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)

A prospective study was performed to determine urinary albumin excretion in a group of 28 patients with systemic sclerosis. At the initial screen one patient had proteinuria and three had microalbuminuria. One year later these abnormalities persisted and in two of of the patients serum creatinine had significantly increased. In addition, a further three patients had developed microalbuminuria. In a control group of 10 patients with primary Raynaud's disease none had microalbuminuria. In a second control group of 16 patients with unrelated skin diseases one patient had microalbuminuria and one proteinuria, but both these patients had a history of hypertension. It is concluded that microalbuminuria is more common in patients with systemic sclerosis than in patients of equivalent age with other dermatological conditions but no vascular disease.
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PMID:Microalbuminuria in systemic sclerosis. 157 87

We studied the long-term effects of the angiotensin-converting enzyme (ACE) inhibitor perindopril, administered for 36 months on glycemic control, creatinine clearance, and albuminuria in hypertensive insulin-treated diabetics. After 1 month treatment with placebo, 39 patients entered the study and received 4-8 mg perindopril/day. Within the first 3 months, diastolic blood pressure was normalized in 80% of the patients. From these, 23 were followed during a total of 3 years on perindopril therapy, and divided in three groups according to their initial urinary albumin excretion rate (AER): 11 had normal AER (less than 15 mg/24 hours), eight had microalbuminuria (AER 15-150 mg/24 hour), and four had AER greater than 150 mg/24 hours and had overt proteinuria. Long-term (3 years) diastolic blood pressure normalization (less than or equal to 90 mm Hg) was achieved throughout the study. Concomitant with blood pressure reduction, a long-term decrease in AER was observed in normo- and microalbuminuric patients. Macroproteinuria was unaffected by perindopril. Glycemic control and creatinine clearance remained stable during the whole study period. No major side effects were observed. We conclude that perindopril safely produces a long-term normalization of elevated blood pressure in hypertensive insulin-treated diabetics without affecting glycemic control. Blood pressure normalization is associated with long-term AER reduction in normo- and microalbuminuric patients.
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PMID:Long-term reduction of microalbuminuria after 3 years of angiotensin-converting enzyme inhibition by perindopril in hypertensive insulin-treated diabetic patients. 158 Feb 74

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

Serum and urinary concentrations of type IV collagen and laminin were measured by enzyme-linked immunosorbent assay (ELISA) in diabetic patients and compared with normal control subjects. In diabetic patients with proteinuria or with renal insufficiency, serum and urinary concentrations of type IV collagen were higher than those of control subjects (p less than 0.005). Furthermore urinary concentrations of type IV collagen and laminin were significantly higher in diabetes, even in the absence of nephropathy, than in normal controls (p less than 0.05). Urinary concentrations of type IV collagen in patients with diabetes and microalbuminuria (0.73 +/- 0.11 mg mmol-1) were significantly higher than in diabetic patients without nephropathy (0.40 +/- 0.060 mg mmol-1) (p less than 0.025). Urinary concentrations of type IV collagen may have a role as an indicator of early diabetic nephropathy. Serum concentrations of type IV collagen in diabetic patients with retinopathy were significantly higher than in normal controls (p less than 0.025). However, urinary concentrations of type IV collagen (p less than 0.05) and serum concentrations of laminin (p less than 0.025) were significantly higher in diabetic patients than normal controls and the difference between patients with and without retinopathy was not significant.
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PMID:Serum and urinary concentrations of type IV collagen and laminin as a marker of microangiopathy in diabetes. 160 Jul 9

