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PubMed2006

High prevalence of albuminuria in population-based patients diagnosed with type 2 diabetes in the Shanghai downtown.

OBJECTIVE: The prevalence of albuminuria and the risk factors associated with albuminuria were evaluated among the Chinese patients diagnosed with type 2 diabetes aged over 30 in the Shanghai downtown. We also evaluated the variability of urinary albumin-to-creatinine ratio (ACR) among the three measurements and the relationship between diabetic retinopathy (DR) and albuminuria. METHODS: The 1039 Chinese patients diagnosed with type 2 diabetes aged over 30 were investigated by randomized cluster sampling in the Shanghai downtown and 1018 patients were analyzed in this study. Body mass measurements including height, weight, waist circumference and hip circumference, resting blood pressure, fasting blood measures, urinary ACR and the digitally stored fundus images were investigated. The prevalence of albuminuria was calculated and the risk factors associated with albuminuria were evaluated by stepwise logistic regression. The concordance of urinary ACR was evaluated by observed agreement. The relationship between albuminuria and DR was also evaluated. RESULTS: (1) The mean age of all patients was 66.10+/-11.54 years and the duration of diabetes was 7.89+/-7.16 years. (2) The prevalence of albuminuria was 49.6% among the Chinese patients diagnosed with type 2 diabetes aged over 30 in the Shanghai downtown, 41.4% with microalbuminuria and 8.2% with macroalbuminuria. (3) Microalbuminuria was significantly associated with systolic blood pressure, gender and waist circumference. Macroalbuminuria was significantly associated with systolic blood pressure and duration of diabetes. (4) Observed agreement among the three urinary ACR measurement for albuminuria staging was 73.3% (first versus second), 64.5% (first versus third) and 77.5% (second versus third). Observed agreement in the albuminuria staging between the single urinary ACR measurement and all three urinary ACR measurements was 85.8% (first versus all three), 87.6% (second versus all three) and 81.9% (third versus all three). (5) The percentage of DR in the macroalbuminuric group (59.2%) was significantly higher than that in the normalbuminuria group (16.1%) and microalbuminuria group (24.6%). (6) The macroalbuminuric patients with DR had significantly increased fasting blood glucose and HbA1c compared with the macroalbuminuric patients without DR. CONCLUSION: The prevalence of microalbuminuria observed in the Chinese patients diagnosed with type 2 diabetes aged over 30 in the Shanghai downtown reached up to 41.4% though the observations in our study might be representative of the diabetic patients of the Shanghai downtown. We agreed that at least two of the three urinary collections were done in a 3- to 6-month period because of the day-to-day variability in albumin excretion. The percentage of DR among the patients with macroalbuminuria was 59.2%, and the macroalbuminuric patients with the significantly high plasma glucose and DR were prone to diagnose DN.

Adult↗
PubMed1999

Induction of albuminuria in mice: synergistic effect of two monoclonal antibodies directed to different domains of aminopeptidase A.

BACKGROUND: Aminopeptidase A is an enzyme that is present on podocytes and is involved in the degradation of angiotensin II. In previous studies in mice, we administered single monoclonal antibodies directed against aminopeptidase A. We observed that only monoclonal antibodies that inhibited aminopeptidase A enzyme activity caused albuminuria. METHODS: In this study, the effects of the combined injections of two monoclonal anti-aminopeptidase A antibodies (mAbs) were studied, using a combination of anti-aminopeptidase A mAbs that were directed against two different domains involved in the aminopeptidase A enzyme activity (ASD-3 or ASD-37) and an anti-aminopeptidase A mAb not related to the enzyme active site (ASD-41). RESULTS: An injection of the combinations ASD-3/37 (total 4 mg, 1:1 ratio) and ASD-37/41 (total 4 mg, 1:1 ratio) in doses that do not cause albuminuria when given alone (4 mg) induced massive albuminuria at day 1 after injection. The combination ASD-3/41 had no effect. This albuminuria was not dependent on systemic immune mediators of inflammation and could not merely be related to a blockade of aminopeptidase A enzyme activity. However, a correlation was observed between the induction of albuminuria and the aggregation of the mAbs injected and aminopeptidase A on the podocytes. An injection of the combinations ASD-3/37 or ASD-37/41 did not cause an increase in systemic blood pressure. The treatment with a combination of enalapril and losartan lowered blood pressure (53 +/- 10 vs. 90 +/- 3 mm Hg in untreated mice) and reduced the acute albuminuria by 55% (11,145 +/- 864 vs. 24,517 +/- 2448 micrograms albumin/18 hr in untreated mice). However, similar effects were observed using triple therapy. Therefore, the reduction of albuminuria by the combined treatment of enalapril/losartan seems to be the consequence of the reduction in the systemic blood pressure. These findings argue against a specific role for angiotensin II in this model. CONCLUSIONS: The combined injection of two mAbs directed against different domains of aminopeptidase A induces a massive albuminuria in mice, which is not merely dependent on angiotensin II. We hypothesize that the direct binding of mAbs to at least two pathogenic domains on aminopeptidase A triggers the podocyte to release mediators that are involved in the observed albuminuria.

