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

1. Twelve patients with the nephrotic syndrome were prescribed for 4 week periods a normal protein diet (NPD) containing 1 g of protein/kg ideal body weight. They were then prescribed for further 4 week periods in random order diets with high (HPD) and low (LPD) protein contents, respectively 2.0 and 0.5 g/kg ideal body weight. 2. Compliance was confirmed by dietary history and measurement of urinary excretion. 3. Serum albumin was the same on all diets. Twenty-four hour urinary protein excretion increased progressively with increasing dietary protein (LPD 6.1 g. NPD 8.2 g. HPD 9.2 g). Recumbent plasma renin activity and serum phosphate were significantly increased on HPD (plasma renin activity: LPD 5.7, NPD 4.6, HPD 8.2 pmol of angiotensin I min-1 1(-1); serum phosphate: LPD 1.27, NPD 1.26, HPD 1.41 mmol/l). 4. There was no evidence of protein-induced hyperfiltration or hyperperfusion: 51Cr-ethylenediaminetetra-acetate and [125I]iodohippurate clearances were similar on all three diets. 5. Since proteinuria, increased plasma renin levels and hyperphosphataemia may contribute to progression of renal failure and because HPD did not improve hypoalbuminaemia, the use of HPD in the nephrotic syndrome should be abandoned. 6. Until it can be established that LPD, which is accompanied by the least proteinuria, does not, with long-term feeding, lead to malnutrition, NPD should be used in the treatment of the nephrotic syndrome.
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PMID:Effect of a high protein diet in patients with the nephrotic syndrome. 280 3

Twenty hypertensive diabetic patients (10 with type I and 10 with type II) were treated with captopril, 50 mg twice a day, for three months. The drug was effective as monotherapy in 16 patients. An additional nine months of follow-up was obtained in 12 of these patients (four with type I and eight with type II) who did not need the addition of diuretics to achieve normal blood pressure. For these patients with long-term treatment, since there was no substantial difference between those with type I and those with type II, the data were pooled. Mean arterial pressure significantly decreased shortly after treatment was begun and the reduction was maintained. No significant change was induced by captopril in urine volume, osmolar clearance, and serum and urinary values of sodium, chloride, calcium, and magnesium, whereas significant reduction was found in fractional excretion of potassium and phosphate. The baseline levels of proteinuria were only slightly elevated, yet they fell in all patients during treatment. All patients maintained satisfactory control of carbohydrate metabolism, and none of them required substantial changes in hypoglycemic treatment. The administration of captopril as monotherapy appears to be an effective and safe way of lowering blood pressure in diabetic hypertensive patients, even in the long term, without effects on renal function and in carbohydrate metabolism.
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PMID:Efficacy of captopril in hypertensive diabetic patients. 306 95

Two patients, one with myeloma (Patient 1) and the other with probable chronic lymphocytic leukemia (Patient 2), had reduced renal tubular phosphate reabsorption in the absence of hyperparathyroidism together with other features of the Fanconi syndrome, as consequences of the nephropathy associated with light-chain proteinuria. Both patients had hypophosphatemic osteomalacia, demonstrated for the first time in this condition by iliac bone histomorphometry after in vivo double tetracycline labeling, despite absence of bone pain or Looser zones. Neither patient was vitamin D-depleted, but plasma calcitriol level was normal in Patient 1 and low in Patient 2; only the latter patient had severe muscle weakness. Complete histologic correction of osteomalacia was achieved by treatment in accordance with the biochemical defects--oral phosphate therapy alone in Patient 1 and combined with calcitriol in Patient 2. Both patients are now symptom-free, five and three years after the initial diagnosis of bone disease and hematogenous malignancy. Thirteen previous instances of the same form of osteomalacia were reviewed; in most cases, the Fanconi syndrome developed before its probable cause became apparent. The Fanconi syndrome has also been reported in two cases of osteomalacia due to mesenchymal tumor, but not in osteomalacia associated with prostatic carcinoma. Light-chain nephropathy and consequent renal tubular dysfunction appears to be a third form of oncogenous osteomalacia.
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PMID:Hypophosphatemic osteomalacia and adult Fanconi syndrome due to light-chain nephropathy. Another form of oncogenous osteomalacia. 310 97

