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)

Many renal structural and functional abnormalities have been associated with sickle cell disease. The patients have an impaired urinary concentrating ability but an intact diluting capacity. There are defects in both urinary acidification and potassium excretion, although overt metabolic acidosis and hyperkalemia occur infrequently. Proximal tubular function is supranormal, as manifested by increased reabsorption of phosphate and increased secretion of creatinine. The former results in mild hyperphosphatemia, while the latter causes substantial overestimation of the glomerular filtration rate (GFR) by creatinine clearance. Both GFR and renal plasma flow are increased in young patients with sickle cell disease, but prostaglandin inhibitors decrease the GFR. The GFR progressively decreases with increasing age. Proteinuria, and even nephrotic syndrome, are relatively frequent; the most common renal lesion in children is focal glomerular sclerosis, which may be associated with progressive deterioration in renal function. Glomerular hyperfiltration has been implicated in the pathogenesis of the glomerular lesions, as well as in the development of renal failure. In patients with end-stage renal disease, both hemodialysis and kidney transplantation have been successful. Recurrent hematuria is a relatively common problem in patients with sickle cell disease. The bleeding usually remits spontaneously, but occasionally requires therapy with aminocaproic acid. Papillary necrosis may occur, and is thought to result from medullary ischemia.
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PMID:Renal abnormalities in sickle cell disease. 217 77

To label specific anionic sites on glomerular capillary wall structures, biotin was covalently linked to sialic acid residues by sequential treatment with mild peroxidation and biotin hydrazide, while carboxyl groups were biotinylated by exposure to the combination of biotin hydrazide and a water-soluble carbodiimide reagent. Optimal specific labeling of rat glomerular structures was obtained with in situ perfusion of the biotinylation reagents, followed by fixation in 4% phosphate-buffered paraformaldehyde, embedment in LR White resin, and post-embedment detection of biotinylated sites using a sequence of anti-biotin antibodies followed by a secondary antibody-colloidal gold conjugate. Attempts to use streptavidin-gold conjugates were not successful. Specificity of labeling was confirmed by enzymatic (neuraminidase) pre-treatment or by modification of carboxyl groups, as evaluated by electron microscopy and by solid-phase assays of solubilized glomerular basement membrane (GBM) components. In two rats with heavy proteinuria induced by doxorubicin (Adriamycin), a marked reduction in sialic acid residues within the GBM and on the epithelial cell surfaces was found, suggesting that reduced charge density attributable to abnormal sialylation may be important in the pathogenesis of nephrotic proteinuria.
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PMID:Affinity cytochemical labeling of glomerular basement membrane anionic sites using specific biotinylation and colloidal gold probes. 230 3

The effects of dietary phosphate binder on deoxycorticosterone (DOC)-salt-hypertensive rats were examined. DOC-treated and non-DOC-treated rats were fed the diet either with or without phosphate binder, dihydroxyaluminum aminoacetate. All rats drank 1% NaCl. DOC-salt-treated rats without binder demonstrated marked glomerular hypertrophy, many globally sclerosed glomeruli, severe proteinuria, focal cardiac fibrosis, and splenomegaly. A significant reduction of glomerular hypertrophy, glomerulosclerosis, severity of proteinuria, splenomegaly, and the myocardial lesion took place when the DOC-salt-treated rats were given phosphate binder. The globally sclerosed glomeruli exhibited remarkable hypertrophy while structurally preserved glomeruli showed little evidence of enlargement. The plasma phosphate level was low in rats with dietary phosphate binder. In conclusion, the dietary phosphate binder ameliorated glomerular hypertrophy, glomerulosclerosis, proteinuria, myocardial fibrosis, and splenomegaly occurring in DOC-salt-treated rats. The data indicated that there was an association between glomerular hypertrophy and glomerulosclerosis in this model. The exact mechanisms of action of the phosphate binder, however, remain far from clear.
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PMID:Prevention of 11-deoxycorticosterone-salt-induced glomerular hypertrophy and glomerulosclerosis by dietary phosphate binder. 231 24