Determinants of proliferative diabetic retinopathy (PDR) that occur during the 2nd decade of insulin-dependent diabetes mellitus (IDDM) (early-onset PDR) were investigated in a nested case-control study. From an inception cohort of patients with juvenile-onset IDDM that now has 15-21 yr diabetes duration, the patients with PDR (cases, n = 74) were selected for study along with a random sample of the patients in the cohort without PDR (control subjects, n = 88). The risk of PDR was associated with poor glycemic control during the first 12 yr of diabetes. Relative to patients in the first quartile of the index of hyperglycemia, those in higher quartiles and nonattenders had a four- to fivefold risk of developing PDR. A striking relationship with cardiovascular autonomic neuropathy (CAN) was found. Relative to patients without CAN, patients with significant and mild CAN had odds ratios of 77.5 and 34.6, respectively. Patients with albumin excretion rates greater than 30 micrograms/min had moderately increased risk of PDR (ranging from 4-fold for microalbuminuria to 7-fold for proteinuria). In contrast, patients with impaired renal function had an extremely high risk of PDR. All 20 of these patients were cases, therefore the odds ratio was infinite. All three factors (poor glycemic control, CAN, and various stages of nephropathy) were associated with PDR in multiple logistic regression analysis. However, in models including glycemic control, the association between microalbuminuria or proteinuria and PDR was weakened. In conclusion, our findings are consistent with a hypothesis that the level of glycemia is a primary determinant of early-onset PDR.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Risk of early-onset proliferative retinopathy in IDDM is closely related to cardiovascular autonomic neuropathy. 160 70

von Willebrand factor (vWF) antigens were quantitatively and qualitatively analyzed in plasma and urine in 41 patients with type I (insulin-dependent) diabetes. The patients were divided into three groups according to their albumin excretion: group N (n = 24) without any excretion (less than 20 micrograms/min), group M (n = 8) with microalbuminuria (20-200 micrograms/min), and group P (n = 9) with persistent albuminuria (greater than 200 micrograms/min). Healthy subjects served as controls (n = 28). The plasma concentration of vWF was higher (p less than 0.05) in the patients with diabetes mellitus than in the controls. Differences between the groups of patients were not statistically significant. The typical multimeric structure described for vWF in normal plasma was observed in all patients. In urine, significantly higher excretion of vWF fragments was observed in the three diabetic study groups as compared with the controls. In group P the patients' urinary vWF/creatinine levels tended to be higher than in groups N and M. Qualitative analysis of urinary vWF fragments demonstrated a similar distribution pattern of fragments, with three distinctive peaks, in the patients of groups N and M and in the controls. The distribution pattern of vWF fragments in group P, however, differed clearly from that in the controls and showed a great variation within the group. The urinary fragments tended to be of a higher molecular weight and several less distinct fragments with the whole spectrum of molecular weight were observed. Because in these patients with proteinuria no qualitative changes appeared in plasma, it is suggested that abnormal degradation of vWF occurred in the kidneys.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:von Willebrand factor antigen in plasma and urine in patients with type I (insulin-dependent) diabetes mellitus with and without nephropathy. 161 Nov 44

Diabetic patients who develop proteinuria show a marked increase in cardiovascular morbidity and mortality. The precise pathogenesis of human diabetic kidney disease and the factors responsible for the susceptibility to it remain, in part, obscure. However, there is now evidence that renal disease clusters in families and that genetic factors may be of central importance in determining susceptibility. Predisposition to arterial hypertension has been suggested as playing a contributory role in the development of kidney disease. Hypertrophic processes may be implicated in the susceptibility to arterial wall damage and glomerular injury in diabetes. Interestingly, fibroblasts of patients with diabetic nephropathy show a higher Na+/H+ antiport activity and a greater 3H-thymidine incorporation into DNA than fibroblasts of diabetic patients without nephropathy. The first clinical signs of renal involvement are the appearance of microalbuminuria and a small elevation in arterial pressure. Mesangial expansion accompanies these changes. Microalbuminuria is associated with abnormalities of lipoprotein profiles and higher Na+/Li+ countertransport rates. The environmental changes brought about by diabetes could lead in susceptible individuals to increased systemic and intraglomerular pressures on the one hand and to mesangial expansion on the other. These two processes would cause proteinuria and glomerulosclerosis. Lipid abnormalities may further aggravate the renal histological damage and, in combination with hypertension, contribute to the accelerated atherosclerosis typical of patients with diabetic kidney disease. A vicious circle would thus be triggered, involving reduction in renal function, further hypertension, proteinuria, glomerular obsolence and hyperlipidaemia, and eventually end-stage renal failure or premature cardiovascular death.
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PMID:Risk factors for renal and cardiovascular disease in diabetic patients. 165 64