Albuminuria↗
PubMed2002

Diurnal variations of glomerular filtration rate and albuminuria in diabetic nephropathy.

BACKGROUND: The aim of our study was to evaluate the diurnal variation in glomerular filtration rate (GFR), and the potential mechanisms responsible for such variations in GFR and albuminuria in diabetic nephropathy. METHODS: In three 24-hour urine samples, divided into a night- and daytime portion, diurnal variation in albuminuria (ELISA) was assessed. Furthermore, during recumbency changes in albuminuria, GFR (51Cr-EDTA plasma clearance) and arterial blood pressure (TM2420) from nighttime (00:00 to 05:00 hours) to subsequent daytime (08:00 to 13:00 hours) were examined in 20 type 1 diabetic patients with diabetic nephropathy. RESULTS: The 24-hour urine collections showed an average rise in albuminuria from night- to daytime of 51% (95% CI; 16 to 95; P < 0.01). During recumbency a non-significant rise was recorded from night- to daytime in albuminuria (22%, -8 to 61, P=0.15), simultaneously with an increase in GFR of 9.0% (3.4 to 14.5, P < 0.005) and mean arterial blood pressure (MABP) of 8.0% (4.3 to 11.7, P < 0.0001). No diurnal variation in fractional clearance of albumin was found. Significant associations between MABP and albuminuria were demonstrated during night- (R2=0.50; P < 0.001) and daytime (R2=0.48; P < 0.005). A linear regression analysis between diurnal variations in MABP and GFR showed that an increase in MABP (of 10%) from night- to daytime was associated with a significant increase in GFR (of 8.0%, 0.2 to 4.1, P < 0.02). CONCLUSIONS: Our study revealed diurnal variations in GFR, albuminuria and MABP in diabetic nephropathy, with lowest values during sleep at night. The observed diurnal variation in albuminuria seems to be explained partly by mechanisms related to orthostasis, and partly by the diurnal variation in GFR and serum albumin concentration. The diurnal variation of blood pressure seems to play a role for the diurnal changes in GFR and albuminuria.

Adolescent↗
PubMed2026

Large-scale AI analysis reveals missed opportunities in albuminuria testing and disease-modifying therapy implementation.

AIMS: Albuminuria is a key diagnostic and prognostic biomarker of chronic kidney disease (CKD), associated with adverse cardiovascular and renal outcomes. Despite guideline recommendations, urine albumin-to-creatinine ratio (UACR) testing is infrequently performed in cardiology. This study assessed the uptake of UACR testing, the estimated prevalence of undiagnosed albuminuria, and the use of disease-modifying therapies in patients with cardio-kidney-metabolic (CKM) disease. METHODS AND RESULTS: We conducted a retrospective cohort study of all adults seen at the cardiology department of a tertiary referral centre between 2019 and 2024. Data were extracted using CTcue, an AI-driven platform. Albuminuria was defined as UACR &#x2265;30 mg/g. A weighted logistic regression model estimated albuminuria prevalence in untested patients. Among 77 351 patients (44.8% female, mean age 64.4 years), only 8.9% had a recorded UACR, of whom 46.4% had albuminuria. Testing rates were low across high-risk groups: 29.9% in diabetes, 21.7% in heart failure, and 13.7% in hypertension. In untested patients, the predicted prevalence of albuminuria was 36.6%, and highest in those with eGFR <30 mL/min/1.73m2 (70.0%), heart failure (47.8%), or diabetes (46.8%). Use of disease-modifying therapies was low, even among patients with confirmed albuminuria. In patients with documented vs. predicted albuminuria, 43.0% vs. 39.1% received renin-angiotensin system inhibitors, 12.8% vs. 5.7% received SGLT2 inhibitors, and <1% in both groups received finerenone. CONCLUSION: Albuminuria is substantially underdetected in cardiology practice, possibly contributing to underuse of effective CKM therapies. Systematic UACR screening with structured treatment protocols may help close this gap and improve outcomes for patients with CKM disease.