A series of blood and urine samples was collected from each of eight normal foals between birth and eight weeks. Blood chemistry relating to renal function was evaluated as well as physical and chemical characteristics of urine. During the first 4d of life it was impractical to suggest meaningful normal values due to wide variation among foals and with time. Serum urea and plasma creatinine fell markedly to levels less than those previously reported for normal adult horses, while urine, mildly hypersthenuric at birth, rapidly became hyposthenuric. There was also a marked proteinuria during the first 48h. After 4d clinicopathological values stabilised. Urea and creatinine remained at subadult levels and hyposthenuria was maintained. While there was some variation with time, generally the urinary activity of gamma-glutamyl transpeptidase (GGT) and alkaline phosphatase (AP) was greater in foals than in adults; plasma potassium, the creatinine clearance ratio of potassium (% Cr K), serum inorganic phosphate and the creatinine clearance ratio of phosphate (% Cr PO4) were greater than in adults while plasma chloride and the creatinine clearance ratio of chloride (% Cr Cl) were lower in foals than in adults. Urinary pH was acidic and epithelial cells and calcium oxalate crystals more prevalent in the urine of foals than in that of adults. The information presented here will be useful in the diagnosis and management of renal disease and azotaemia in foals.
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PMID:Indices of renal function: values in eight normal foals from birth to 56 days. 239 72

Peripheral mononuclear blood cells isolated from nephrotic subjects with minimal-change nephrotic syndrome (selective proteinuria greater than 3.5 g/24 h) or various other forms of glomerulonephritis (non-selective proteinuria greater than 3.5 g/24 h) were stimulated with concanavalin A and cultured for 20 h in the presence of kidney tissue under standard conditions. Identical cultures were developed with phosphate-buffered saline from normal control donors. Triplicate cultures of each subject (3 X 10(6) cells/ml) were incubated with or without 5, 10, or 20 micrograms/ml concanavalin A per milliliter serum-free tissue culture medium upon cryostat sections from normal rat kidney. The cells were subsequently removed, and the tissue sections were washed and stained for sialoprotein using the colloidal iron method and evaluated for stainability of glomerular polyanion using light microscopy. The results show that peripheral mononuclear blood cells from subjects with minimal-change nephrotic syndrome had affected glomerular polyanion in vitro during incubation with kidney tissue in a significantly (p less than or equal to 0.005) higher number of cases (15/17) as compared with the number of glomerulonephritis patients who scored positive in 4 out of 14 cases, whereas this was the case in 3 out of 18 cases of the normal donors. It is concluded that stimulated cellular immune reactivity of peripheral mononuclear blood cells from subjects with minimal-change nephrotic syndrome in vitro is associated with the potential impairment in vitro of an important part of the glomerular filtration barrier. Since this cellular activity occurred to a significant lesser extent in other nephrotic subjects, this response is not related to the nephrotic state per se.
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PMID:Loss of glomerular polyanion in vitro induced by mononuclear blood cells from patients with minimal-change nephrotic syndrome. 242 34

In 75 bitches with pyometra single urine samples were examined for gamma-glutamyl transferase (gamma-GT), protein, glucose, specific gravity, bacteria, red blood cells and white blood cells. Serum samples were examined for urea, creatinine, inorganic phosphate and gamma-GT. Biochemical findings were compared with the degree of illness (clinical signs). Twenty one bitches had no signs of renal disease. Seventeen showed only glomerular damage indicated by proteinuria without signs of proximal tubular damage. Thirty seven bitches had increased urinary gamma-GT levels, indicating proximal tubular lesions, which were associated with proteinuria in 35 and renal failure in 16 of them, and worse clinical findings. In all bitches with pyometra serum levels of gamma-GT were comparable to values in control bitches. Glomerular dysfunction seemed to precede proximal tubular lesions, so that gamma-GT-uria in bitches with pyometra was not an early but rather a late indication of a more profound degree of renal dysfunction, that is, proximal tubular renal damage developed after glomerular dysfunction and preceding renal failure.
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PMID:Urinary gamma-glutamyl transferase and the degree of renal dysfunction in 75 bitches with pyometra. 256 10

