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)

We examined renal abnormalities in Greek patients with sickle-cell beta thalassemia (S-beta thal). A total of 17 patients aged 16-59 years suffering from S-beta thal and 17 age- and sex-matched healthy controls were studied. In all individuals we carried out a detailed study of renal function including electrolytes in serum and urine, concentrating or diluting ability, urine acidification ability, glomerular filtration rate (GFR), and hormones [such as plasma renin activity (PRA), serum aldosterone, and erythropoietin (EPO)]. Though the GFR did not differ significantly in patients and controls, half the patients had either supranormal or subnormal values. Serum potassium and uric acid were significantly higher in patients than controls. Serum phosphorus was similar in both groups, though patients with S-beta thal had significantly lower phosphate excretion indices. All patients were unable to maximally concentrate the urine, and seven also had limited ability to maximally dilute it. Five patients had incomplete distal renal tubular acidosis. Four had mild proteinuria, and six had microalbuminuria. Serum EPO and aldosterone were higher in S-beta thal patients than controls, but there was no difference in PRA between the two groups. There was a strong correlation between hemoglobin concentration and EPO levels, which was strongest in patients with GFR < 50 ml/min. We conclude that patients with S-beta thal, like sickle-cell anemia patients, present multiple abnormalities of renal function.
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PMID:Renal abnormalities in patients with sickle cell-beta thalassemia. 923 25

With the increasing use of ifosfamide in pediatric tumors, nephrotoxicity became the point of interest since it may cause chronic morbidity. In this study, the renal glomerular and tubular functions of 25 cases with solid tumors aged between 2-17 years (median 9) who were treated with ifosfamide, were investigated. For this purpose, routine blood urea, creatinine, calcium, phosphorus, electrolytes, urinary creatinine, phosphorus, glucose, protein and urinary retinol binding protein as well as microglobulin were evaluated. Except for two patients who had hypophosphatemia, phosphaturia, and proteinuria, all the cases had normal blood biochemistry, creatinine clearance, tubular phosphate reabsorption; and none had proteinuria, hematuria, or glycosuria. In spite of these findings, urine beta 2 microglobulin and retinol binding protein were found to be high in 11 patients and this elevation persisted during the following one year in 8 cases whose treatments were stopped and their levels increased in three patients who continued to receive fosfamide therapy. In correlation with the increasing cumulative dose of ifosfamide (32-126 g/m2), urinary retinol binding protein or beta 2 microglobulin of patients who are treated with ifosfamide may predict the existence of renal toxicity even if other routine renal function tests are normal. Thus, the periodic evaluation of urinary beta 2 microglobulin and retinol binding protein in patients receiving chemotherapy containing ifosfamide is recommended.
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PMID:Renal dysfunctions secondary to ifosfamide treatment in children. 926 52

Study group consisted of 63 women in the III trimester of pregnancy (gestational age 29-40 weeks). 32 subjects with PIH (investigated group) were compared to control group consisted of 30 healthy patients with uneventful course of gestation. Women with PIH had no proteinuria nor oedema, their mean blood pressure remained at the level of 161 +/- 16.7/98 +/- 12.8 mm Hg. Concentration of calcium, phosphorus and magnesium in serum blood and urine were determined. It was stated that due to renal impairment observed during PIH, calcium urine excretion and calcium concentration in blood serum are decreased while serum inorganic phosphorus levels are increased. No changes in magnesium and ionised calcium homeostasis were seen in the course of PIH.
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PMID:[Homeostasis of calcium-phosphorus-magnesium in women with pregnancy induced hypertension]. 928 28

