Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0033687 (proteinuria)
 24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report ophthalmological findings in 15 cases of nephropathia epidemica. The patients, 13 men and 2 women, were 20 to 62 (mean 30) years of age. The onset of the disease was characterized by high fever, nausea, headache, abdominal pain, backache, somnolence, red throat, proteinuria, and oliguria. The symptoms subsided rapidly during the polyuria stage. Transitory myopia occurred in 8 patients (53%). Conjunctival injection and haemorrhages were seen in 3 patients (20%). One patient had acute glaucoma with oedema in the cornea and shallowing of the anterior chamber, with subsequent anterior uveitis and haemorrhages in the ocular fundus, and another patients had acute glaucoma. Three patients had photophobia which occurred in 2 patients without any glaucoma or anterior uveitis.
 ...
PMID:Ophthalmological findings in nephropathia epidemica in Lapland. 653 41

Chronic renal failure was diagnosed in 6 young Standard Poodles from 2 related litters. Clinically, the disease was characterized by polydipsia, polyuria, anorexia, lethargy, vomiting, and bony deformities suggestive of fibrous osteodystrophy. Laboratory evaluation revealed azotemia and hypercholesterolemia in all 6 dogs and nonregenerative anemia in 3 dogs. Two dogs had hyperphosphatemia and another 2 were hypercalcemic. Isosthenuria and proteinuria were found in both dogs for which urinalyses were available. The kidneys were characterized pathologically by interstitial fibrosis, variable interstitial infiltrates of lymphocytes and plasma cells, tubular atrophy, tubular dilatation, tubular basement membrane mineralization, cystic glomerular atrophy, and immaturity of glomeruli, with inconspicuous capillary lumens.
 ...
PMID:Juvenile renal disease in related Standard Poodles. 662 80

A single s.c. injection of 1-(2-chloroethyl)-3-(trans-4-methylcyclohexyl)-1-nitrosourea (MeCCNU; 20-140 mg/kg) resulted in rapid decreases in renal function as well as leading to a chronic progressive nephropathy in male Fischer 344 rats. Disturbances in renal function were proportional to the dose of MeCCNU administered and included impaired tubular transport of p-aminohippuric acid, a decrease in urine concentrating ability, an increase in urine pH, polyuria, proteinuria and enzymuria. The tubular accumulation of p-aminohippuric acid by kidney slices was decreased as early as 1 hr after MeCCNU administration (100 mg/kg), was maximal within 12 hr and remained depressed for at least 28 days after a single injection of either 40 or 80 mg/kg. Changes in other measures of renal function (increased lactate dehydrogenase excretion, alkalinuria and decreased urine concentrating ability) were delayed from 1 to 6 days after MeCCNU administration and in some cases progressed in severity throughout the 28-day duration of the experiment. The delay between the first evidence of renal damage (decreased p-aminohippuric acid uptake) and the subsequent appearance of enzymuria, proteinuria, polyuria and alkalinuria appears to correspond to a similar delay between the initial insult and the eventual development of cellular necrosis and other histopathological changes. These results demonstrate that MeCCNU is a nephrotoxicant in rats and indicate that even a single acute dose may lead to chronic and irreversible effects on the kidney. The in vivo toxicity model defined herein appears to be an appropriate one for further study of the mechanism of nephrotoxicity of MeCCNU.
 ...
PMID:Nephrotoxicity of 1-(2-chloroethyl)-3-(trans-4-methylcyclohexyl)-1-nitrosourea (MeCCNU) in the Fischer 344 rat. 663 21