Humans↗
PubMed2001

Albuminuria in mice after injection of antibodies against aminopeptidase A: role of angiotensin II.

It has been shown that injection of combinations of anti-aminopeptidase A (APA) monoclonal antibodies (mAb) that inhibit the enzyme activity induces an acute albuminuria in mice. This albuminuria is not dependent on inflammatory cells, complement, or the coagulation system. APA is an important regulator of the renin-angiotensin system because it is involved in the degradation of angiotensin II (Ang II). This study examined the potential role of glomerular Ang II in the induction of albuminuria. The relation among renal Ang II, glomerular APAX enzyme activity, and albuminuria was examined first. Injection of the nephritogenic combinations ASD-3/37 and ASD-37/41 in BALB/c mice induced albuminuria, whereas the non-nephritogenic combination ASD-3/41 had no effect. There was no clear relation between the inhibition of glomerular APA activity and albuminuria, yet it was evident that intrarenal Ang II levels were significantly increased in albuminuric mice and not in nonalbuminuric mice. As a next step, anti-APA mAb were administered to angiotensinogen-deficient mice that do not produce Ang II, and kidney morphology and albuminuria were determined. Angiotensinogen-deficient mice also developed albuminuria upon ASD-37/41 administration. Altogether, these findings clearly demonstrate that Ang II is not required for the induction of albuminuria upon injection of enzyme-inhibiting anti-APA mAb.

Albuminuria↗
PubMed1993

Long-term effects of protein-restricted diet on albuminuria and renal function in IDDM patients without clinical nephropathy and hypertension.

OBJECTIVE: To determine the long-term effects of an LPD on albuminuria and renal hemodynamics in IDDM patients without nephropathy. RESEARCH DESIGN AND METHODS: We selected 31 patients with overnight albuminuria between 10 and 200 g/min and without hypertension from a referral-based diabetic clinic. One participant dropped out. A 2-yr randomized prospective study was conducted on 14 patients assigned to an LPD (0.6 g.kg-1.day-1) and 16 patients assigned to continue their UPD. Protein intake was assessed by using urinary urea excretion. Albuminuria (three overnight collections) was measured at baseline and on seven occasions thereafter. GFR and ERPF were measured annually using [125I]iothalamate and [131I]hippuran, respectively. RESULTS: In the LPD group, protein intake decreased from 1.05 +/- 0.32 to 0.79 +/- 0.16 g.kg-1.day-1 (P < 0.005), but only seven participants consumed < 0.8 g.kg-1.day-1. Protein intake was unaltered in the UPD group (P < 0.001 vs. LPD). Baseline albuminuria and renal hemodynamics were not different in the groups. In the LPD group albuminuria decreased from 36 (95% CI, 16-83) to 30 micrograms/min (95% CI, 14-67) (P < 0.05). After adjustment for MAP and diabetes duration, the decrease in albuminuria in the LPD group was 26% (95% CI, 13-36) (P < 0.001), which was significantly different from the 5% (95% CI, -10-22) change in the UPD group (P < 0.005 vs. LPD). Multiple regression analysis showed the actual decrease in protein intake lessened (P < 0.005), whereas prevailing MAP accelerated albuminuria (P < 0.001). Low-protein intake independently reduced ERPF (P = 0.009) and GFR (indirectly via ERPF, P < 0.001) after 1 yr. Only minor changes in renal hemodynamics occurred in the second yr. CONCLUSIONS: This study suggests that long-term dietary protein restriction beneficially reduces albuminuria and renal hemodynamics in IDDM patients with mildly elevated albuminuria. Systemic BP counteracts these effects even in the absence of hypertension. Suboptimal compliance limits diet efficacy.

Adult↗
PubMedDate not supplied

Lipid abnormalities in insulin-dependent diabetic patients with albuminuria.

