Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0730345 (microalbuminuria)
4,018 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To determine whether or not urinary Alanine aminopeptidase (AAP) could be used as an early marker for diabetic nephropathy, urinary AAP, microalbumin and N-acetyl-beta-D-glucosaminidase (NAG) were measured in 132 diabetic patients and 59 normal subjects. Urinary AAP, microalbumin and NAG in the diabetic patients and the normal subjects were 15.5 +/- 11.7 U/g. Cr and 9.1 +/- 6.9 (P less than 0.01), 27.4 +/- 35.5 mg/g. Cr and 8.4 +/- 4.4 (P = 0.0001), 10. 3 +/- 9.5 U/g. Cr and 3.9 +/- 2.1 (P = 0.0001), respectively. AAP had a moderate correlation with NAG (r = 0.58, P = 0.0001). AAP, microalbumin and NAG showed a slight positive correlation with age (AAP: r = 0.25, P less than 0.01, microalbumin: r = 0.32, P less than 0.01, NAG: r = 0.21, P less than 0.05), although it is significant, and AAP had a positive correlation with urinary protein concentration (r = 0.45, P = 0.0001) in diabetic patients. However, AAP in diabetic patients without proteinuria was higher than that in age-matched normal subjects. Urinary AAP was correlated with the indices of renal tubular damage like NAG, alpha 1-microglobulin and beta 2-microglobulin, so it seemed to be tubular origin but in the patients with clinical proteinuria, it might be partially glomerular origin. Since urine AAP increased in some patients without microalbuminuria and was not influenced by control of blood sugar, AAP could be used as an early marker of diabetic nephropath y in addition to microalbumin and NAG, but the effect of age should be considered in its estimation as in the case of NAG.
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PMID:[Clinical evaluation of urinary alanine aminopeptidase in the patients with diabetes mellitus-comparison among AAP microalbumin and N-acetyl-beta-D-glucosaminidase]. 168 Jul 83

To evaluate effects of acute loading of different proteins on renal function, glomerular filtration rate (GFR), albumin excretion rate (AER), and concentrations of plasma amino acids, 11 normal volunteers and 20 diabetic patients were studied before and after eating 1.0 g/kg body weight of either tuna fish meal or bean curd on separate days. In normal subjects, the mean baseline GFR was 115.8 +/- 9.5 ml/min/1.73 m2, and the mean GFRs after ingestion of tuna fish meal were 134.1 +/- 15.5 (1 hr), 146.2 +/- 18.8 (2 hr), and 157.8 +/- 21.2 (3 hr), respectively. GFR did not significantly increase in normal subjects after ingestion of bean curd. GFR in diabetic patients with normoalbuminuria after ingestion of each protein was similar to the response in normal subjects. In diabetic patients with microalbuminuria, GFR did not significantly increase after ingestion of each protein. In diabetes with macroalbuminuria, GFR decreased after ingestion of tuna fish meal and did not significantly change after intake of bean curd. In both normal subjects and diabetic patients, urinary AER did not increase after each kind of protein loading. Plasma concentrations of alanine, glycine, and arginine, known to induce glomerular hyperfiltration, increased to a greater degree after ingestion of tuna fish meal than after administration of bean curd. These findings suggest that responses of GFR to acute protein loading may differ according to the amino acid composition of the protein ingested and to the stage of diabetic nephropathy.
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PMID:Effects of acute protein loads of different sources on renal function of patients with diabetic nephropathy. 260 33

The knowledge of renal function in the course of BMT is poor. We prospectively investigated glomerular and tubular function in 42 children who underwent BMT because of malignancy. Seventeen children were transplanted autologously. Investigations were performed before and immediately after the conditioning regimen. Inulin and creatinine clearance, albuminuria, urine excretion of alpha 1-microglobulin, beta-N-acetylglucosaminidase, alanine-aminopeptidase, intestinal alkaline phosphatase, and Tamm-Horsfall-Protein as well as sodium- and phosphatreabsorption were measured. The patients were classified regarding use of total body irradiation (tTBI) in the conditioning regimen. BEFORE CR: Glomerular filtration rate (GFR) was not influenced by the underlying diagnosis or previous treatment. Mean GFR was elevated compared with the reference group. Microalbuminuria was elevated in 15% of patients, and mean levels were higher than in the reference group. Proximal tubular dysfunction was indicated by an elevated excretion of alpha 1-MG in 54%, of beta-NAG in 66%, of AAP in 40%, and of IAP in 47%. Fractional sodium excretion was abnormal in 21%, phosphate reabsorption in 5% and THP-excretion in 7% of the patients. AFTER CR: Creatinine clearance was not affected by CR. After CR alpha 1-MG, beta-NAG, FENa, AAP, and IAP were increased compared with values before CR. TP/Clcr was decreased. Excretion of THP was not altered by CR. In patients without fTBI there was a greater increase in alpha 1-MG excretion and decrease in phosphate reabsorption after CR compared with patients conditioned with fTBI. We conclude that significant proximal tubular dysfunction is present in about 50-60% of patients before and in nearly all alter CR. Distal tubular function was less severely affected. Severity of nephrotoxicity after CR did not correlate with pre-existing abnormalities.
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PMID:Renal function after conditioning therapy for bone marrow transplantation in childhood. 907 24

