Urine drug testing in an athlete leads to the diagnosis of unsuspected mediastinal germ cell tumor.
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Adolescent↗
Biomedical subjects
George Jerums
Publications and source records attributed to George Jerums.
Diastolic dysfunction is associated with anaemia in patients with Type II diabetes.
Anaemia is common in patients with diabetes and associated with an increased risk of diabetic complications. Although the role of anaemia in heart failure is established, we hypothesize that anaemia also contributes to an increased risk of cardiac dysfunction in patients with Type II diabetes. In the present study, 228 consecutive adults with diabetes were investigated using transthoracic echocardiography. Echocardiographic parameters were correlated with the Hb (haemoglobin) level and adjusted for other risk factors for cardiac dysfunction using multivariate analysis. More than one in five patients (23%) had anaemia, which was an independent risk factor for cardiac dysfunction on echocardiography. Over one-third of all patients with evidence of abnormal cardiac function (diastolic and/or systolic dysfunction) on echocardiography had anaemia compared with <5% of patients with normal echocardiographic findings. Most patients with anaemia had cardiac dysfunction (94%), with the major abnormality being diastolic dysfunction associated with an increased left ventricular mass and impaired relaxation indices. A continuous association between diastolic function and Hb was also observed in patients without anaemia. In patients with a history of cardiovascular disease, systolic dysfunction was twice as common in patients with anaemia. Anaemia was also correlated with plasma markers of cardiac risk, including BNP (brain natriuretic peptide), CRP (C-reactive protein) and AVP (arginine vasopressin). Notably, the predictive utility of these markers was eliminated after adjusting for Hb. Consequently, the inexpensive measurement of Hb may be a useful tool to identify diabetic patients at increased risk of cardiac dysfunction.
Aged↗
The epidemiology of hemoglobin levels in patients with type 2 diabetes.
BACKGROUND: Anemia is a common finding in patients with diabetes, for whom it constitutes an additional burden. The aim of this study is to clarify the natural history of anemia in patients with type 2 diabetes and describe factors that predict a decrease in hemoglobin (Hb) levels. METHODS: A 5-year prospective cohort study was designed as a follow-up of 503 individuals with type 2 diabetes in a single diabetes clinic. In addition to standard management, a full blood count was obtained at each routine visit. No intervention was undertaken to modify Hb levels. RESULTS: At baseline, 12% of patients had anemia, and an additional 13% developed anemia during follow-up. Overall Hb levels decreased by -0.07 +/- 0.01 g/dL/y, suggesting that anemia is the end point of a process that begins more than 10 years previously with the initiation of vascular damage. The greatest decreases in Hb levels were seen in patients with macroalbuminuria, renal impairment, or established macrovascular disease at baseline (all P < 0.01). In patients with microvascular disease, decreasing Hb levels tracked with decreasing glomerular filtration rates (GFRs). Patients with an estimated GFR greater than 90 mL/min/1.73 m2 (>1.5 mL/s) or normoalbuminuria had stable Hb levels during the 5-year follow-up. In patients with anemia in our cohort who were managed conservatively, Hb levels decreased by 0.09 +/- 0.03 g/dL/y. This decrease was associated with HbA1c levels, but not renal function. CONCLUSION: This study defines the natural history of Hb levels in patients with type 2 diabetes. Early identification of anemia may be achieved by means of annual or biannual screening in high-risk groups with nephropathy, advanced age, or macrovascular disease. These data are important for developing a rational response to the prevention and management of anemia.
Adult↗
Is nonalbuminuric renal insufficiency in type 2 diabetes related to an increase in intrarenal vascular disease?