The relationship between serum lipid, lipoprotein, and apolipoprotein levels and abnormalities of renal function has been investigated in 112 insulin-dependent (type I) diabetic patients. They were subdivided into three matched groups according to the amount of albuminuria: group A (albuminuria less than 20 micrograms/min), group B (albuminuria between 20 and 150 micrograms/min; Albustix negative), and group C (albuminuria greater than 150 micrograms/min; Albustix positive). Twenty-one nondiabetic subjects with albuminuria above 150 micrograms/min but without nephrotic syndrome and/or renal failure and 77 healthy subjects were also studied. Mean total and LDL cholesterol, triglycerides, and apo B were higher, while HDL cholesterol and HDL/LDL cholesterol ratio were lower in group C than in groups A and B; the apo A/apo B ratio was lower in group C than in group A. Differences in apo B and in apo A/apo B ratio were found between groups A and B. No correlation between lipid parameters and amount of albuminuria was observed. Significant differences in lipid concentrations were also found in diabetic patients when compared with nondiabetic subjects with albuminuria and with healthy subjects. The present study confirmed previous reports of lipid disorders in insulin-dependent (type I) diabetes; however, the most important observation was the finding of albuminuria-related differences in lipid parameters in diabetic patients without renal failure. We think that the greater lipid abnormalities observed in diabetic patients with larger amounts of albuminuria might be the consequence both of impairment of glomerular permeability and of the diabetic state.

Adult↗
PubMed1984

Glycaemia, arterial pressure and micro-albuminuria in type 1 (insulin-dependent) diabetes mellitus.

Plasma glucose control and arterial pressure were assessed in 28 Type 1 (insulin-dependent) diabetic patients with different degrees of micro-albuminuria. They were divided into two groups according to their urinary albumin excretion rate: a low micro-albuminuria group (n = 16) with albumin excretion ranging between 12.1 and 28.9 micrograms/min and a high micro-albuminuria group (n = 12) with albumin excretion between 32.4 and 91.3 micrograms/min. The groups were matched for age, sex and duration of diabetes with the same number of normo-albuminuric (2.0-10.4 micrograms/min) diabetic control subjects. Both the low and high micro-albuminuria groups had significantly higher glycosylated haemoglobin levels and mean plasma glucose concentrations during a 24-h profile than their respective normo-albuminuric control subjects. A correlation between glycosylated haemoglobin level and urinary albumin excretion rate was found in the whole study group (r = 0.48; p less than 0.001). Arterial pressure (both systolic and diastolic) was significantly higher in the high micro-albuminuria group than in either the control group or the low micro-albuminuria group. A significant correlation was found between arterial pressure and albumin excretion rate in the whole study population (r = 0.49; p less than 0.001) as well as in the pooled micro-albuminuria groups (r = 0.43; p less than 0.05). Multiple regression analysis showed that glycosylated haemoglobin and arterial pressure levels were independently correlated with albumin excretion rates. Diabetic patients with micro-albuminuria of any degree have worse glycaemic control than normo-albuminuric patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1993

Lack of albuminuria in the early heterologous phase of anti-GBM nephritis in beige mice.

Passive anti-glomerular basement membrane (GBM) nephritis in the mouse is accompanied by acute massive albuminuria in the early heterologous phase. As we have previously shown, this albuminuria does not occur in the beige mutant of the C57BL/6J strain which is deficient for the leukocytic neutral proteinases elastase and cathepsin G. To address the question whether an intrinsic defect in the polymorphonuclear granulocyte (PMN) or local factors in the beige kidney are responsible for the lack of albuminuria in the beige mouse strain, we conducted reciprocal bone marrow transplantations (BMT) in beige and congenic control mice. Injection of anti-GBM antibody resulted in only slight albuminuria (89 +/- 47 micrograms/18 hours; N = 6) in normal (that is, non-irradiated, non-reconstituted) beige mice. By contrast, in beige mice, reconstituted with bone marrow (BM) from control mice, acute albuminuria developed (3032 +/- 1408 micrograms/18 hours; N = 8), to a degree comparable to that in non-irradiated control mice (4411 +/- 3405 micrograms/18 hours; N = 6, P < 0.01). Albuminuria in control mice, reconstituted with beige BM, was in the range of the normal beige mice (112 +/- 55 micrograms/18 hours; N = 9). Reconstitution with syngeneic bone marrow demonstrated that BMT by itself did not influence the level of albuminuria. All mice showed similar morphological lesions, with comparable influx of PMN in the glomeruli two hours after antibody injection. Elastase activities of PMN extracts in BMT groups were not different from those in donor mice. We conclude that the absence of albuminuria in beige mice is caused by an intrinsic defect in leukocytic neutral proteinase activity.