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

Bedside methods for the detection of microalbuminuria such as Microbumintest (TM) have the advantage of simplicity but not the specificity of radio-immunoassay. In the present study we assessed whether apparently inappropriate positive Microbumintest results in the presence of low urinary albumin concentrations could be accounted for by non-albumin proteinuria of glomerular or renal tubular origin. Urinary albumin and transferrin were considered to indicate glomerular proteinuria, and alpha-1-microglobulin and N-acetyl-beta-D-glucosaminidase to reflect tubular proteinuria. Microbumintest had a sensitivity of 100% and specificity of 67% to detect a urinary albumin concentration of 40 mg/l. Samples with albumin concentration less than 40 mg/l contained more total protein: 110 (78-155) v 60 (35-104) mg/l p less than 0.0001 (geometric means with 1 SD range), more albumin: 11.7 (5.1-26.8) v 5.4 (2.8-10.4) mg/l p less than 0.005 and more transferrin: 496 (191-1284) v 174 (78-389) micrograms/l p less than 0.001, in those testing positive with Microbumintest than in those testing negative. Microbumintest had a sensitivity of 82% and specificity of 75% to detect an albumin concentration of 20 mg/l. In samples containing less than or equal to 20 mg/l albumin, the mean albumin concentration was no greater in those testing positive compared with those testing negative. However, total protein: 108 (72-161) v 60 (34-105) mg/l p less than 0.001, and transferrin: 326 (148-715) v 157 (78-316) micrograms/l p = 0.01 both remained increased in samples testing positive compared with those testing negative.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Microbumintest and non-albumin proteinuria in diabetes. 172 Mar 63

In this article, we analyze the blood pressure (BP) threshold for the start of antihypertensive treatment in insulin-dependent diabetes mellitus (IDDM) patients, with particular emphasis on those with persistent microalbuminuria or proteinuria (incipient and overt nephropathy, respectively). In such individuals, there is a clear increase in the prevalence of hypertension and in actual measured BP values that is not observed in normoalbuminuric patients. In 94 young healthy adults (less than 45 yr of age), average mean +/- SD arterial pressure (MAP; diastolic + 1/3 pulse pressure) was approximately 90.0 +/- 8.1 mmHg, closely corresponding to large population studies. In microalbuminuric IDDM patients, MAP values between approximately 105 and approximately 95 mmHg have been found in different studies, and the level has progressively decreased in various studies between 1984 and 1990 with similar BP-measuring techniques. Somewhat higher values are seen in patients with proteinuria, who are also consistently characterized by reduced glomerular filtration rate (GFR). A clear correlation is found between MAP plotted against the increased rate of microalbuminuria (%/yr) in incipient nephropathy and against fall rate of GFR (ml.min-1.mo-1) in proteinuric patients. In the natural history of renal disease, different cutoff points in MAP for start of progression are observed: greater than 95 mmHg for the start of progression of microalbuminuria and greater than 105 mmHg for the decrease in GFR. During antihypertensive treatment, there is reduction or no progression in microalbuminuria with MAP of approximately 90-95 mmHg and only a limited fall in GFR with MAP of approximately 100 mmHg. However, certain antihypertensive drugs (angiotensin-converting enzyme inhibitors) may have specific renoprotective actions, reducing microalbuminuria at rather low BP levels or even independent of BP reduction. The optimal way of monitoring BP may be by 24-h ambulatory recording.
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PMID:Renal factors influencing blood pressure threshold and choice of treatment for hypertension in IDDM. 174 53


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