Sixty five women were in the third trimester of pregnancy (29-40 weeks of gestation) submitted to the study including 35 with primary hypertension (the studied group) and 30 healthy (control group). The following parameters were measured in blood serum and urine from 24 hrs, collection: total Ca and Ca++, inorganic phosphorus (Pi) and magnesium. Generally accepted micromethods were used; Ca++ was measured using AVL type 9140 analyser. Women of the studied group presented mean blood pressure 164 +/- 14/106 +/- 9.7 mm Hg and did not have proteinuria and oedema. They presented decreased concentrations of total Ca (p < 0.004) and ionised Ca++ (p < 0.004), and an increase of Pi (p < 0.002) in blood serum. No differences in magnesium concentrations were found. Distinct decrease of calcium excretion in urine was found in hypertensive women (4.50 +/- 2.76 vs 6.60 +/- 3.4 mmol/24 hrs, p < 0.024). No alterations in phosphorus and magnesium urine excretion were observed in women with hypertension (women of both groups had the same volume of 24 urine). Our study concludes the main alterations in calcium-phosphorus-magnesium homeostasis in pregnant women with primary hypertension are the calcium homeostasis alterations. Phosphorus homeostasis is less affected while magnesium distribution does not change. Hypocalciuria might be related to impaired glomerular filtration in this pathology in pregnancy. Hypocalciuria and lowered serum concentrations of total Ca and ionised Ca++ might prove general deficiency of this element in pregnancy complicated by primary hypertension.
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PMID:[Calcium, phosphorus and magnesium in pregnant women with primary hypertension]. 929 44

The course of chronic renal failure is generally progressive and mediated by several factors that operate in combination. Several extrarenal events which may cause transient or permanent deterioration of renal function, are important, because their correction may slow the progression of renal disease e.g. volume disorders, infection, nephrotoxic agents. In progression of chronic renal disease leading factors are hypertension, proteinuria and high protein/phosphorus intake. Number of evidence suggests that ameliorating hypertension, reducing proteinuria slow the progression of chronic renal failure. Clinical studies in diabetic nephropathy demonstrated that the renoprotective effect of ACE inhibitors was independent of their effect of systemic blood pressure. In ESRD patients access for renal replacement therapy should be obtained as early as possible. An A-V fistula may take several weeks to mature especially in diabetic or elderly patients. Early dialysis has been advocated in diabetic patients. In general, patients can start ESRD therapy when residual kidney function drops to 5-10% of normal value. High quality of dialysis should be provided to the uremic patient with respect of successful renal transplantation.
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PMID:[Current therapy of chronic renal failure]. 987 58

We describe a familial syndrome in two brothers who were investigated after the casual discovery of tubular proteinuria in their 1st month of life. During a follow-up of 20 and 11 years, respectively, the two children grew well and were asymptomatic, but developed the same biochemical abnormalities, i.e., tubular proteinuria and hyperphosphaturia, progressive decrease in serum phosphorus below the normal values for age, and an increase in serum 1,25-dihydroxyvitamin D levels over normal values. Moreover, hyperabsorptive hypercalciuria and systemic osteopenia developed and progressively worsened. In both children, at a different age, medullary nephrocalcinosis appeared. The oldest boy suffered a progressive decrease in urinary concentration ability and in glomerular filtration rate. Oral phosphate supplementation led to reversal of all biochemical abnormalities, with the exception of decreased phosphate tubular reabsorption and tubular proteinuria. With long-term phosphate supplementation, a normal bone mass was reached, while progression of nephrocalcinosis was arrested and impairment of renal function was slowed down. In a family study (siblings and parents), the only detectable abnormality was microglobinuria in the mother, thus suggesting a X-linked inheritance of this disorder. In the two probands a mutation within the renal chloride channel gene (CLCN5) was discovered.
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PMID:A familial syndrome due to Arg648Stop mutation in the X-linked renal chloride channel gene. 1078 36

Sickle cell anemia and the related hemoglobinopathies are associated with a large spectrum of renal abnormalities. The patients have impaired urinary concentrating ability, defects in urinary acidification and potassium excretion, and supranormal proximal tubular function. The latter is manifest by increased secretion of creatinine and by reabsorption of phosphorus and beta(2)-microglobulin. Young patients with sickle cell disease (SCD) have supranormal renal hemodynamics with elevations in both effective renal plasma flow (ERPF) and glomerular filtration rate (GFR). These parameters decrease with age as well as following the administration of prostaglandin inhibitors. Proteinuria, a common finding in adults with sickle cell disease, may progress to the nephrotic syndrome. Proteinuria, hypertension, and increasing anemia predict end-stage renal disease (ESRD). While ESRD can be managed by dialysis and/or renal transplantation, there may be an increased rate of complications in renal transplant recipients with SCD. Hematuria is seen in individuals with all of the SCDs as well as with sickle cell trait. In most cases the etiology of the hematuria turns out to be benign. However, there does appear to be an increased association between SCD and renal medullary carcinoma. Therefore, those SCD patients who present with hematuria should initially undergo a thorough evaluation in order to exclude this aggressive neoplasm. Papillary necrosis may occur due to medullary ischemia and infarction. Erythropoietin levels are usually lower than expected for their degree of anemia and decrease further as renal function deteriorates. An abnormal balance of renal prostaglandins may be responsible for some of the changes in sickle cell nephropathy. Acute renal failure is a component of the acute multiorgan failure syndrome (MOFS). Finally, progression of sickle cell nephropathy to ESRD may be slowed by adequate control of hypertension and proteinuria. However, the prevention of the renal complications of SCD will require a cure for this genetic disorder.
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PMID:Renal abnormalities in sickle cell disease. 1142 1