Albuminuria↗
PubMed2002

Albuminuria and renal insufficiency prevalence guides population screening: results from the NHANES III.

BACKGROUND: A number of screening criteria, applied either at a single point in time or serially, can be used for the purpose of identifying individuals at risk of end-stage renal disease (ESRD). This study focused on two such criteria measured on a single occasion, proteinuria and renal insufficiency, and examined their prevalence in a sample representative of the adult U.S. non-institutionalized population. Such knowledge guides the utility of population screening to prevent ESRD. METHODS: The prevalence of albuminuria (microalbuminuria and macroalbuminuria from a random urine albumin-to-creatinine ratio) and renal insufficiency [glomerular filtration rate (GFR) estimated from serum creatinine] was determined in different age categories in various adult screening groups in the cross-sectional Third National Health and Nutrition Examination Survey (NHANES III). RESULTS: A total of 14,622 adult participants were included in the analysis. In the general population, 8.3% and 1.0% of participants demonstrated microalbuminuria and macroalbuminuria, respectively. To identify one case of albuminuria, one would need to screen three persons with diabetes mellitus, seven non-diabetic hypertensive persons, or six persons over the age of 60. When albuminuria and renal insufficiency were considered together, it was clear that these tests were identifying different segments of the population; 37% of participants with a GFR less than 30 mL/min/1.73 m2 demonstrated no albuminuria. Non-albuminuric renal insufficiency was most evident in the ages of 60 to 79; 34% of diabetics, and 63% of non-diabetic hypertensives with a GFR less than 30 mL/min/1.73 m2 demonstrated no albuminuria. CONCLUSIONS: Albuminuria is prevalent, and when considered together, screening tests of albuminuria and renal insufficiency measured on a single occasion identify different segments of the population. The prevalence of albuminuria and renal insufficiency in populations of interest should be considered, as this knowledge has implications for the effectiveness of screening.

Adult↗
PubMed2002

Impaired coronary endothelial function in a rat model of spontaneous albuminuria.

BACKGROUND: Albuminuria is an independent risk factor of coronary artery disease and has been proposed to reflect a general endothelial disorder. The Munich Wistar Frömter (MWF) rat strain develops spontaneous albuminuria and, therefore, may be an interesting experimental model to study alterations of endothelial function under conditions of increased albuminuria. Our aim was to investigate if the MWF strain shows generalized endothelial dysfunction or endothelial dysfunction localized to the coronary vascular bed, and if so, determine which endothelial dilative mediators are involved. METHODS: Coronary and mesenteric arteries were investigated for endothelium-dependent relaxation and the contribution of prostacyclin, nitric oxide (NO) and endothelium-dependent hyperpolarization (EDH) in MWF rats compared to normal Wistar rats. In addition, as MWF rats show increased blood pressure, spontaneously hypertensive rats (SHR) with similar hypertension but without increased albuminuria also were studied. RESULTS: Maximal total endothelium-dependent relaxation of coronary arteries was strongly impaired in MWF rats (55 +/- 3%) compared to Wistar (89 +/- 5%) and SHR (89 +/- 2%) P < 0.05, respectively. The NO-mediated relaxation as well as the relaxation mediated by EDH were significantly lower in coronary arteries from MWF compared to Wistar. In mesenteric arteries of MWF the endothelium-dependent relaxation was intact. CONCLUSIONS: The strong impairment of coronary endothelium-dependent relaxation in the MWF model of spontaneous albuminuria may be due to defects in production or activity of NO and EDH. The intact mesenteric endothelium-dependent relaxation suggests that increased albuminuria may not be related to generalized endothelial vasodilator dysfunction in this model. Selective impairment of coronary endothelial function in a setting of spontaneous albuminuria may be a feature of the MWF that may be employed to further study cause-effect relations between albuminuria and coronary artery disease.

Albuminuria↗
PubMed1999

Albuminuria, cardiovascular morbidity and mortality in diabetic and non-diabetic subjects in a rural general practice.