OBJECTIVE: To investigate the role of intrarenal vascular disease in the pathogenesis of nonalbuminuric renal insufficiency in type 2 diabetes. RESEARCH DESIGN AND METHODS: We studied 325 unselected clinic patients who had sufficient clinical and biochemical information to calculate an estimated glomerular filtration rate (eGFR) using the Modified Diet in Renal Disease six-variable formula, at least two estimations of urinary albumin excretion rates (AER), and a renal duplex scan to estimate the resistance index of the interlobar renal arteries. The resistance index, measured as part of a complications surveillance program, was compared in patients with an eGFR < or >or=60 ml/min per 1.73 m(2) who were further stratified into normo- (AER <20), micro- (20-200), or macroalbuminuria (> 200 microg/min) categories. RESULTS: Patients with an eGFR <60 ml/min per 1.73 m(2) had a higher resistance index of the renal interlobar arteries compared with patients with an eGFR >or=60 ml/min per 1.73 m(2). However, the resistance index was elevated to a similar extent in patients with an eGFR <60 ml/min per 1.73 m(2) regardless of albuminuric status (normo- 0.74 +/- 0.01, micro- 0.73 +/- 0.01, and macroalbuminuria resistance index 0.75 +/- 0.11). Multiple regression analysis revealed that increased age (P < 0.0001), elevated BMI (P = 0.0001), decreased eGFR (P < 0.01), and decreased diastolic blood pressure (P < 0.01), but not an increased AER, were independently associated with an elevated resistance index in patients with impaired renal function. CONCLUSIONS: Subjects with type 2 diabetes and reduced glomerular filtration rate had similar degrees of intrarenal vascular disease, as measured by the intrarenal arterial resistance index, regardless of their AER status. The pathological mechanisms that determine the relationship between impaired renal function and AER status in subjects with type 2 diabetes remain to be elucidated.
Aged↗
Androgenic correlates of genetic variation in the gene encoding 5alpha-reductase type 1.
Androgens determine male secondary sexual characteristics and influence a variety of metabolic pathways. Circulating levels of androgens are highly heritable; however, the genes involved are largely unknown. The 5alpha-reductase enzymes types 1 and 2 responsible for converting testosterone to the more potent androgen dihydrotestosterone are encoded by the SRD5A1 and SRD5A2 genes, respectively. We performed indirect genetic association studies of SRD5A1 and SRD5A2 and the dihydrotestosterone/testosterone ratio that reflects the activity of 5alpha-reductase in 57 males with type 2 diabetes. We found evidence of significant association between a single nucleotide polymorphism in SRD5A1 and the dihydrotestosterone/testosterone ratio (median 0.10, interquartile range 0.08 vs. median 0.06, interquartile range 0.04, P = 0.009). The polymorphism was not associated with any diabetic phenotypes. These results suggest that functional genetic variants might exist in or around SRD5A1 that affect the activity of the 5alpha-reductase enzyme type 1 and influence androgen levels.
3-Oxo-5-alpha-Steroid 4-Dehydrogenase↗
Modulation of soluble receptor for advanced glycation end products by angiotensin-converting enzyme-1 inhibition in diabetic nephropathy.
Recent studies have identified that first-line renoprotective agents that interrupt the renin-angiotensin system not only reduce BP but also can attenuate advanced glycation end product (AGE) accumulation. This study used in vitro, preclinical, and human approaches to explore the potential effects of these agents on the modulation of the receptor for AGE (RAGE). Bovine aortic endothelial cells that were exposed to the angiotensin-converting enzyme inhibitor (ACEi) ramiprilat in the presence of high glucose demonstrated a significant increase in soluble RAGE (sRAGE) secreted into the medium. In streptozotocin-induced diabetic rats, ramipril treatment (ACEi) at 3 mg/L for 24 wk reduced the accumulation of skin collagen-linked carboxymethyllysine and pentosidine, as well as circulating and renal AGE. Renal gene upregulation of total RAGE (all three splice variants) was observed in ACEi-treated animals. There was a specific increase in the gene expression of the splice variant C-truncated RAGE (sRAGE). There were also increases in sRAGE protein identified within renal cells with ACEi treatment, which showed AGE-binding ability. This was associated with decreases in renal full-length RAGE protein from ACEi-treated rats. Decreases in plasma soluble RAGE that were significantly increased by ACEi treatment were also identified in diabetic rats. Similarly, there was a significant increase in plasma sRAGE in patients who had type 1 diabetes and were treated with the ACEi perindopril. Complexes between sRAGE and carboxymethyllysine were identified in human and rodent diabetic plasma. It is postulated that ACE inhibition reduces the accumulation of AGE in diabetes partly by increasing the production and secretion of sRAGE into plasma.
