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)

In seven patients on maintenance hemodialysis, de novo recurrent renal stone formation was observed. In all patients, the underlying disease was glomerulonephritis, with or without the nephrotic syndrome. All patients had considerable persistent proteinuria. The stones consisted predominantly of protein, as revealed by amino acid analysis, and had a negligible carbohydrate and lipid content. Only in some specimens, X-ray diffraction and scanning electron microscopy revealed the presence of small amounts of whewellit (calcium oxalate monohydrate) and/or uric acid. In semithin sections, the stones had a laminated texture and exhibited structural anisotropy under polarized light. With transmission electron microscopy, they were found to consist of peculair microfibrils. The proteinaceous material differed from fibrin or Tamm-Horsfall-protein, as indicated by ultrastructure, carbohydrate analysis, and amino acid analysis. Symptomatic de novo matrix stone formation constitutes another complication of dialyzed patients which has not been reported so far.
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PMID:Urinary matrix calculi consisting of microfibrillar protein in patients on maintenance hemodialysis. 54 10

Hyperoxaluria is frequently seen in patients with inflammatory bowel disease, or after resection of the ileum. It is assumed to be responsible for the development of nephrolithiasis, nephrocalcinosis (oxalate nephrosis) and progressive renal impairment in these patients. Steatorrhea may aggravate the severity of hyperoxaluria. A 60-year-old male underwent massive resection of the jejunum and ileum 10 years prior to admission, due to strangulation of the small bowel, with occlusion of the superior mesenteric artery. He remained well except for steatorrhea which developed two-and-a-half years prior to admission, when microhematuria, proteinuria and oxaluria developed progressively. Since that time, the nephrolithiasis, nephrocalcinosis and renal failure have continued to worsen despite therapy with oxalate restriction and oxalate-binding agents. A renal biopsy, performed late in the clinical course, showed severe changes in the renal parenchyma. The decline in renal function proved irreversible. The unusual metabolic consequences of massive resection of the small intestine and their mechanisms are discussed.
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PMID:Hyperoxaluria, nephrolithiasis, nephrocalcinosis and renal failure after massive resection of the small intestine: report of a case. 136 95

In 26 healthy individuals and 114 patients with urolithiasis, total urine protein levels were measured in a single sample by using the stain ponceau S. The findings were statistically analyzed. The levels of the protein were found to be 27-80 mg/l in the healthy individuals, while the distribution of the data was asymmetric as viewed from high values. The patients with urolithiasis exhibited their protein levels according to the type of nephrolithiasis. Proteinuria was demonstrated to be less pronounced in patients with oxalate and urate nephrolithiasis than in patients with coral phosphate calculi. There was a substantial asymmetry in the distribution of total urine protein for all the examined groups of urolithiasis patients, as well as great dispersion values, which fails to regard the parameter alone as a diagnostic criterion for the type of nephrolithiasis. At the same time it was noted that simultaneous examination of the levels of total protein, uric acid, potassium, and sodium enabled the type of a concrement (oxalate or phosphate) to be in vivo estimated with approximately 85% probability.
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PMID:[Total urinary protein in different types of nephrolithiasis]. 194 15

The exact role of urinary proteins in kidney stone formation remains an area of controversy. Some investigators believe that urinary proteins are selectively incorporated within urinary calculi and as such have an active role in stone formation. Other investigators believe that urinary proteins are nonspecifically adsorbed into urinary crystals and thus have only a passive role in stone formation. In the current investigation a previously described stone-forming animal model (hyperoxaluric rat) was utilized along with an animal model for renal tubular injury (gentamicin nephrotoxicity) in an effort to clarify the role of urinary proteins in kidney stone formation. Urine specimens were collected before and after the induction of stone formation and after the induction of renal tubular injury. The purified proteins from each urine specimen were separated in two dimensions by electrophoresis resulting in a characteristic "map" of protein spots for each urine specimen. All animals in the stone-forming group had pathologic evidence of early stone formation (diffuse intranephronic calculosis). Early stone formation was consistently associated with a reduction in the excretion of low molecular weight urinary proteins (30,000 dalton and less than 20,000 dalton ranges). Alcian blue staining confirmed the presence of matrix within clumps of intranephronic calcium oxalate crystals. Renal tubular injury was associated with an increase in the excretion of low molecular weight proteins (approximate 20,000 dalton range) consistent with classical tubular proteinuria. These results suggest that low molecular weight urinary proteins are selectively incorporated within the crystalline structure of the stone early during its formation.
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PMID:The evaluation of urinary protein patterns in a stone-forming animal model using two-dimensional polyacrylamide gel electrophoresis. 200 20

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

A prospective multicenter study was designed to determine the frequency and prognostic importance of hypercalciuria in children with hematuria. Urinary calcium excretion was examined in 215 patients with unexplained isolated hematuria (no proteinuria, urolithiasis, infection or systemic disorder). Hypercalciuria (urinary calcium excretion greater than 4 mg/kg/day) was identified in 76 patients (35%). Compared to patients with normal urinary calcium excretion, children with hematuria and hypercalciuria were characterized by male preponderance, white race, family history of urolithiasis, gross hematuria and calcium oxalate crystals. Renal biopsies were performed in 10 patients with urinary calcium excretion 0.4 to 2.5 mg/kg/day; three had IgA glomerulonephritis, three had glomerular basement membrane thinning, one had proliferative glomerulonephritis and three were normal. Renal biopsies in three patients with hypercalciuria showed focal segmental glomerulosclerosis, hereditary nephritis or no abnormalities. Oral calcium loading tests showed renal hypercalciuria in 26 patients, absorptive hypercalciuria in 15 patients and were not diagnostic in 35 patients. Serum parathyroid hormone, bicarbonate and phosphorus and urinary cyclic adenosine monophosphate concentrations were similar in the three groups of hypercalciuric patients. Urinary calcium excretion after one week of dietary calcium restriction was higher (5.8 mg/kg/day) in renal hypercalciuria than in other hypercalciuric patients (3.4 mg/kg/day), P less than 0.01. One to four years follow-up was available for 184 patients. Eight of 60 hypercalciuric patients developed urolithiasis or renal colic compared to 2 of 124 patients with normal urinary calcium excretion (P less than 0.001). Hypercalciuria is commonly associated with isolated hematuria and represents a risk factor for future urolithiasis in children with hematuria.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Idiopathic hypercalciuria: association with isolated hematuria and risk for urolithiasis in children. The Southwest Pediatric Nephrology Study Group. 240 91