We evaluated the relationship of an alanine or valine polymorphism at amino acid sequence 16 [Val(16)Ala] of manganese superoxide dismutase (Mn-SOD) with diabetes and diabetic nephropathy in Japanese type 2 diabetic patients. Val(16)Ala genotyping of Mn-SOD was done by polymerase chain reaction-restriction fragment length polymorphism with a restriction enzyme ( Bsaw I) in 478 Japanese type 2 diabetic patients and 261 nondiabetic Japanese healthy subjects. The genotype distribution of diabetic and nondiabetic subjects was then compared, and the association of genotype with diabetic nephropathy was evaluated in the diabetic patients. The allele frequency and genotype of the diabetic patients were not different from those of the healthy nondiabetic subjects. The VV type showed a significantly higher frequency in the diabetic patients with nephropathy than did the AA or VA type [VV type: normoalbuminuria 70.8%, microalbuminuria 84.8% (P = 0.0057), macroalbuminuria 84.1% (P = 0.0128)]. Furthermore, logistic regression analysis showed that this polymorphism is associated with diabetic nephropathy independently (odds ratio = 0.461925, P = 0.03). Accordingly, the Val(16)Ala polymorphism of Mn-SOD may be unrelated to the etiology of type 2 diabetes, but it seems to be associated with diabetic nephropathy in Japanese type 2 diabetic patients.
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PMID:The polymorphism of manganese superoxide dismutase is associated with diabetic nephropathy in Japanese type 2 diabetic patients. 1262 25

There is a high prevalence of diabetes mellitus in the population of Saudi Arabia with the majority having non-insulin dependent diabetes mellitus (NIDDM). Random mid-day urine samples were obtained from 100 male [37 insulin dependants DM (IDDM) and 63 NIDDM] and 100 female (51 IDDM and 49 NIDDM) diabetic patients. Eighty-four patients were hypertensive (46 males and 28 females). One hundred and fifty-five subjects, not under medication and without clinical evidence of renal disease, hypertension, or diabetes mellitus were used as controls. Two urinary enzymes, N-acetyl-beta-D-glucosaminidase (NAG) and alanine amino-peptidase (AAP) were measured in the urine, together with total protein and creatinine concentration. Microalbuminuria, glucose and pH were measured using test strips. Increased levels of both NAG and AAP were found in the diabetic subjects. Increased excretion of both these enzymes as well as microalbuminuria was found in the hypertensive groups. The high levels of urinary enzymes found, suggest that renal complications were prevalent in the groups studied. Because of the high incidence of diabetes in Saudi Arabia, a screening program should be established which would include urinary biomarkers for the early detection of renal damage.
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PMID:Urinary enzymes and microalbuminuria as indicators of renal involvement in patients with diabetes mellitus in saudi arabia. 1820 62

The aim of the present study was to evaluate the relationship of the manganese superoxide dismutase (MnSOD) Val16Ala (V16A) polymorphism with type 2 diabetes mellitus (T2DM) and diabetic nephropathy (DN) in Chinese patients, a case-control study was performed. This case-control study included 172 non-diabetic (non-DM) subjects and 257 T2DM patients with or without DN. Among T2DM patients, 154 had DN [albumin excretion rate (AER) >or= 30 mg/24 h] and 103 did not (AER < 30 mg/24 h), but the latter with known diabetes duration >or=10 years. The DN patients were further divided into groups with microalbuminuria (DN-1; n = 92; 300 > AER >or= 30 mg/24 h) and overt albuminuria nephropathy (DN-2; n = 62; AER >or= 300 mg/24 h). PCR-restriction fragment length polymorphism (RFLP) was used to detect genotypes of the V16A polymorphism for all subjects. The genotypic distributions of the V16A polymorphism in non-DM and T2DM subjects were in Hardy-Weinberg equilibrium and Ala allelic frequencies did not differ (11.9% vs. 9.1%; P > 0.05). The AA+VA genotypic frequencies of DN patients were significantly lower than those of non-DN patients (11.6% vs. 24.3%; P = 0.008). Multiple logistic regression analysis revealed that except for HbA1C, triglyceride, and BMI, which were high risk factors for the development of DN, the AA+VA genotype of the MnSOD-V16A polymorphism was an independent protective factor from the development of DN (odds ratio = 0.42; 95% CI = 0.18-0.95; P = 0.037) in T2DM patients. Our results suggested that the MnSOD-V16A polymorphism is associated with decreased risk of diabetic nephropathy in Chinese patients with type 2 diabetes.
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PMID:The manganese superoxide dismutase Val16Ala polymorphism is associated with decreased risk of diabetic nephropathy in Chinese patients with type 2 diabetes. 1898 29

Patients and Methods: A retrospective chart review of 32 GSD- I patients, followed at the American University of Beirut Medical Center, between 2007 and 2018 was conducted. Diagnosis was confirmed by enzymatic and/or genetic studies. Clinical presentation, growth, and kidney outcome were assessed. All patients were evaluated for body mass index, blood parameters of metabolic control including uric acid, alanine, lactic acid, and triglycerides in blood. Kidney evaluation included creatinine clearance, microalbuminuria, citraturia, and calciuria as well as urine microalbumin/creatinine ratio. Results: Almost one third of GSD-I patients developed microalbuminuria. This was detected below 7 months of age in 36% of patients who required early treatment with ACEI with significant reduction in albuminuria. Kidney stones were present in 6% and were associated with hypercalciuria and hypocitraturia. Poor metabolic control reflected by hyperuricemia, lactic acidosis, and hyperalaninemia were noted only in patients who developed microalbuminuria. Conclusion: Glomerular injury may appear in early infancy in poorly controlled patients. Adequate metabolic control and ACEI therapy may improve kidney outcome in GSD I patients. Plasma alanine appears to be a promising and reliable marker reflecting metabolic control in GSD-I patients.
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PMID:Kidney and Metabolic Phenotypes in Glycogen Storage Disease Type-I Patients. 3304 26