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Query: UMLS:C0730345 (microalbuminuria)
 4,018 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To clarify the ultrastructural changes in renal proximal tubules causing microalbuminuria in the early stage of diabetic nephropathy, three different groups of rats were prepared: rats with streptozotocin (STZ)-induced diabetes given no treatment (DMut; n = 7), rats with STZ-induced diabetes treated with insulin (DMt; n = 7), and non-diabetic rats injected with citrate buffer (control; n = 7). In each group, the laboratory findings, ATP content of the renal cortex, and the size of proximal tubule cells and their nuclei and mitochondria (MT) were determined. In two weeks after the start of the study, MT in renal proximal tubules showed diffuse enlargement in the DMut group as compared with those in the control group. Renal cortical ATP content, fractional sodium excretion (FENa), urinary excretion of beta 2-microglobulin and albumin were also increased significantly in the DMut group relative to the controls. In the DMt group, most of the examined parameters returned almost to normal. There were positive correlations between each of the following parameters: hyperglycemia and MT enlargement, MT enlargement and increased cortical ATP content, increased cortical ATP content and increased FENa, increased FENa and increased urinary excretion of beta 2-microglobulin and albumin. On the basis of these results, we conclude that mitochondrial enlargement, resulting from disturbed metabolism of ATP, may reduce active transport in renal proximal tubules, which, in turn, may impair reabsorption in the tubules. This would cause urinary excretion of low-molecular-weight proteins and microalbumin in the early stage of diabetic nephropathy.
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PMID:Correlation between mitochondrial enlargement in renal proximal tubules and microalbuminuria in rats with early streptozotocin-induced diabetes. 129 Mar 23

Nephropathies associated with human immunodeficiency syndrome (HIVAN) are characterized by gross proteinuria, lack of change in blood pressure, and various histologic lesions. The present study prospectively measured microalbuminuria in 72 HIV-seropositive patients (3 asymptomatic, 32 AIDS-related complex, 37 AIDS) screened for Phase I clinical pharmacology studies. There were 14 patients (19.4%) that had abnormal urinary levels of microalbumin; 7 of these patients (50%) had proteinuria similar to those values found in diabetic nephrotic syndrome. Microalbumin levels were not correlated with race, sex, risk factors of AIDS, disease history, or concurrent drug therapy. In contrast, urinary microalbumin levels were correlated with CD 4 T-cell and WBC counts, tumor necrosis factor alpha and beta 2-microglobulin levels, suggesting an association between AIDS progression and microalbuminuria. By monitoring urinary microalbumin levels, those patients susceptible to the development of nephrotic syndrome could be identified and prophylactic measures initiated.
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PMID:Incidence of microalbuminuria in ambulatory patients with acquired immunodeficiency syndrome. 151 82

In metabolic disorders such as diabetes mellitus (DM) and obesity, renal abnormalities may also occur even when renal dysfunction is not be detected by conventional urinalysis. By use of immunological technique, an investigation was made on the subclinical abnormality in the excretion of urinary proteins in DM and obese (OB) subjects. Urinary excretion of the proteins (albumin, IgG, IgG4, beta 2-microglobulin) and fractional clearances (clearance ratios to creatinine clearance) at sitting position were respectively measured. Albumin excretion rate (AER) and fractional albumin clearance were higher in DM and OB than normal controls (NC). In non-diabetic subjects (OB+NC), body mass index (BMI) significantly positively correlated with AER and fractional albumin clearance. In DM, not only AER and fractional albumin clearance but also IgG4 excretion rate and fractional IgG4 clearance positively correlated with BMI. In DM with BMI less than 22 Kg/m2, HbA1C significantly correlated with AER, IgG4 excretion rate, and fractional albumin and IgG4 clearances. The data suggest that microproteinuria in DM and OB may be of glomerular origin. In DM, in the light of an increase in urinary excretion of negatively charged IgG4, it is also suggested that proteinuria is attributed to the alteration of charge barrier as well as to that of glomerular hemodynamics. Lastly but not least , obesity-related factor should also be taken into account in the development of microalbuminuria of the diabetic patient.
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PMID:[A study on microproteinuria among diabetic and obese subjects without clinically overt proteinuria]. 158 64