The time course for the onset of N-(3,5-dichlorophenyl)succinimide (NDPS)-induced nephrotoxicity was studied in male Sprague-Dawley rats. The ability of rats to recover from a single nephrotoxic dose (100 or 200 mg/kg) of NDPS also was examined. One hour following NDPS administration (200 mg/kg, i.p.), p-aminohippurate (PAH) accumulation by renal cortical slices was decreased 51%. Changes in renal morphology, proteinuria, hematuria, and diuresis were observed at 3 h. Renal damage at 6 h was similar to that seen at 24 h with tubular necrosis greater than that observed at 3 h and some lumina plugged with PAS+ material. Accumulation of both PAH and tetraethylammonium (TEA) by renal cortical slices was decreased; and proteinuria, hematuria, and polyuria were increased at 6 h and 24 h. Blood urea nitrogen (BUN) was not increased until 24 h. Renal function began to return to normal in rats receiving NDPS (100 mg/kg, i.p.) by 48 h, and functional recovery was complete by 168 h, although slight morphological changes were still evident. However, not all rats receiving NDPS (200 mg/kg, i.p.) recovered by 168 h, and some rats (3 of 7) died of renal failure between 96 h and 168 h. Widespread tubular necrosis and increased kidney weight were also present in this group at 168 h. Thus, NDPS-induced nephrotoxicity was evident by 1 h, established by 6 h and maximum between 24 h and 48 h. Recovery from NDPS-induced nephropathy was found to be dose-dependent, and incomplete in some animals at a dose of 200 mg/kg.
 ...
PMID:Onset of and recovery from acute N-(3,5-dichlorophenyl)succinimide-induced nephrotoxicity in Sprague-Dawley rats. 671 May 45

The mechanism of cadmium-metallothionein (CdMT)-mediated nephrotoxicity is being studied in rats using an acute dose regimen. Results of metabolism studies have shown that injected CdMT is rapidly degraded by the kidney with the release of Cd2+ into the cell cytoplasm. Ultrastructural studies indicate that an increase in the number of small lysosomes is the first measurable effect of CdMT in the kidney at 1 hr. This is followed by an increase in the number of small vesicles at 4 hr. It is proposed that these effects are the result of decreased primary lysosome formation and an inhibition of the fusion of pinocytotic vesicles with cell lysosomes by Cd. Functional alterations measured 8 hr after CdMT injection include an increase in urine volume and increased excretion of the low molecular weight protein, RNAase. Prior induction of renal MT by Zn pretreatment prevents the induction of polyuria and low molecular weight proteinuria by CdMT. These data provide further evidence that CdMT nephrotoxicity occurs as a result of Cd2+ toxicity within the cell.
 ...
PMID:Intracellular metabolism and effects of circulating cadmium-metallothionein in the kidney. 673 65

Renal failure was diagnosed in 22 young Doberman Pinscher dogs. The clinical findings were anorexia, weight loss, vomiting, lethargy, polydipsia, polyuria, and dehydration. Laboratory findings were azotemia, hyperphosphatemia, lymphopenia, nonregenerative anemia, hypercholesterolemia, and proteinuria. The kidneys were characterized pathologically by glomerular sclerosis, cystic glomerular atrophy, tubular dilatation, tubular atrophy, mononuclear interstitial inflammation, interstitial fibrosis, interstitial mineralization, and hyperplasia of the collecting duct epithelium.
 ...
PMID:Juvenile renal disease in Doberman Pinscher dogs. 683 84

The antibiotics of the aminoglycoside group are all potentially nephrotoxic. Aminoglycosides are exclusively excreted via the kidneys by glomerular filtration. On passing the proximal tubular cells of the nephron, an active reabsorption and intracellular concentration, 10-20 times the serum concentration, take place. Aminoglycosides are trapped in the lysozymes and inhibit cell metabolism. Functional changes are at first discrete, comprising polyuria, slight proteinuria, enzymuria and glycosuria. With more progressive changes the glomerular filtration rate decreases, followed by increased blood urea and serum-creatinine. The urine contains protein, casts and shedded tubular cells. Ultimately, but rarely, oligo-anuric renal failure may be encountered. Compared with gentamicin, the newer aminoglycosides, amikacin, tobramycin and netilmicin show in animal experiments a decreasing nephrotoxicity in the mentioned order. Extensive studies have demonstrated that netilmicin may be the drug with the least nephrotoxic potential. Clinical studies confirm that netilmicin is less nephrotoxic than gentamicin and compares favourably with tobramycin and amikacin. A survey of the literature is given.
 ...
PMID:The effect of netilmicin and other aminoglycosides on renal function. A survey of the literature on the nephrotoxicity of netilmicin. 701 May 49

