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Query: UMLS:C0033687 (proteinuria)
24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

Gentamicin-associated acute renal failure was diagnosed in 10 dogs. The disease was characterized by a poor prognosis and lengthy hospitalization. Hypoalbuminemia, disorders of potassium homeostasis, proteinuria, hematuria, and cylindruria were common during therapy for renal failure. Fever and dehydration were the most commonly identified potential predisposing factors.
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PMID:Gentamicin-associated acute renal failure in the dog. 398

Animal studies involving concurrent pathophysiologic states, including experimental renal dysfunction, are useful for a proper understanding of the mechanisms of gentamicin nephrotoxicity and acute renal failure. This study examined gentamicin nephrotoxicity in a model of glomerular dysfunction in rats. Administration of medium molecular weight polyvinyl alcohol (PVA) produced a glomerulopathy, with characteristic accumulation of macromolecular PVA in the glomerular mesangium without altering glomerular filtration or causing proteinuria. Subsequent daily doses of gentamicin ranging from 0 to 120 mg/kg elicited a dose-response nephrotoxicity in both control and PVA-pretreated rats after 6 or 12 days of drug. Based on statistical analysis of renal clearances of creatinine, urea, sodium, and potassium; serum creatinine and urea nitrogen; urinary N-acetyl-beta-D-glucosaminidase excretion (6 days only); in vitro renal cortical transport of tetraethylammonium (TEA) (6 days); and quantified light-microscopic data (12 days), PVA induced an early (6 days) sensitivity to gentamicin nephrotoxicity. By 12 days, there were no differences in the responses of control and PVA rats to gentamicin. Single-dose gentamicin clearance, volume of distribution, and half-life were not altered by PVA and renal concentrations at 6 days were generally lower in these rats. Results of TEA transport studies tend to rule out PVA-induced metabolic lesions in the proximal tubular epithelium as the mechanism for the early sensitivity. This investigation demonstrates altered gentamicin nephrotoxicity in rats with an otherwise benign glomerulopathy and, combined with similar conclusions from a related study in subtotally nephrectomized rats, presents further evidence that the underlying pathophysiologic state of the kidney is an important factor in the renal response to nephrotoxins.
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PMID:Dose-response studies of gentamicin nephrotoxicity in rats with experimental renal dysfunction. II. Polyvinyl alcohol glomerulopathy. 402 16

We report the first comparative study on enalapril maleate, a new angiotensin converting enzyme inhibitor, in patients with uncomplicated mild to moderate essential hypertension. Fifty-four patients were randomly assigned to treatment with enalapril or propranolol for 16 weeks following a placebo run-in-phase. The study was double-blind. Enalapril and propranolol both reduced blood pressure, though the changes were significantly treated with enalapril were normotensive at the end of the study. Enalapril treatment was associated with a significant reduction in weight. Both drugs raised plasma potassium and urea. No haematological abnormalities occurred with enalapril and there were no reports of rash, taste disturbance or proteinuria. At the end of the trial the mean daily dose of enalapril was 20 mg and that of propranolol was 180 mg.
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PMID:Enalapril in essential hypertension: a comparative study with propranolol. Enalapril in Hypertension Study Group (UK). 633 82

The plasma renin activity (PRA) was determined by radioimmunoassay in 102 subjects with normal blood pressure. In this group, 56 were female and 46 male, their ages ranged between 13 and 90 years, they were not receiving any medication and their diet contained normal amounts of sodium and potassium. In addition to the PRA measurements, their weight, height, blood pressure, hemoglobin, hematocrit, serum and urinary sodium, potassium, chloride as well as proteinuria and creatinine clearance were studied. A significative correlation was found between the PRA and age. However, no correlation was found between PRA and urinary sodium. The subjects were also divided in three groups: I. less than 30 years old. II. between 30 and 60 years old, and III. over 60 years. A significative correlation between PRA and urinary sodium was found in group II. These results in group II could be explained by the finding of a daily urinary sodium excretion below 250 mEq. Age has a definite influence between PRA and urinary sodium. We found that important changes in the response of the yuxtaglomerular apparatus to the intake of sodium develop around the age of 60. In group II is where we found a more stable equilibrium in PRA. In group I, the response of the PRA to a low intake of sodium was faster and violent, where as in group III the response was slower. Finally we think it is very important in these type of studies to follow very strict methodology, because it is the only way to establish comparisons between the different ethnic groups.
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PMID:[Relation between plasma renin and other variables. An evaluation in the Venezuelan population]. 634 63