To study the relations between renal tubular disorder and glomerular dysfunction in the early phase of insulin-dependent diabetes mellitus (IDDM), we performed concomitant measurements of urinary beta-D-N-acetyl glucosaminidase (NAG), beta 2-microglobulin (BMG), and microalbumin in 29 of pediatric patients with IDDM, 15 normal controls, and 83 patients with non-diabetic ketoacidosis. Urinary NAG levels were significantly elevated in the IDDM patients compared with controls. Urinary BMG levels were also elevated in IDDM, however, they were not as prominent as NAG levels. Although urinary microalbumin levels were elevated in the IDDM patients, statistical analysis did not show any significant difference between the IDDM patients and controls. Urinary NAG and BMG concentrations were also increased in patients with non-diabetic ketoacidosis, suggesting a toxic effect of ketone bodies to renal tubular cells. Statistically significant correlations were noted both between urinary NAG and microalbumin and between urinary BMG and microalbumin. These results suggest that, in early phase of IDDM, microalbuminuria is preceded by elevations in urinary NAG and BMG levels, and that keton bodies have deleterious effects on renal tubular cells.
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PMID:Study on the relation between renal tubular disorders and glomerular dysfunction in the early phase of insulin-dependent diabetes mellitus in children. 159 97

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

The present investigation was performed to confirm the relationship between the circadian variation of microproteinuria and physical activity. Urine samples from 10 normal male volunteers, collected during six consecutive 4-h periods, were examined for albumin, alpha 1-, beta 2-microglobulin, NAG, electrolytes and hormones. The fluctuations in heart rate (HR) and blood pressure (BP) over 24-h were measured at 30-min and 1-h intervals, respectively. Energy expenditure (EE) was calculated using the equation of regression between HR and oxygen uptake measured on another day. The variations of HR (delta HR) and EE (delta EE) based on a 24-h average (bpm and kcal/kg/h) were used as indices of change in physical activity during an ordinary day. The correlation coefficients between delta HR and the variations of albumin (delta Alb) and beta 2-microglobulin (delta beta 2M) from the 24-h average (micrograms/h.cr 1 mg) were 0.619 and 0.670 (p less than 0.001), respectively. Increased excretions of both glomerular and tubular proteins were correlated with the increase in HR and/or EE during daytime activity. During rest time at night, the variations in alpha 1M, beta 2M and NAG excretion were different from the variations in albumin. A temporary inhibition of tubular protein excretion was observed only in the early morning (04:00-08:00), although albumin excretion was inhibited throughout the nighttime. These findings suggested that physical activity may influence the diurnal variations in protein excretions, that albuminuria may be more sensitive to daytime activity, and that fluctuation of tubular protein excretion may be preferably controlled by an endogenous mechanism. Timed overnight or first-morning urine may be recommendable as a sample for determination of microalbuminuria for screening of clinical diabetic nephropathy.
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PMID:[Circadian variations of urinary excretions of microproteins and N-acetyl-beta-D-glucosaminidase (NAG) during the ordinary activity day]. 169 14

The renal effects of the prostaglandin synthesis inhibitor naproxen was investigated in eight patients with incipient type I diabetes nephropathy. The patients were treated with 1000 mg naproxen daily for 4 days in a placebo-controlled double-blind cross-over study. Naproxen reduced urinary prostaglandin E2 (PGE2) excretion by 60%, from 276 ng/24 h to 110 ng/24 h (P less than 0.05). Plasma renin activity (PRA) was reduced by 45% (P less than 0.05). Glomerular filtration (GFR) (single bolus 99mTc-DTPA technique) and effective renal plasma flow (ERPF) (131I-Hippuran clearance) were unchanged by naproxen. Microalbuminuria and renal albumin clearance was unchanged as was also urinary excretion of sodium, glandular kallikrein and beta 2-microglobulin (beta 2-M). Our results show that albumin excretion in incipient diabetic nephropathy is not solely dependent on the renal prostaglandin system. The difference in action between naproxen in this study and indomethacin in previous reports, could be caused by renal actions of indomethacin independent of the prostaglandin system.
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PMID:Effects of short-term treatment with naproxen on kidney function in insulin-dependent diabetic patients with microalbuminuria. 181 19