In a study of the effect of a low-protein diet on the progression of renal disease 19 insulin-dependent diabetic patients with persistent clinical proteinuria were observed for 12-39 (mean 29) months while they were on a normal-protein diet (1.13 [0.06] g/kg per day), then for 12-49 (mean 33) months on a low-protein diet (0.67 [0.03] g/kg per day). The low-protein diet had no adverse effect on nutrition or glycosylated haemoglobin concentration. Mean supine blood pressure (BP) fell slightly on the low-protein diet and was probably due to the start or modification of antihypertensive medication in 9 patients. The mean rate of decline in glomerular filtration rate fell from 0.61 (SEM 0.14) ml/min per month with the normal-protein diet to 0.14 (0.08) with the low-protein diet, and this effect remained highly significant after adjustment for blood pressure, energy intake, and glycosylated haemoglobin. The rise in the fractional clearance of albumin during a normal-protein diet stopped with the low-protein diet, and there was a significant fall in albumin excretion from 467 (95% CI 234-895) micrograms/24 h on the normal-protein to 340 (138-719) on the low-protein diet. Thus, a low-protein diet, with its reduction in protein and possibly other dietary components such as phosphate or fat, seems to retard the rate of decline of glomerular filtration rate in diabetic nephropathy independently of blood pressure changes and glycaemic control.
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PMID:Restriction of dietary protein and progression of renal failure in diabetic nephropathy. 196 36

Since the first description of tubular proteinuria in 1958, much progress has been made with regard to diagnostic means for detecting small changes in the function of the proximal tubule. Small increases in the excretion of low-molecular-weight proteins can now be determined with great accuracy. Determination of total protein is an economic way of screening large populations but does not give specific information on the type of damage. Determinations of glucose, phosphate and amino acids are relatively insensitive methods, since their excretion is also dependent on diet and nutritional status. Determination of high-molecular-weight enzymes released from damaged tubular cells may be of use for studies of acute as well as chronic effects of nephrotoxic agents, but more data are needed.
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PMID:Markers of tubular dysfunction. 265 26

The triad of insulin, diet and exercise has been the basis for treatment of diabetes for several decades. However, the choice of sporting activities for young diabetics requires an understanding of: (a) the energy metabolism and the adaptation to physical activity in the healthy; (b) the metabolic adaptation during physical activity in the diabetic child; and (c) the practical recommendations concerning diet and insulin that have to be learned by the children themselves. The healthy child utilises immediately available substrates, such as ATP and creatine phosphate in much the same fashion as the adult. However, the capacity for anaerobic degradation of glycogen and glucose seems limited in the muscles of children relative to that of adults. Consequently, the adaptation to resistance exercise should be undertaken with prudence in children and adolescents. In diabetic children, an adequate insulin therapy is required to allow the full benefit of muscular activity on glucose assimilation and to reach the same level of physical performance as the non-diabetic. In the case of insufficient metabolic control, exercise can provoke severe hypoglycaemic episodes, even after muscle activity has ceased, or increase glucose levels and lead to ketoacidosis. Regular physical training induces a reduction in postexercise proteinuria measured in diabetic adolescents but its role in metabolic control remains controversial. If a diabetic child or adolescent follows individual recommendations concerning diet and insulin, he or she can perform physical activity much the same as a young non-diabetic. These recommendations include: (a) self-measurement of blood glucose concentration before and after exercise; (b) ingestion of carbohydrates before, during, and after exercise; (c) reduction of the insulin dose during and immediately after exercise; and (d) not choosing an injection site involved with muscular work. The only prohibited sports are those which constitute a danger to the diabetic child by provoking an eventual hypoglycaemia. The best sports are those that require progressive physical effort and that are spread out over several hours.
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PMID:Sport and the diabetic child. 265 64

Chronic renal failure was diagnosed in 15 Bull terrier dogs. The dogs ranged in age from one to 8 years. History and clinical findings typically included lethargy, anorexia, polyuria, polydipsia and weight loss. Affected dogs were azotaemic, had elevated serum phosphate and cholesterol, and proteinuria was apparent in all dogs tested (13/13). The concentration of urine was consistently in the nil to minimally concentrated range (specific gravities 1.011-1.017). In those dogs necropsied, both kidneys were approximately two-thirds normal size, tough in consistency, with a pale cortex and a finely nodular capsular surface. Histologically, there was marked nephron loss, diffuse interstitial fibrosis and focal dense radial fibrosis which was especially evident in the renal medulla. Tubular dilation was widespread with focal mineralisation of tubular epithelium and adjacent basement membranes. Glomeruli were often shrunken and segmentally fibrotic. Some Bowman's spaces were extremely dilated. Many less severely affected glomeruli had thickened basement membranes.
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PMID:Chronic renal disease in bull terriers. 277 60


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