Renal failure, proteinuria and proximal tubular acidosis are the features of cidofovir renal toxicity, its main side-effect. Proteinuria occurs in more than 40 per cent of patients and correlates with early renal dysfunction. A fall in serum potassium, bicarbonate, uric acid, calcium and phosphorus levels associated with glucosuria is the hallmark of proximal tubular acidosis. Most of the patients exhibit only glucosuria. Renal failure, diagnosed in 12 per cent of treated patients, is a late feature, usually discovered after the onset of proteinuria and glucosuria. Prevention of cidofovir-induced renal toxicity involves a search for other risk factors, probenecid treatment, and requires an optimal hydration status.
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PMID:[Renal tolerance of cidofovir]. 1070 41

Nephropathic cystinosis is a metabolic disease related to lysosomal cystine accumulation in almost all tissues of the body. The first symptoms set up from 5 or 6 months of age including anorexia vomiting polyurodipsia and failure to thrive associated with a proximal tubulopathy (glycosuria, tubular proteinuria, loss of bicarbonate, potassium, phosphorus, etc.) Treatment by cysteamine dramatically changed the prognostic. If started early this treatment allows to delay and possibly to prevent the spontaneous evolution towards end stage renal disease between 6 and 12 years of age and to avoid the growth failure. On the long term the disease involves other organs: eyes, thyroid endocrine pancreas, muscle and central nervous system. The diagnosis of cystinosis is based on the cystine leukocyte assay allowing also the follow up and the adjustment of the treatment. Prenatal diagnosis is possible on chorionic sample. The gene of this recessive disease, mapping on chromosome 17 was recently identified. This gene encodes a protein of the lysosomal membrane involved in the transport of cystine out of the lysosome. There is a juvenile, late onset, form of cystinosis its main symptom is proteinuria with variable tubular alterations. The so called adult form is asymptomatic its only symptom is corneal deposits most often found by chance examination.
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PMID:[Cystinosis from childhood to adulthood]. 1073 Feb 75

The occurrence of renal diabetic complications was studied in diabetic nonobese IIM/FmeSS (eSS) rats. The results were compared with eumetabolic Wistar rats paired by sex and age. Between 6 and 12 months of age, eSS male rats had higher fructosamine values and glucose intolerance as well as increasing proteinuria and uremia. Enhancement in water, calcium and phosphorus fractional excretion with a concomitant lower sodium excretion, was observed from 12 months of age on. 18- and 21-month-old eSS rats exhibited fasting hyperglycaemia and rising values of fructosamine, glucose intolerance and glycosuria. Simultaneously, a notorious worsening of proteinuria as well as alterations in glomerular filtration were verified. Optic microscopy of 12-month-old eSS rat kidneys showed areas of tubular dilatation with protein cylinders. In 21-month-old eSS animals, kidneys appeared overtly damaged. Increased capsular, glomerular and Henle's thin loop diameters were verified in 12- and 21-month-old eSS rats. Glomeruli showed diffuse hypertrophy of mesangial tissue and thickening of the basement membrane. Areas of markedly atrophic and dilated tubules containing acidophilic proteinaceous material were observed. At age of 21 months, kidneys of eumetabolic Wistar control rats presented foci of interstitial and pielic inflammatory infiltrates.
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PMID:Onset and evolution of nephropathy in rats with spontaneous diabetes mellitus. 1087 81


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