Persistent proteinuria is strongly associated with increased mortality in insulin dependent diabetes, and risk of this condition can be predicted many years in advance by subclinical increases in albumin excretion rate (microalbuminuria). Eight normotensive insulin dependent diabetics with microalbuminuria who had overnight albumin excretion rates of between 15 and 200 micrograms/min underwent a three week randomised crossover study of their normal protein diet (median 92 (range 55-117) g/day) and a low protein diet (47 (38-57) g/day). Both diets were isoenergetic, and the low protein diet was supplemented with calcium and phosphate. Median overnight albumin excretion rate fell from 23.0 (15.0-170.1) micrograms/min during the normal diet to 15.4 (4.1-97.8) micrograms/min during the low protein diet. No consistent change was found in urinary excretion of beta 2 microglobulin during the two diets. The reduction in albumin excretion rate was accompanied by a significant fall in median glomerular filtration rate and fractional renal clearance of albumin. Kidney volume remained unchanged. There were no significant changes in glycaemic control or arterial blood pressure. In these few patients restriction of dietary protein had a beneficial effect on microalbuminuria, independent of changes in glucose concentrations and arterial blood pressure.
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PMID:Effect of protein restriction in insulin dependent diabetics at risk of nephropathy. 310 47

The progression of renal failure was analyzed in 108 patients with mild to moderate renal impairment, none of whom had received any form of dietary protein, phosphate restriction or immunosuppressive treatment. The reciprocal of plasma creatinine was plotted against time using a minimum of six plasma creatinine values taken over at least six months (mean 13 values over 41 months). Plots indicated there was linear deterioration in 70 patients, non-linear deterioration in 15 and stable renal function in 24. Progressive renal failure was common in patients with glomerulonephritis, diabetic nephropathy, chronic pyelonephritis and polycystic kidney disease. Most patients with hypertensive nephrosclerosis, analgesic nephropathy and renal impairment following acute renal failure were stable. Among those with progressive impairment the mean rates of deterioration were significantly faster for patients with glomerulonephritis and diabetic nephropathy compared to those with chronic pyelonephritis, polycystic kidney disease and undiagnosed renal disease (p less than 0.01). Hence the underlying renal pathological changes appear to be important in determining progression of renal failure and also the subsequent rate of deterioration. For those with linear progression of renal failure there was a significant correlation between 24-h urinary protein excretion and the rate of deterioration. This relationship held for glomerulonephritis and chronic pyelonephritis as separate diagnostic groups only. Proteinuria, therefore, may be a useful prognostic index for the rate of progression of established renal failure. Calcium phosphate product correlated poorly with the rate of deterioration. We were unable to demonstrate a relationship between spontaneous protein intake and deterioration of renal function. However, patients prescribed high protein diets were not included in dietary analysis and we cannot, therefore, exclude the possibility that a high dietary protein intake may accelerate renal failure. Similarly we were unable to show a significant relationship between blood pressure and progression of renal failure although there were weak correlations between mean arterial pressure and rate of deterioration for chronic pyelonephritis and glomerulonephritis.
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PMID:Renal pathology and proteinuria determine progression in untreated mild/moderate chronic renal failure. 320 6

The effects of hypertension on the course of early chronic renal failure were evaluated in 233 patients with renal disease of diverse etiology, followed for 12-166 months (mean 51.35) on protein-restricted diet. On entry, 174 patients (74.6%) were hypertensive and 59 (25.4%) were normotensive. Serum creatinine levels rose from 2.40 +/- 1.11 to 4.84 +/- 3.26 mg/dl in the overall population. Deterioration of renal function was more evident in hypertensives (percent increase in serum creatinine 112.8, monthly increase 0.053 mg/dl) than in normotensives (percent increase 70.9, monthly increase 0.032 mg/dl). This difference, however, was not statistically significant. Progression of renal failure was significantly faster in hypertensive than in normotensive patients in the groups of polycystic kidney disease and chronic renal failure of unknown etiology. The actuarial renal survival probability at 72 months was 77% in normotensives and 47% in hypertensives. Among the 84 patients (36.1%) who had a fast deterioration of renal failure, 71 (84.5%) were hypertensive. In conclusion, hypertension seems to play an important role in worsening the prognosis of patients with renal parenchymal disease and early chronic renal failure. It is still difficult to separate the exact role of hypertension from the constellation of pathogenetic factors (such as the underlying renal disease, the magnitude and duration of proteinuria, the inadequate dietary contents of protein and phosphate) which may affect the progression of chronic renal disease in man.
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PMID:Role of hypertension on the progression of renal disease in man. 320 72

Dietary phosphate restriction has been shown to be effective in preventing proteinuria, renal histological changes, and progressive renal functional deterioration in experimental renal disease. By use of rats and dogs, this effect has been noted in renal ablation, glomerulonephritis, and an experimental type of diabetic renal disease. Although a beneficial effect of dietary phosphate restriction for human renal disease has not been established, the fact that it is effective in multiple types of experimental renal disease in two distinct species suggests that phosphate restriction could be effective in retarding the progression of renal failure in man.
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PMID:Effect of dietary phosphate restriction on renal function and deterioration. 327 32

