Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:Q92565 (GFR)
 4,179 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Conservative management of chronic renal failure in children is essentially based on dietary prescription including recommendations for high caloric intake and a certain limitation of protein intake according to GFR in order to avoid any extra loading with nitrogen wastes. Prescriptions for sodium potassium and water have to be adjusted on their residual output. Prevention of osteodystrophy needs supplement of calcium, chelation of phosphorus with aluminium hydroxide and the prescription of vitamin D or its active derivatives. High blood pressure when present must be carefully controlled. Drugs, when necessary, have to be given with a dosage taking into account the level of renal failure. Finally, the mode of life of the uremic child should be as close to normal as possible.
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PMID:Conservative treatment of chronic renal insufficiency in children. 4 67

Renal responses to reducing dietary nitrogen were studied in four ewes during intravenous infusion of arginine vasopressin. The fall in urea excretion and in plasma urea concentration was accompanied by significant reduction in GFR and in urine osmolality. The fraction of filtered urea reabsorbed increased despite reduction in the urea U/P concentration ratio and this increase was sustained when the urea U/P ratio was further reduced at higher urine flows observed when the drinking water was replaced with saline. This procedure also sustained the RPF which in the absence of additional salt was significantly reduced on the low protein diet. It is suggested that the fall in GFR and the increase in the fraction of filtered urea reabsorbsed may contribute to nitrogen economy and that the increase in fractional reabsorption and the reduction in urine osmolality on the low protein diet provided evidence of active reabsorption of urea by renal tubules.
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PMID:The effects of reducing dietary nitrogen and of increasing sodium chloride intake on urea excretion and reabsorption and on urine osmolality in sheep. 24 64

This experiment was designed to test whether protein consumption reduces the amount of filtered calcium reabsorbed by the kidney. Nine subjects were each fed meals containing 18 g protein and 54 g protein. The intake of energy, sodium, calcium, phosphorus, magnesium and zinc was similar in the two meals. For 4 hours after the meal, measurements were made of serum calcium (total and filterable), serum creatinine, and urinary calcium, creatinine, zinc and nitrogen. Calcium reabsorption was calculated in five clearance periods, as (filterable calcium X GFR) minus urinary calcium. Urinary calcium, zinc and nitrogen were significantly higher between 2 and 4 hours after consumption of the high protein meal. Protein level did not affect urine pH or volume, serum total or filterable calcium & or GFR. The percentage reabsorption of filtered calcium was significantly lower 0.5 hours after the high protein meal, so that at 2.5 hours, reabsorption was 98.0% compared to 98.7% after the lower protein meal. We conclude that protein consumption reduces the amount of calcium reabsorbed by the kidney.
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PMID:Reduction of renal calcium reabsorption in man by consumption of dietary protein. 45 88

Observations on the influence of extrauterine life upon renal functional maturation in the human being were made in 49 newborn infants of 25 to 41 weeks' GA during the first 48 hours of life, and in serial studies of 12 of these infants whose GA at birth was less than or equal to 34 weeks. GFR was found to be uniformly low in infants born prior to 34 weeks' GA, and increased rapidly after 34 weeks' GA. Glucosuria was found to occur commonly in infants less than or equal to 30 weeks' GA. Glomerulotubular balance for glucose was noted in every infant studied, regardless of GA or length of time since birth. Mean values for TRP at every age prior to feeding was greater than or equal to 85%, and decreased concomitantly with the rise in serum phosphate concentrations after feedings were introduced. The urinary excretion of alpha amino nitrogen was greatest in infants less than 34 weeks' GA. These studies suggest that renal functional development in the human infant is closely related to conceptional (GA + postnatal age) age, and that the pattern of renal functional development for the premature infant during extrauterine life is similar to that of the fetus in utero of corresponding conceptional age.
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PMID:Developmental patterns of renal functional maturation compared in the human neonate. 64 17

The importance of humoral factors, including urea, in the adaptations in electrolyte excretion which occur with acute or chronic reduction in nephron mass was studied using isovolemic cross-circulation in 38 pairs of anesthetized rats. After initial clearance studies, donor rats with acute (48 h) three-quarter nephrectomy or sham operation, acute urea loading, or chronic (2-3 wk) three-quarter nephrectomy or sham operation, underwent cross-circulation with normal recipient animals. Donor rats with acute three-quarter nephrectomy caused a marked natriuresis-kaliuresis in normal recipients. Natriuresis resulted from inhibition of tubular reabsorption independent of changes in GFR or renal plasma flow. Urea was a major but not the only factor involved in the cross-circulation natriuresis-kaliuresis. The severity of reduction in nephron mass, as indicated by the GFR of the donor rat, correlated with the increase in electrolyte excretion in the recipient. Donor rats with chronic three-quarter nephrectomy produced a slight but significant natriuresis in recipients which was much less than that seen with acute three-quarter nephrectomy. Since the GFR and blood urea nitrogen level of donors with acute and chronic renal insufficiency were similar, it was evident that the chronicity of reduced nephron mass, through mechanisms that are not clear, had a significant effect on the level of circulating natriuretic and kaliuretic factors in renal insufficiency.
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PMID:Cross-circulation study of natriuretic factors in rats with reduced nephron mass. 72 64