Acute renal failure was diagnosed by clinical, necropsy and histological criteria in 39 flocks (20 low ground, 13 hill and six marginal upland) in areas served by six veterinary investigation centres. Forty-eight lambs of 12 different breeds or crosses were investigated. The mean age of affected lambs was 38 days (range seven to 84 days); 21 lambs (44 per cent) were aged seven to 28 days, while only eight (17 per cent) were older than two months. Mortality in clinically affected lambs was almost 100 per cent, with no response to various treatments. Histological examination showed that 40 lambs (83 per cent) had nephrosis, while the rest had toxic tubular necrosis, interstitial nephritis or tubular damage associated with oxalate crystal deposits. Only about half of the lambs had any evidence of enteric infections or enteropathy. Acutely ill lambs had azotaemia, haemoconcentration and proteinuria; some lambs had glycosuria or haematuria. Samples of plasma from 22 lambs with nephrosis were compared with similar samples from 82 incontact but asymptomatic lambs. The clinically affected group had significantly elevated plasma urea, creatinine, total protein, globulin, phosphorus and chloride concentrations and significantly reduced plasma calcium concentrations compared with healthy lambs. Affected lambs had a significant reduction also in the calcium:phosphorus ratio. No significant differences between groups was found in plasma concentrations of albumin, glucose, lactate, glycerol, creatine kinase, alkaline phosphatase, sodium, potassium or magnesium.
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PMID:Acute nephropathy in young lambs. 291 11

Clinicopathologic findings were retrospectively evaluated in 26 cats and 24 dogs with ethylene glycol intoxication. Common clinical signs were ataxia, depression, vomiting, and hypothermia. Characteristic alterations in the hemogram and serum chemical profile included neutrophilia, lymphopenia, azotemia, hyperphosphatemia, hypocalcemia, hyperglycemia, and decreased whole blood bicarbonate. Common urinalysis findings included isosthenuria, proteinuria, glucosuria, hematuria, calcium oxalate and hippurate crystalluria, and the presence of renal epithelial cells, white blood cells, and granular and cellular casts in the urine sediment. The high death rate (78%) was attributed to delays in presentation, diagnosis, and therapy.
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PMID:Clinicopathologic findings in dogs and cats with ethylene glycol intoxication. 669 34

The calcium oxalate stone formation is induced in rats by a single injection of sodium oxalate (i.p., 7 mg/100 g body weight). There was increase in kidney oxalate concentration and kidney mitochondrial oxalate binding activity with increased lipid peroxidation. Histopathological observations showed larger aggregates of calcium oxalate crystals in the renal tubules. At 12 hours after oxalate administration a maximal crystal deposition in the renal tubule with denuded epithelium, lymphocytic infiltration and blood were observed. Increased blood urea and creatinine indicated kidney failure after oxalate administration. Calcium oxalate crystalluria, hematuria, and proteinuria with casts were observed. Renal antioxidants vitamin E, ascorbic acid and glutathione were significantly decreased on oxalate challenge. Pretreatment with vitamin E provided only partial protection from calcium oxalate deposition. Pretreatment with vitamin E and mannitol together protected the renal tubules completely from calcium oxalate deposition by normalizing the tissue oxalate concentration and mitochondrial oxalate binding activity and increasing the concentration of antioxidants on oxalate challenge.
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PMID:Effect of vitamin E and mannitol on renal calcium oxalate retention in experimental nephrolithiasis. 942 53

Infantile oxalosis is a rare, autosomal recessive disorder. We present three unrelated cases of infantile oxalosis and their families, emphasizing its place as a cause of acute renal failure in infancy, and showing the clinical heterogeneity of the disease within the same family. The affected infants (two males, one female) were 2.5, 3.5, and five months old. Two families had first degree parental consanguinity; two revealed a history of nephrolithiasis; and one of these two had a member who received liver and kidney transplants because of primary hyperoxaluria type I. All the patients presented with the symptoms and findings of acute renal failure. Their hemoglobin levels were between 6.8-9.6 g/dl, urinalysis revealed (+) to ( +) proteinuria and microscopic hematuria. All had metabolic acidosis with BUN levels 67-113 mg/dl and creatinine 3.5-7.7 mg/dl. The abdominal ultrasonographies revealed normal sized hyperechogenic kidneys with the loss of corticomedullary junctions. Calcium oxalate crystals were demonstrated in retina and bone marrow of two patients, and in renal parenchyma of all the patients. The patients were treated with peritoneal dialysis. Renal functions continued to be abnormal (BUN: 47-168 mg/dl, creatinine: 2.8-11 mg/dl) after dialysis, and the outcome was fatal in all. In the presented families, because of the variation of the clinical presentation and the fatal outcome, presence of the multiple genetic loci appeared to be most likely. Further molecular studies will clarify the heterogeneity of this disorder.
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PMID:Fatal outcome of infantile oxalosis: case reports from three families and a review of literature. 967 29


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