Urinary excretion of kallikrein (UKal), sodium, potassium, protein, and creatinine, as well as the kidney content of kallikrein and renin, was studied in spontaneously hypertensive FH/Wjd (FH) male and female rats and in age- and sex-matched normal Wistar rats. With the exception of 1-month-old rats UKal excretion was significantly lower in FH rats than in Wistar rats. FH females also excreted less UKal than Wistar females. No UKal inhibitor or increased degradation of this enzyme in the urine of FH rats was detected. There was no difference in creatinine clearance, blood urea nitrogen, or serum electrolytes, and calcium between 5-month-old FH and Wistar males. Wistar rat kidneys contained about twice as much kallikrein as FH rat kidneys. From the age of 2 months FH males excreted more sodium, as well as urine, than all other groups. No differences in potassium excretion were observed. Only FH males, 4 months and older, developed proteinuria. FH males and females became hypertensive at the ages of 2 and 4.5 months, respectively. Plasma renin activity, as well as renal renin activity, was significantly lower in FH than in Wistar males. In conclusion, the decrease in UKal activity which precedes the onset of hypertension suggests that the abnormality in the renal kallikrein system may be involved in the pathogenesis of hypertension in FH rats.
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PMID:Urinary and renal kallikrein in hypertensive fawn-hooded (FH/Wjd) rats. 636 17

Proteinuria is a side effect of captopril treatment in hypertensive patients. The possibility of reproducing the same renal abnormality with captopril was examined in SHR. Oral administration of captopril at 100 mg/kg for 14 days failed to aggravate proteinuria pre-existing in SHR. Also, captopril treatment failed to potentiate or facilitate development of massive proteinuria invoked by puromycin aminonucleoside in SHR. Captopril had little or no demonstrable effects on serum electrolyte concentrations, excretion of urine, sodium and potassium, endogenous creatinine clearance, body weight, and food and water consumption. However, ketone bodies were consistently present in urine and several lethalities occurred during multiple dosing of captopril in SHR.
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PMID:Effect of captopril on pre-existing and aminonucleoside-induced proteinuria in spontaneously hypertensive rats. 645 43

The cause of the morphological changes and functional defects in the renal tubule seen in patients with severe potassium depletion is unknown. In man and animals potassium status is a major factor regulating ammonia synthesis in the kidney and urinary ammonium excretion. A primary effect of potassium depletion is to cause an increase in ammoniagenesis by the renal tubular cells. It is proposed that the vacuolation of the renal tubular cells and the functional defects of tubular proteinuria, polyuria, resistance to arginine vasopressin, renal resistance to the action of parathyroid hormone, and increased urinary excretion of N-acetyl-beta-glucosaminidase found in potassium depletion are secondary effects caused by high concentrations of ammonia in the renal tubular cells.
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PMID:Increased ammoniagenesis and the renal tubular effects of potassium depletion. 651 81

Interstitial nephritis consequent to rifampin was associated with potassium wasting, an acidifying defect, high fractional uric acid excretion, and glucosuria, indicating a multiplicity of renal tubular transport abnormalities. Enlarged kidneys on sonogram and proteinuria were also observed.
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PMID:Potassium wasting and other renal tubular defects with rifampin nephrotoxicity. 651 18

The characteristics of end-stage renal disease (ESRD) complicating spinal cord injury (SCI) were studied retrospectively in 43 male hemodialysis patients. A control group of male patients dialyzed in the same institution were studied for comparison. The SCI patients had significantly lower serum creatinine concentrations and daily urinary creatinine excretion than the control group, despite comparable creatinine clearances. Therefore, serum creatinine, when compared with the familiar values in non-SCI patients, may greatly underestimate the severity of the renal impairment. Urine output was higher, urine specific gravity lower, and renal glucosuria more common in the SCI patients. 24-hour urinary protein excretion was higher and serum albumin was lower in the SCI patients, with 48% of the patients exhibiting nephrotic range proteinuria. Urine pH was markedly elevated, and pyuria and bacteriuria were present in all SCI patients. Fractional excretion of potassium (159 +/- 16%) exceeded its filtered load in most SCI patients.
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PMID:Features of residual renal function in end-stage renal failure associated with spinal cord injury. 652 25


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