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)

"Minamata disease" was found among the residents along Minamata bay contaminated with the effluent from an industrial plant using mercury. The patients were suffering from various neurologic disorders primarily due to organic mercury poisoning. Evidence is described of renal tubular dysfunction associated with this disease by the immunochemical demonstration or renal tubular epithelial antigen and beta-2-microglobulin in the urine. Nineteen patients with Minamata disease and 35 diseased and healthy control subjects were examined. The contents of urinary renal tubular epithelial antigen and beta-2-microglobulin, and the ratios of these proteins to albumin in individuals with Minamata disease were significantly different from the levels in healthy control subjects (P less than 0.05) were identical to those found in patients with tubular and the values, proteinuria. These results indicate that Minamata disease is associated with renal tubular dysfunction, and also suggest that these procedures would be useful for screening the nephrotoxicity in the environmental exposure of heavy metals.
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PMID:Renal tubular dysfunction in Minamata disease. Detection of renal tubular antigen and beta-2-microglobin in the urine. 6 93

The renal handling of beta-2-microglobulin, amylase and albumin was studied in patients with acute pancreatitis. The data were compared with results obtained from patients with glomerular proteinuria and from patients with tubular proteinuria. Initially during acute pancreatitis, the clearance ratio (clearance protein/clearance creatinine) for beta-2-microglobulin was increased dramatically (77-fold) compared to normals. After four to seven days this ratio had fallen and was elevated only 7-fold. The corresponding figures for amylase were 3.3 and 1.8 times and for albumin 9 and 5 times respectively. In glomerular disease, the clearance ratios for beta-2-microglobulin, amylase and albumin were increased 6, 1.1, and 154 times and in tubular disease 448, 1.1, and 28 times, respectively. The electrophoretic pattern of the urinary proteins during pancreatitis was mostly normal. In a few cases, slight tubular proteinuria was noticed. Amylase activity in serum and urine from patients with pancreatitis was found to sediment, (S20,W = 4.6) in a sucrose gradient, identical to amylase from normal serum and urine. The marked increase in the excretion of beta-2-microglobulin probably reflects interference of the kidney function at the proximal tubular level. Determinations of this protein in urine may be of value in studies of kidney dysfunction that can accompany pancreatitis.
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PMID:Renal handling of beta-2-microglobulin, amylase and albumin in acute pancreatitis. 8 64

The proteinuria of fifteen patients treated with just aminoglycoside or aminoglycoside and either penicillin or cephalosporin was studied. The proteinuria was analysed by means of immunoelectrophoresis, acetate cellulose electrophoresis, thin-layer polyacrylamide gel electrophoresis and sodium dodecylsulphate acrylamide gel electrophoresis. We observed a urinary excretion of free immunoglobulin light chains and an increased urinary excretion of lysozyme in all cases. The increase in urinary excretion of beta-2-microglobulin and retinol-binding-protein appeared only in patients treated with aminoglycoside and cephalosporin. These disturbances disappeared a few days after the treatment was discontinued.
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PMID:Low molecular weight proteins as urinary markers of aminoglycoside nephrotoxicity in man. 9 49

Decreased GFR and TmG and increased beta-2-microglobulin excretion were found in a worker with a nine-year exposure to cadmium. The patient's recent marked weight loss and other multiple symptoms could not be explained on these abnormalities or by results of other specialized studies. Increased urinary beta-2-microglobulin without proteinuria but with elevated blood and urine cadmium levels in this patient raises questions about which biological indicators will prove to be most helpful in effectively monitoring cadmium workers.
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PMID:Cadmium nephropathy--a clinical evaluation. 22 57

Low molecular weight (LMW) proteinurias vary widely in their microprotein composition. In general, there is little correlation between a given microprotein composition and a defined clinical disease (with the exception of the predominant beta-2-microglobulin in Wilson's disease). Free immunoglobulin light chains are a practically invariable component of, and may be the only detectable LMW protein in, 'tubular' proteinuria. The origins and significance of some frequently occurring urinary LMW proteins are discussed.
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PMID:Low molecular weight proteinuria. 123 88

The kidney is considered the critical organ following long term occupational or environmental exposure to cadmium. Tubular dysfunction in the form of low molecular weight proteinuria is the earliest manifestation of cadmium nephrotoxicity. The current acceptable critical concentration of cadmium in the urine is 10 ug Cd/g creatinine. The aim of this paper is to identify the presence of tubular dysfunction among workers with less than 10 ug Cd/g creatinine. The exposed group of 92 workers were from a nickel-cadmium battery factory. The control group of 122 workers were factory and sedentary office workers with no known history of exposure to nephrotoxic agents. The urinary excretion of N-acetyl-D-glucosaminidase (NAG), beta-2-microglobulin (beta 2m) and alpha-1-microglobulins (alpha 1m) were measured from morning spot urine samples. The age, sex and race adjusted NAG and alpha 1m showed increasing trend with rising urinary cadmium levels. Levels were significantly raised when the urinary cadmium was above 5 ug Cd/g creatinine. A similar trend was seen with increasing length of exposure. Renal tubular dysfunction is present among cadmium exposed workers with levels below the current critical concentration.
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PMID:Renal tubular function of cadmium exposed workers. 128 95

