of immunoreactive TxB2 was also significantly higher in nephrotic than in normal animals. Administration of a selective Tx synthetase inhibitor, UK-38,485, from day 14 to day 18 after adriamycin resulted in a significant reduction of proteinuria compared with pretreatment values. Glomerular synthesis and urinary excretion of TxB2 were normal during the UK-38,485 treatment. Additional experiments showed that elevated glomerular synthesis and urinary excretion of TxB2 were not a consequence of increased substrate availability. Maximal stimulation of the renin-angiotensin axis with furosemide increased glomerular TxB2 synthesis in normal rats, which was significantly lower than in nephrotic animals. Finally, experiments using a unilateral model of adriamycin nephrosis indicated that the enhancement of glomerular TxB2 synthesis is not simply a consequence of the nephrotic syndrome. We conclude that: there is an abnormality of glomerular AA metabolism in nephritic syndrome, which leads to increased TxA2 production; the increased Tx generation correlates with protein excretion and might be responsible for altering the glomerular basement membrane permeability to protein; and the alteration found in isolated glomeruli probably reflects a modification in vivo, in that urinary excretion of immunoreactive TxB2 is also consistently increased in adriamycin nephrosis.
 ...
PMID:Increased glomerular thromboxane synthesis as a possible cause of proteinuria in experimental nephrosis. 403 7

Toxemia was induced in 13 of 20 pregnant ewes by the stress of a change in environment and food deprivation late in pregnancy. Of the toxemic ewes, eight developed prominent neurological findings with convulsions, motor weakness, and blindness, whereas five ewes developed azotemia without neurological signs. Proteinuria and azotemia occurred in all but one of the toxemic animals. Seven animals did not develop clinical or laboratory evidence of toxemia. Hypertension did not occur with the onset of toxemia but all toxemic animals showed glomerular changes by light and electron microscopy. These abnormalities, which were similar to those seen in human preeclampsia, included endothelial cell swelling, focal reduplication of the basement membrane, and fusion of the epithelial cell foot processes. The toxemia could not be attributed to changes in hematocrit, plasma glucose, Na, Cl, CO(2), K, Ca, fibrinogen, arterial pH, lactate, or pyruvate concentrations. Cardiac output fell only in ewes with prominent neurological signs. Plasma renin rose strikingly in animals developing toxemia, without change in substrate concentration. In contrast to human and other species, sheep uterus and amniotic fluid contained no detectable quantities of renin. Thus in response to stress the pregnant ewe develops a toxemia which in the absence of hypertension has clinical and pathological similarities to human preeclampsia.
 ...
PMID:Toxemia of pregnancy in sheep: a clinical, physiological, and pathological study. 538 29

The epidemiology, pathogenesis, significance and management of hypertension in diabetic subjects are discussed. In Type 1 diabetes the presence of diastolic hypertension is closely related to the presence of diabetic nephropathy, from the stage of persistent proteinuria onwards. There may also be some elevation of systolic pressure. The apparent increased prevalence of hypertension in Type 2 diabetes is largely explicable, directly or indirectly, by obesity but there may be an excess of systolic hypertension among elderly patients. Hypertension in the diabetic population is associated with an increased incidence of both microvascular and macrovascular complications, but whether the high blood pressure is causal is not clear. The possible roles of sodium and insulin, the renin-angiotensin system, catecholamines and physical factors are explored. All current antihypertensive agents have additional limitations and disadvantages when used in diabetic patients: diuretics and beta-blockers are probably the initial drugs of choice. Only in the case of diabetic nephropathy is there yet reasonable evidence of antihypertensive treatment reducing the rate of progression of the disease.
 ...
PMID:Diabetes and arterial hypertension. 613 Oct 4


<< Previous 1 2 3 4 5 6 7 8 9 10