OBJECTIVES: The aim of this study was to estimate the frequency of albuminuria in patients with and without diabetes mellitus, answering the question: 'How relevant for general practice are epidemiological findings that albuminuria is a significant risk indicator for the development of cardiovascular syndromes?'. METHOD: The relationship between albuminuria and vascular disease was studied in two groups of subjects: one group consisted of 138 patients with diabetes mellitus and the other of 160 patients without diabetes, randomly selected from a stratified sample comparable with known diabetics by age, sex and profession. The groups were examined in the same way and mortality was followed over 5 years (1994-1998). RESULTS: Albuminuria was significantly more often present in diabetics (P < 0.0001). Peripheral arterial occlusive disease was diagnosed in 27.3% of patients with diabetes mellitus, and in 8.8% of the control group (P < 0.001). In the diabetic group 40 (29%) had microalbuminuria, but only 20 (12.5%) of the other group had the condition. In the presence of albuminuria, the incidence of arterial occlusive disease was 53.6%, but in those without it was only 9.8%. CONCLUSIONS: Our study has demonstrated that albuminuria is frequently present with diabetes mellitus, peripheral arterial occlusive disease, hypertension, coronary heart disease, hyperlipidaemia and in cases with increased concentration of blood fibrinogen. The albuminuria was significantly more frequent in those who died in the observed 5-year period after first examination. Although albuminuria indicates higher risks of cardiovascular morbidity and mortality in diabetics and in non-diabetics, it is necessary to study further how useful is this evidence for general practice.

Adult↗
PubMed2005

The effects of highly active antiretroviral therapy on albuminuria in HIV-infected persons: results from a randomized trial.

BACKGROUND: Human immunodeficiency virus (HIV)-infected patients receiving highly active antiretroviral therapy (HAART) regimens, especially those containing protease inhibitors (PIs), are at increased risk for cardiovascular events. Albuminuria is a known independent predictor for the development of cardiovascular disease and may potentially increase in patients receiving PIs. Alternatively, albuminuria may improve with HAART as a result of treating renal parenchymal HIV infection. Longitudinal studies have not been performed previously addressing the effects of HAART on albuminuria. METHODS: We evaluated the effects of HAART on albumin to creatinine ratios (ACRs) during the initial 64 weeks of therapy in 68 previously untreated HIV-infected subjects, without pre-existing diagnosed diabetes or hypertension, enrolled in a randomized trial comparing PI-based (n = 32) with non-PI-based (n = 36) HAART regimens. We also estimated the prevalence of albuminuria, defined as an ACR > or =3.4 mg/mmol, in these subjects prior to initiation of HAART. RESULTS: The changes in ACR over the initial 64 weeks of therapy in those receiving PIs [0.0 mg/mmol (-0.4, 0.3)] and in those not receiving PIs [0.0 mg/mmol (-0.5, 0.3)] were not significantly different. There was also no significant difference in the change in the ACR in the group as a whole. However, albuminuria at baseline was found in seven (10%) subjects. Five of these seven subjects had substantial improvements in ACR, ranging from 45 to 95%, with HAART use; three subjects had resolution of albuminuria. ACR at baseline significantly correlated with the baseline HIV-1 RNA level (r = 0.25; P = 0.04) and negatively with CD4 cell count (r = -0.25; P = 0.04). CONCLUSION: Albuminuria in HIV-infected, treatment-naïve patients was found more frequently than expected and may be influenced by baseline immune status. Although we did not observe an effect of HAART on ACR during the first 64 weeks of therapy, we cannot exclude the possibility that HAART may be beneficial in those patients with significant albuminuria prior to treatment. Research in larger cohorts is required to investigate more definitively the associations between immune status, antiretroviral therapies and renal function in HIV-infected patients.

Adult↗
PubMed1992

Micro-albuminuria and the organ-damage concept in antihypertensive therapy for patients with insulin-dependent diabetes mellitus.