Male Sprague-Dawley rats were exposed to high-dose (0.5%) lead acetate for periods ranging from 1 to 9 months; then lead exposure was discontinued, and animals were sacrificed after 12 months. Controls were pair-fed. Two additional groups of low-dose (0.01%) and high-dose (0.5%) rats were exposed to lead for 6 months, then lead was discontinued and the rats were treated with three 5-day courses of 0.5% DMSA (dimercaptosuccinic acid) over the next 6 months. Controls were rats exposed to lead for 6 months, then removed from exposure for 6 months without receiving DMSA. Low-dose lead-treated rats showed no significant pathological changes with or without DMSA treatment, but exhibited a significant increase in GFR after DMSA. High-dose lead-treated animals showed no functional or pathological changes when lead exposure was discontinued after 1 month. However, when duration of exposure was 6 or 9 months, GFR was decreased and serum creatinine and urea nitrogen were increased as compared to controls. Tubulointerstitial disease was severe. Administration of DMSA resulted in an improvement in GFR and a decrease in albuminuria, together with a reduction in size and number of nuclear inclusion bodies in proximal tubules. However, tubulointerstitial scarring was only minimally reduced. It may be concluded that, except for brief initial exposure, discontinuation of high-dose lead exposure fails to reverse lead-induced renal damage. Treatment with the chelator, DMSA, improves renal function but has less effect on pathological alterations. As GFR improved after DMSA treatment in both low-dose and high-dose lead-treated rats, irrespective of the degree of pathological alterations, it may be concluded that the DMSA effect is most likely mediated by hemodynamic changes.
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PMID:Experimental model of lead nephropathy. II. Effect of removal from lead exposure and chelation treatment with dimercaptosuccinic acid (DMSA). 131 91

In 77 untreated patients (16 males and 61 females, aged 12 to 65 years) with hyperthyroid Graves' disease, and in 107 control subjects (36 males and 71 females, aged 13 to 78 years), blood urea nitrogen (BUN), serum creatinine (Scr) levels, and BUN to Scr ratios (BUN/Scr) were determined. In 53 patients, the determinations were performed before treatment and after restoration of euthyroidism by treatment with an antithyroid drug. In addition, in seven untreated patients and seven normal subjects, renal clearances of creatinine (Ccr), urea nitrogen (Cun), inulin (Cin), and p-aminohippurate (CPAH) were also determined. The distal tubule delivery of chloride (DTD) and the distal fractional chloride reabsorption (DFCR) were also measured in these subjects: DTD = (CH2O + Ccl)/Cin x 100, and DFCR = CH20/(H20 + Ccl) x 100, where CH20 and Ccl stand for clearances of H2O and chloride, respectively. BUN was significantly elevated, while Scr was significantly depressed, in untreated patients with hyperthyroid Graves' disease. Accordingly, the BUN/Scr was markedly elevated. Restoration of euthyroidism accompanied the normalization of all these abnormalities. Ccr and Cun were significantly elevated, but Cin (glomerular filtration rate [GFR]) was slightly, but insignificantly, elevated in the patients. As a result, the ratios Ccr/Cin and Cun/Cin were significantly greater in the patients than in controls (Ccr/Cin, 1.42 v 1.00; Cun/Cin, 0.92 v 0.68). The amounts of urinary creatinine and urea nitrogen (UN) excretion were decreased and increased, respectively, and DTD was significantly depressed, but DFCR was unchanged in the patients. We conclude that BUN is elevated, Scr is depressed, and the BUN/Scr is increased in hyperthyroidism.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Alteration of renal function in hyperthyroidism: increased tubular secretion of creatinine and decreased distal tubule delivery of chloride. 155 47