The effect of the mucolytic agent bromhexine, 72 mg daily for one month, on albumin excretion in insulin dependent diabetes was investigated in a double-blind, randomised, cross-over, placebo-controlled study. Nine patients with normal albumin excretion [overnight albumin excretion rate 3.2 (2.1-8.8) micrograms/min.; mean (range)], six with microalbuminuria [36 (22-95) micrograms/min.] and six with macroalbuminuria [321 (201-1215) micrograms/min.] participated. Albumin excretion was similar after treatment with bromhexine and placebo in all 3 groups [normoalbuminurics 3.6 (1.7-13.5) versus 3.3 (1.9-13.2) micrograms/min.; microalbuminurics 40 (20-128) versus 37 (20-103); macroalbuminurics 396 (247-2160) versus 443 (292-2592)]. Excretion of beta 2-microglobulin and creatinine clearance were identical at the end of each treatment. Blood glucose control and blood pressure remained constant throughout the study in the 3 groups. We conclude that bromhexine 72 mg daily for 1 month had no effect on albumin excretion in IDDM patients with normal and pathological albuminuria.
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PMID:The effect of bromhexine on albumin excretion in insulin dependent diabetes. 188 76

The nature and origin of proteinuria in diabetes mellitus have been investigated by measuring the urinary excretion of seven specific proteins of low (beta 2-microglobin, retinol-binding protein) or high molecular weight (albumin, transferrin, hemopexin and IgG). Using the Alcian Blue binding test, we also measured negative charges on red blood cell (RBC) membrane which according to recent studies might mirror the glomerular polyanion charge. A group of 190 diabetics was examined, including 90 patients with type I diabetes, 23 type II diabetics treated with diet and/or hypoglycaemic agents and 77 longstanding type II diabetics requiring insulin therapy. With the exception of beta 2-microglobulin all proteins measured were excreted in the urine of diabetics in significantly higher amounts than in controls. The assay of transferrin proved the most sensitive (58% positive) followed by albumin (49%), IgG (34%), hemopexin (28%) and retinol-binding protein (26%). Practically the same ranking was obtained when only type I diabetics were considered. RBC membrane negative charges were diminished in diabetics and negatively correlated with the urinary excretion of albumin (r = -0.61, n = 190). RBC charges were also negatively correlated with other urinary proteins of high molecular mass (r between - 0.5 and - 0.2) but presented no relation with urinary beta 2-microglobulin or retinol-binding protein. The loss of RBC charges in diabetics most likely reflects the concomitant depletion of the glomerular polyanion responsible for the increased glomerular leakage of high molecular mass plasma proteins. The preferential increase in transferrin excretion together with the progressive rise in the urinary excretion of IgG lead us to postulate that the loss of glomerular polyanion in diabetes is accompanied, from the early stage, by a progressive decrease in the size-selectivity of the glomerular filter. The urinary excretion of retinol-binding protein was weakly correlated with albuminuria (r = 0.26, n = 186). Eight % of diabetics showed an elevation of urinary retinol-binding protein without evidence of microalbuminuria, which clearly demonstrates that a proximal tubular impairment can occur independently of the glomerular alterations in the course of diabetic nephropathy.
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PMID:Urinary proteins and red blood cell membrane negative charges in diabetes mellitus. 225 3

In 109 patients with insulin-dependent diabetes mellitus (IDDM), we measured the urinary excretion of albumin, the low molecular weight proteins (LMWP) retinol-binding protein (RBP) and beta 2-microglobulin (beta 2m), and brush-border antigens (BBA) revealed by monoclonal antibodies. All such markers of kidney damage and/or dysfunction were higher in diabetic patients than in 44 controls. Increased urinary levels of BBA (p = 0.0001) were associated with higher values of albumin (p = 0.0002), RBP (p = 0.0005) and, to a lesser extent, of beta 2m (p = 0.1), different combinations of values above the reference limits being observed. Some 30 and 40% of patients with and without microalbuminuria, respectively, also exhibited signs of tubulopathy. Although under certain circumstances tubular defects may give rise to small increases in albuminuria, the most likely explanation for our findings is the coexistence of glomerular and tubular damage in some patients with IDDM. Neither the prognostic value nor the pathophysiological meaning of tubular damage and/or dysfunction can be assessed by the present study, owing to its cross-sectional design. Tubular markers thus deserve further studies to clarify whether in diabetic patients they indicate a more severe or diffuse kidney impairment.
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PMID:Urinary excretion of brush-border antigen and plasma proteins in early stages of diabetic nephropathy. 237 16


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