Cadmium, an important environmental toxic agent has the kidney as its most important target organ. It is concentrated mainly in the renal cortex. Excessive renal accumulation of cadmium causes well defined morphological and ultrastructural pathological changes in the proximal tubules. Functional changes accompanying cadmium nephropathy include proteinuria, enzymuria, aminoaciduria, glycosuria, polyuria, hepercalciuria, increased urinary uric acid, and cadmium. The observed proteinuria has two components: low molecular weight proteinuria of tubular origin (excess excretion of proteins such as B2-microglobulin) and high molecular weight proteinuria of glomerular origin, (excretion of proteins such as albumin, IgG, transferrin, etc.) The proposed mechanisms of cadmium nephropathy are reviewed. The involvement of metallothionein in cadmium nephropathy and the nephrotoxic effects of cadmium-thionein are discussed.
 ...
PMID:Cadmium nephropathy. 701 69

The development of proteinuria and its response to insulin therapy in acute experimental diabetes was examined in 11 female rats by sequentially measuring 24 h excretion of glucose and total protein before diabetes, during 5-37 days of acute streptozotocin diabetes, during and after 7-14 days of continuous subcutaneous insulin administration. Induction of diabetes promptly resulted in marked polyuria (78 +/- 9 ml/24 h), and glycosuria (6.6 +/- 0.7 g/24 h), while proteinuria quadrupled (from 4.7 +/- 0.7 to 18.8 +/- 1.8 mg/24 h, p less than 0.001). Concurrent with amelioration of polyuria and glycosuria by insulin treatment, proteinuria decreased strikingly (8.5 +/- 1.2 mg/24 h, p less than 0.001) Polyuria and glycosuria resumed after discontinuing continuous subcutaneous insulin, and proteinuria promptly returned to pretreatment levels (19.0 +/- 2.5 mg/24 h). Similarly decreased proteinuria (8.8 +/- 0.9 mg/24 h) recurred in five rats retreated with insulin after 100 days of diabetes. Elevated proteinuria was not associated with lysozymuria or consistent changes in glomerular filtration rate. The rapid fluctuations in proteinuria attending acute diabetes and its effective treatment suggest that metabolic aberrations of diabetes may directly effect renal handling of proteins.
 ...
PMID:Proteinuria in the acutely diabetic rat and its response to insulin treatment. 702 30

Tissue pharmakinetics, morphology of renal lesions and clinical picture of aminoglycoside-induced tubulopathy are described. Almost completely filtered by the glomerulus, they are eliminated in active form and about a third are reabsorbed along the proximal convoluted tubule, thus reaching maximum concentration in the renal cortex in the sixth hour as the drug disappears from the circulation. They are located inside the lysosomes of the convoluted tubule cells where some typical formations called myeloid bodies are present. Cellular lesions are, however, only produced by high doses after, first, clinical manifestations of tubular disturbance such as polyuria, tubular proteinuria, enzymuria, followed, if the toxic insult persists, by renal insufficiency. This can present clinically as progressive renal function deterioration dependent on the dose-time factor. This deterioration is usually not oliguric and it may also present as a sudden oliguric renal insufficiency. The now fully documented risk factors are discussed as well as the duration of treatment (not more than 11 days), the dosage (3 mg/kg/die), the dosage intervals, the age factor (the elderly being shown to be more highly sensitive to the drug), the association with other aminoglycosides or diuretics or cephalosporin. It is very important to diagnose already existing nephropathies or renal insufficiency, in which case dosages must be appropriately reduced. The nephrological history of the patient and control of urea and creatinine clearances before the start of treatment (in addition, obviously, to functional control of the eighth pair of cranial nerves) are essential for all patients receiving courses of aminoglycoside therapy. It is also necessary to check renal function by daily measurements of creatinaemia and urine. These precautions are valid for all aminoglycosides including those that have come on to the market most recently.
 ...
PMID:[Renal tolerance for aminoglycosides]. 705 26


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>