Proteinuria is the clinical hallmark of diabetic nephropathy and the harbinger of progressive renal disease. Therefore, the present study was designed to examine the effect of phosphate restriction on the proteinuria of streptozotocin-induced diabetes mellitus in the rat. Uninephrectomy was performed in experimental and control groups to worsen the degree of diabetic nephropathy. Proteinuria was prevented in Sprague-Dawley rats treated with the intestinal phosphate binder, dihydroxyaluminum aminoacetate (DHAAA) (24.75 +/- 20.35 mg/d at 3 months v control, 77.45 +/- 44.72 mg/d, P less than 0.001); an effect that was independent of protein and caloric intake, plasma albumin and lipids, severity of diabetes, mean arterial pressures, cardiac output, and renal calcium accumulation. The effect of DHAAA on protein excretion and glomerular hemodynamics was examined in similarly prepared Munich-Wistar rats; these rats did not tolerate long-term studies. Three weeks of DHAAA again caused a consistent fall in proteinuria (5.98 +/- 7.28 v 34.94 +/- 24.28 mg/d) and in transmembrane hydraulic pressure difference (41.1 +/- 1.2 v 46.4 +/- 2.8 mm Hg, P less than 0.005). In conclusion, phosphate restriction significantly decreases the proteinuria of Sprague-Dawley and Munich-Wistar uninephrectomized rats with streptozotocin-induced diabetes mellitus. Micropuncture of Munich-Wistar rats suggests that a reduction of intraglomerular pressure may be at least partially responsible for such an effect.
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PMID:Phosphate restriction reduces proteinuria of the uninephrectomized, diabetic rat. 337 33

Recent clinical investigations have demonstrated that an early restriction of dietary protein intake may reduce the rate of progression of chronic renal failure in humans. In this study the effects of a restricted-protein diet on kidney function in type I diabetic patients with clinical nephropathy were evaluated. Sixteen patients (9 men, 7 women) with mean age 37.1 +/- 9.8 yr, mean duration of diabetes 17.7 +/- 6.6 yr, proteinuria greater than 0.5 g/24 h, and serum creatinine concentration of 0.7-1.9 mg/dl were studied. Patients were randomly divided into two groups. The low-protein diet (LPD) group comprised seven patients who were kept for 4.5 +/- 1 mo on a diet containing 0.71 +/- 0.12 g X kg-1 X day-1 protein. The normal-protein diet (NPD) group comprised nine patients as controls maintained for 11.7 +/- 7 mo on their usual diabetic diet containing 1.44 +/- 0.12 g X kg-1 X day-1 protein. All patients were studied every 1-2 mo. Metabolic control was assessed by evaluation of 5-8 blood glucose determinations/day and by glycosylated hemoglobin, whereas renal function was evaluated by albumin, IgG and beta 2-microglobulin urinary excretion rates, serum creatinine concentration, and creatinine clearance. At each visit, serum concentrations of total protein, albumin, phosphate, calcium, and electrolytes and weight and blood pressure were also measured. A significant reduction (434 +/- 244 to 205 +/- 212 micrograms/min, mean +/- SD) in albumin excretion rate was found in all LPD patients after dietary protein restriction, with a significant reincrease (689 +/- 201 micrograms/min) in the same patients several months after interruption of diet.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Reduced albuminuria after dietary protein restriction in insulin-dependent diabetic patients with clinical nephropathy. 362 97

Twelve patients with chronic renal failure who exhibited a progressive decline in 24-hour creatinine clearance, despite being given for 2 to 10 months a diet containing 0.3 g per kg ideal weight of protein and 7 to 9 g mg per kg ideal weight of phosphorus, supplemented with vitamins, CaCO3, and 10 g per day of essential amino acids, were changed to a supplement containing predominantly ketoacids. In six patients whose serum creatinine was 7.5 mg/dl or greater at changeover, progression continued unabated. In six patients with serum creatinine levels at changeover of 6.6 to 7.4 mg/dl, one was non-compliant with the diet and progressed to dialysis. In the other five, progression, measured as the rate of change of a bimonthly radioisotope clearance, has been undetectable during the ensuing one to two years. There has been no change in urea appearance, blood pressure, phosphaturia or proteinuria. Nutrition has been maintained. Thus this ketoacid supplemented regimen apparently halted the progression of moderately-severe chronic renal failure for at least a year in a small group of patients in whom restriction of protein and phosphate intake without ketoacids failed to halt progression. In more severe renal failure, no effect on progression was seen.
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PMID:Progression of chronic renal failure in patients given ketoacids following amino acids. 362 95


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