OBJECT OF TREATMENT: Antihypertensive treatment in hypertensive patients with insulin-dependent diabetes mellitus is intended to prevent long-term complications, particularly diabetic nephropathy. DIABETIC HYPERTENSIVES WITH ABNORMAL ALBUMINURIA: Antihypertensive therapy, particularly with angiotensin converting enzyme (ACE) inhibitors, typically produces a permanent reduction in the decline of the glomerular filtration rate (GFR) in diabetic patients with abnormal albuminuria. The rate of decline in the GFR during antihypertensive treatment is a well accepted end-point in diabetic renal disease. DIABETIC HYPERTENSIVES WITHOUT ABNORMAL ALBUMINURIA: In insulin-dependent diabetic patients with essential hypertension but with normal urinary albumin excretion there is no reduction in the GFR. Longitudinal studies have shown a fall in the GFR only in the presence of significantly increased urinary albumin excretion. ABNORMAL ALBUMINURIA AS A MARKER OF INCIPIENT NEPHROPATHY: Micro-albuminuria and proteinuria may be pathogenetic factors in the development of nephropathy, leading eventually to end-stage renal failure in diabetic patients. Measurements of micro-albuminuria and proteinuria, in addition to blood pressure recordings, might therefore be used as indications for initiating antihypertensive treatment. NEED TO MONITOR PATIENTS FOR ABNORMAL ALBUMINURIA: Transglomerular macromolecular traffic may produce mesangial damage, with subsequent glomerulopathy and diabetic nephropathy. Thus, close monitoring for micro-albuminuria and proteinuria is desirable in the management of diabetic hypertensive patients.

Albuminuria↗
PubMed2004

Albuminuria is evident in the early stages of diabetes onset: results from the Australian Diabetes, Obesity, and Lifestyle Study (AusDiab).

BACKGROUND: Albuminuria is a common complication of diabetes and a leading cause of end-stage renal disease. We determined the prevalence of and factors associated with albuminuria in an Australian population and examined the association of albuminuria with glucose tolerance. METHODS: The Australian Diabetes, Obesity, and Lifestyle Study included 11,247 adults aged 25 years and older from 42 randomly selected areas of Australia. Microalbuminuria is defined as an albumin-creatinine ratio of 22 to 220 mg/g (2.5 to 25 mg/mmol) in men and 31 to 220 mg/g (3.5 to 25 mg/mmol) in women, and macroalbuminuria is defined as an albumin-creatinine ratio of 220 mg/g or greater (> or =25.0 mg/mmol). RESULTS: Overall, 25.3% of patients with diabetes mellitus (known [KDM] and newly diagnosed [NDM], type 1 and type 2) had evidence of albuminuria (21.0%, microalbuminuria; 4.3%, macroalbuminuria). Prevalence increased with increasing glycemia (normal glucose tolerance [NGT], 5.1%; impaired fasting glucose [IFG], 9.3%; impaired glucose tolerance, 11.0%; NDM, 17.8%; and KDM, 32.6% [type 2 only]). Patients with diabetes (KDM and NDM) and IFG had an increased risk for albuminuria compared with those with NGT independent of age, sex, and other known risk factors for albuminuria. Logistic regression modeling identified age, duration of diabetes, systolic blood pressure, current smoking, body mass index, and glycated hemoglobin level as independent risk factors for albuminuria. CONCLUSION: This Australian population-based study shows that albuminuria is common among patients with established diabetes, is present before the onset of diabetes, and becomes more prevalent with worsening glucose tolerance.

Aged↗
PubMedDate not supplied

[Captopril reduction of albuminuria in type-II diabetics with diabetic nephropathy].

This study was to search if captopril (C) reduces albuminuria in a group of type II diabetics with diabetic nephropathy (DN). Eleven type II diabetics with DN and hypertension, with albuminuria over 0.30 g/L/24th, fasten blood glucose under 250 mg/dL, serum albumin over 3 g/dL, without infection, cardiac failure or diuretic treatment, were treated with C for six months, as the only treatment for hypertension and albuminuria. Every month, albuminuria in a 24h urinary collection, medium arterial pressure (MAP), serum creatinine and fasten blood glucose were measured. Ten women and one man with 60 (50-70) years of average age (0 to 100th percentile), with 18 (8-35) years of diabetic disease, and 4 (1-7) years of clinic hypertension were studied. Before the treatment with C they had albuminuria of 6.9 (0.7 to 12.5) g/L/24h, MAP of 119.7 (93.2 to 139) mmHg, serum creatinine of 2.2 (0.7 to 7.5) mg/dL and glucose of 168 (78 to 250) mg/dL. After 6 months with C, they had albuminuria of 3.5 (0.2 to 9.6) g/L/24h (p less than 0.01), MAP of 113.4 (92.9 to 132.4) mmHg (p = 0.5), serum creatinine of 2.3 (0.5 to 6.4) mg/dL (p = 0.23) and glucose of 133 (87.5 to 239) mg/dL (p = 0.32). The MAP showed a predictive relation over albuminuria (p = less than 0.004). During the six months of study, C reduced albuminuria in type II diabetics with hypertension and diabetic nephropathy.