The Modification of Diet in Renal Disease (MDRD) Study is a multicenter clinical trial designed to assess acceptance, safety, and efficacy of restricted protein and phosphorus diets in patients with progressive renal disease. The Feasibility Study was designed to test procedures and recruitment strategies and to estimate sample size for the Full-Scale Trial. The Feasibility Study was not designed to compare rates of progression of renal disease among diet groups. Patients aged 18 to 75 years, with a glomerular filtration rate (GFR; measured by 125I-iothalamate clearance) between 7.5 and 80 mL/min/1.73 m2, and a previous progressive increase in serum creatinine, were eligible for enrollment. Compliance with prescribed dietary protein intake was calculated from urea nitrogen appearance (UNA). Nutritional status was monitored by anthropometry and serum proteins. Progression of renal disease was calculated as the rate of decline of GFR. Ninety-six patients met all of the eligibility requirements and were randomized to study diets. Follow-up was conducted for a mean duration of 14 months (range, 2 to 22 months). Although most patients did not achieve the prescribed protein intake, marked changes in intake were observed among patients assigned to the low-protein diets, and mean estimated protein intake differed significantly among diet groups. No patients became malnourished. Mean rates of decline in GFR were relatively slow, and variability among individuals was high. As expected, the number of patients enrolled was too small to determine if the rate of decline in GFR was significantly slower among patients assigned to the restricted protein and phosphorus diets. The rate of decline in GFR was significantly inversely correlated with long-term average mean arterial blood pressure (MAP), even among patients whose blood pressure was controlled to levels within the normal range. However, because patients were not randomly assigned blood pressure goals, it was not possible to determine whether a causal relationship exists. Based on the experience gained during the Feasibility Study, the design for the Full-Scale Study includes two studies of defined by patients' baseline levels of renal function. Within each study, patients will be assigned randomly to one of two diets, and within each diet group, to one of two levels of blood pressure control. Based on variability of rates of decline in GFR slopes observed during the Feasibility Study, 800 patients with follow-up periods of up to 4 years will be required for the Full-Scale Trial.
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PMID:The Modification of Diet in Renal Disease Study: design, methods, and results from the feasibility study. 162 75

To maintain nitrogen equilibrium when prescribed a low protein diet (LPD), metabolic adaptations occur involving a reduction protein turnover, principally decreased muscle protein degradation. Studies suggest that in patients with chronic renal failure (CRF) uncomplicated by metabolic acidosis (MA), these adaptive responses are intact. Because MA stimulates muscle proteolysis, this study examined the hypothesis that in CRF complicated by MA, the adaptation to LPD may be impaired, inducing a nitrogen wasting state. Six adults with CRF (mean GFR: 12.8 +/- 1.5 ml/min) and MA (mean serum bicarbonate: 17.0 +/- 1.0 mM/liter) receiving an unrestricted diet (protein intake: 1.2 g/kg body wt/day) were converted to an isocaloric LPD (protein: 0.6 g/kg body wt/day). Two weeks later total urinary nitrogen losses decreased, but skeletal muscle protein catabolism (SMPC), assessed from the urinary 3-methyl histidine:creatinine ratio, increased, demonstrating impairment in the adaptive down-regulation of SMPC. The LPD was continued for a further two weeks and MA was corrected with oral sodium bicarbonate (mean serum bicarbonate: 24.3 +/- 1.2 mM/liter). Correcting MA decreased SMPC to a level below that measured prior to protein restriction. The decreased SMPC was paralleled by further decreases in urinary nitrogen losses, confirming that MA impaired nitrogen utilization. It is concluded that MA can override the expected metabolic adaptive response to a LPD. The associated impairment of nitrogen utilization not only diminishes the efficacy of the diet, but also accelerates the loss of lean body mass.
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PMID:Metabolic acidosis and skeletal muscle adaptation to low protein diets in chronic uremia. 174 30

Thirty-seven young healthy subjects with normal renal function were studied to assess the quantitative effect of protein intake on creatinine clearance. A standard 24-h urine collection and blood sample at the end of the collection were obtained for creatinine and urea concentrations. Correlations between creatinine clearance and urinary urea nitrogen excretion (r = 0.8; P less than 0.0001) and calculated protein intake (r = 0.8; P less than 0.0001) were observed. A significant relationship between creatinine clearance and urea nitrogen excretion was also demonstrated in 28 elderly healthy subjects and 33 patients with renal disease. To demonstrate a cause and effect between urea nitrogen excretion and creatinine clearance in healthy subjects, 18 of the 37 healthy subjects repeated the 24-h urine collection and blood sample after ingesting 5 g of urea in addition to their usual diet. Mean urinary urea nitrogen excretion increased from a mean value of 9.8 +/- 4.0 to 11.8 +/- 4.0 g/day. There was a strong correlation between the changes in urea nitrogen excretion and the changes in creatinine clearance. In acute studies with oral protein loading, there was a significant correlation between creatinine clearance and urinary urea nitrogen excretion. It was concluded that protein intake has a direct and quantitative effect on creatinine clearance in healthy subjects. In normal humans, it is likely that GFR is not a fixed function. Thus, a low creatinine clearance is not a categorical sign of renal disease. A low creatinine clearance adjusted for urea nitrogen excretion may be a useful clinical tool to assess renal function.
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PMID:Effect of diet on creatinine clearance and excretion in young and elderly healthy subjects and in patients with renal disease. 850 21


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