The insulin-like growth factors (IGFs) are important mitogens that are present in many body fluids, where they are commonly bound with high affinity to IGF binding proteins (IGFBPs). We investigated human urine for the presence of IGFBPs. Western ligand blots of concentrated, dialyzed normal urine disclosed the presence of two major bands with IGF binding activity, one at 40-44 kilodaltons and another at 31 kDa. Deglycosylation with endoglycosidase F, and immunoprecipitation with alpha HEC1 antibody revealed these proteins to be hIGFBP-3 and hIGFBP-2, respectively. Comparison of IGFBPs in normal serum and urine showed a reversal of the hIGFBP-2/hIGFBP-3 ratio in urine compared to serum, with hIGFBP-2 being the predominant binding protein in normal urine. The 150 kDa form of hIGFBP-3 was absent in normal urine. In patients with renal disease, the urinary IGFBP (U-IGFBP) pattern was altered. Patients with glomerular disease and proteinuria had elevated U-hIGFBP-3, whereas patients with renal failure who displayed increased urinary beta-2-microglobulin had a dramatic increase in U-hIGFBP-1, in the face of normal serum IGFBP profiles. In conclusion, we have documented the presence of IGFBPs in the urine of normal and diseased individuals. The presence of IGFBPs in urine may complicate the assessment of IGF measurements in urine. U-IGFBPs may be potential clinical markers in renal diseases. Additional studies are required before the origin of urinary IGFBPs in both normal and pathological conditions will be definitively established.
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PMID:Characterization of urinary insulin-like growth factor binding proteins. 137 23

At the time of kidney biopsy the pattern of urinary protein excretion (UPE) and renal function were studied in 54 patients (age 16-62 years) with IgA nephropathy (IgAN). Serum and urinary albumin (alb), IgG, beta-2-microglobulin and creatinine were analysed, and excretion rates (UV) and clearances were calculated. The glomerular filtration rate (GFR) was determined by plasma 51Cr-EDTA clearance (51Cr-EDTA) and by 24-hour creatinine clearance (C-Cr 24 h). Glomerular mesangial (volume expansion and cell proliferation), tubulo-interstitial (fibrosis and inflammation) and vascular lesions were classified semiquantitatively on a five-degree scale, and the percentage of glomeruli showing global sclerosis, segmental sclerosis and cellular crescents was calculated. One third of our patients had reduced renal function, three patients uremia and 70 per cent of the patients overt albuminuria. The mean GFR was reduced in microalbuminurics and further decreased in albuminurics and nephrotics. A lower GFR and more proteinuria were found in the patients with more advanced morphological lesions also when the uremic patients were excluded. Segmental glomerular sclerosis correlated with GFR as well as with UalbV and UIgGV, while global sclerosis correlated only with GFR. UalbV and UIgGV also correlated with the extent of interstitial damage but not with mesangial lesions. In summary an accurate determination of GFR and UPE at the time of the kidney biopsy may give an indication of the extent of renal damage. A lowered GFR was also found in mild proteinuria.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Proteinuria and renal function in relation to renal morphology. A clinicopathological study of IgA nephropathy at the time of kidney biopsy. 822 72

We report a case of sarcoid granulomatous tubulointerstitial nephritis diagnosed by renal biopsy. A 60-year-old man presented with productive cough, and exertional dyspnea of 3 months duration. A chest X-ray film revealed diffuse reticulonodular infiltrates in both lung fields. A transbronchial lung biopsy specimen showed inflammation of the alveolar septum associated with non-caseating granulomas. The patient also had tubular proteinuria and glucosuria. Ga-scintigraphy demonstrated an abnormal accumulation of gallium in both lungs and kidneys. Renal function tests revealed tubular dysfunction. Tubulointerstitial nephropathy was suspected. A renal biopsy specimen exhibited tubulointerstitial nephritis associated with numerous non-caseating granulomas, similar to the findings of the lung biopsy specimen. No glomerular abnormalities were evident. Later, a scalene node biopsy confirmed the diagnosis of sarcoidosis. Prednisolone therapy yielded a favorable outcome for both the renal and pulmonary involvement. During the corticosteroid therapy, measurement of the urinary beta-2-microglobulin concentration proved a valuable monitoring tool for assessing the recovery of the tubular impairment.
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PMID:[A case of sarcoid granulomatous interstitial nephritis improved by steroid therapy]. 174 21

Glomerular filtration rate (GFR) was measured by two methods in 9 children with diabetic ketoacidosis (DKA), directly by true creatinine clearance and indirectly by means of serum beta-2-microglobulin levels. We found significantly reduced GFR in the first hours of DKA. The rapid improvement in GFR after fluid and electrolyte replacement indicates that volume depletion is the major cause of low filtration rate. In spite of the reduced GFR we observed pronounced albuminuria and low molecular weight (LMW) proteinuria. We conclude that the pathological albuminuria and microalbuminuria in DKA are caused not by glomerular hyperfiltration but by tubular dysfunction.
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PMID:Reduced glomerular filtration and elevated urinary protein excretion in diabetic ketoacidosis. 211 97


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