Albuminuria↗
PubMed1990

Effect of protein kinase C modulators on the leucocyte Na+/H+ antiport in type 1 (insulin-dependent) diabetic subjects with albuminuria.

It is uncertain why only one third of Type 1 (insulin-dependent) diabetic patients develop nephropathy. One suggestion is the inheritance of a predisposition to essential hypertension. We have previously found elevated Na+/H+ antiport activity and a raised intracellular pH in leucocytes from hypertensive and Type 1 diabetic subjects with albuminuria using a novel double ionophore fluorimetric technique. These changes are not found in Type 1 diabetic subjects without albuminuria. We wished to test the effect of a protein kinase C inhibitor staurosporine (100 nmol/l) on the elevated antiport activity, and the degree of stimulation achieved by exogenous diacyl glycerol. Raised leucocyte Na+/H+ antiport activity of Type 1 diabetic subjects with albuminuria (73.8 +/- 17.2 mmol.l-1.min-1) was restored to normal levels with staurosporine (54.9 +/- 17.9 mmol.l-1.min-1, p less than 0.001). The leucocyte Na+/H+ antiport activity of diabetic subjects without albuminuria fell significantly also with staurosporine but to a lesser extent (57.3 +/- 11.6 to 50.0 +/- 12.8 mmol/l, p less than 0.003). In contrast, leucocytes from normal control subjects showed no change in antiport activity with staurosporine (54.3 +/- 8.5 to 52.6 +/- 10.4 mmol.l-1.min-1). Dioctanoyl glycerol stimulated the leucocyte Na+/H+ antiport in normal subjects and diabetic patients without albuminuria, with significantly less stimulation in diabetic patients with albuminuria. We conclude that reversal by staurosporine of the elevated Na+/H+ antiport activity in Type 1 diabetic subjects with albuminuria could indicate a role for protein kinase C in activating the antiport. This hypothesis is supported by the reduced stimulation of the antiport by dioctanoyl glycerol in this group of patients.

Albuminuria↗
PubMed2003

Angiotensin-converting enzyme genotype, albuminuria and plasma fibrinogen in type 2 diabetes mellitus.

AIMS: Increased fibrinogen level is considered an important atherosclerosis risk factor. Patients with type 2 diabetes frequently have increased fibrinogen levels. The aim of the present study was to examine the effect of angiotensin-converting enzyme (ACE) gene polymorphism and the effects of the diabetic environment on plasma fibrinogen in type 2 diabetes. PATIENTS AND METHODS: The study group included 125 patients with type 2 diabetes (40 men, 85 women). The average age of patients was 62 +/- 10 years. Fibrinogen concentration was determined with the thrombin coagulation test. ACE insertion/deletion (I/D) polymorphism was detected using polymerase chain reaction (PCR) assay. RESULTS: II homozygotes (n = 17) had the highest mean fibrinogen levels, ID heterozygotes (n = 75) had medium levels and DD homozygotes (n = 33) had the lowest (p = 0.054, ANOVA). II homozygotes also had significantly higher mean fibrinogen level than ID/DD carriers (4.3 +/- 1.7 vs. 3.5 +/- 1.3 g/l; p = 0.015). The indices of renal functions, i.e. albuminuria (r = 0.37; p < 0.0001) and serum creatinine (r = 0.22; p = 0.015), significantly correlated with fibrinogen levels. The correlation between albuminuria and fibrinogen was significant in the subgroups with genotypes II (r = 0.76; p = 0.001) and ID (r = 0.37, p = 0.002), whereas in the subgroup of DD homozygotes this relationship did not reach statistical significance. In the multivariate regression analysis with age, sex, BMI, creatinine, albuminuria and ACE genotype as independent variables, albuminuria was the only significant predictor of fibrinogen level (p < 0.0001). After interaction between the ACE genotype and albuminuria was included into multivariate analysis, the interaction became the only independent predictor of plasma fibrinogen level (p < 0.0001) in the model, and the model explained 25% of the plasma fibrinogen variance. CONCLUSION: ACE gene polymorphism is associated with plasma fibrinogen level in type 2 diabetes. This association is mediated by an interaction between ACE genotype and albuminuria. Diabetes patients with genotypes II or ID have increased plasma fibrinogen in the presence of albuminuria.

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