Alternative Splicing↗
Anemia with impaired erythropoietin response in diabetic patients.
BACKGROUND: Diabetes mellitus is associated with an increased prevalence of anemia, particularly in patients with nephropathy. We undertook this survey to determine the relationship between anemia and the renal production of erythropoietin in patients with diabetes mellitus. METHODS: The clinical data of 722 patients were obtained, including markers of diabetic complications. Erythropoietin levels were measured in the same samples. Patients with a full blood cell count, iron indexes, and renal function within the normal range (n = 151) were used to define the reference range for this population. Anemic patients who had erythropoietin levels within this range were defined as having an "inappropriate erythropoietin response to anemia." RESULTS: Of the 722 patients, 168 (23.3%) had anemia, of whom 130 (77.4%) had erythropoietin levels inappropriately within the normal range. Although 55.4% of anemic patients had moderate renal impairment, erythropoietin levels were also inappropriately low in 69.2% of anemic patients with normal renal function. However, most of these patients (17 of 26) had diabetic kidney disease, as denoted by albuminuria. CONCLUSIONS: The failure to produce erythropoietin in response to a declining hemoglobin level is a common contributor to anemia in patients with diabetes mellitus. This seems to be a manifestation of diabetic kidney disease, in the presence or absence of renal impairment.
Aged↗
Increased tubular organic ion clearance following chronic ACE inhibition in patients with type 1 diabetes.
BACKGROUND: The tubular excretion of creatinine significantly contributes to its clearance. Administration of an angtiotensin-converting enzyme (ACE) inhibitor is associated with increased organic ion clearance in experimental diabetes. This study examines the effect and implications of chronic ACE inhibition on renal organic ion excretion in patients with type 1 diabetes. METHODS: Samples were obtained from the Melbourne Diabetic Nephropathy Study Group (MDNSG) that randomized patients to receive perindopril (N= 11), nifedipine (N= 11), or placebo (N= 8). Albumin excretion rate, creatinine clearance, and isotopic glomerular filtration rate (GFR) were assessed at baseline and after 24 months. In addition, the clearance of the endogenous cations N-methylynicotinamide (NMN), creatinine, and the anion hippurate were determined by high-performance liquid chromatography (HPLC). RESULTS: Following treatment with the ACE inhibitor, perindopril, renal clearance of NMN was increased (+96%) (P < 0.05). There was no difference in patients treated with nifedipine (P= 0.25) and NMN clearance fell in the placebo-treated patients (-26%) (P < 0.05). Changes in NMN clearance were unaffected after adjusting for the effects of perindopril on GFR. However, they were attenuated after adjusting for hippurate clearance, a marker of renal blood flow. This effect of perindopril on NMN clearance was seen in both men and women, regardless of baseline clearance and was correlated with reduced albuminuria following perindopril treatment. CONCLUSION: Organic ion clearance is increased in patients with diabetes following chronic ACE inhibition. This is consistent with experimental models showing increased ion transporter expression and improved tubular blood flow, following blockade of the renin-angiotensin system (RAS). These findings may have implications for the interpretation of creatinine-based indices in patients with diabetes.
Angiotensin-Converting Enzyme Inhibitors↗
Low-molecular weight advanced glycation end products: markers of tissue AGE accumulation and more?
Incomplete digestion of advanced glycation end product (AGE)-modified protein results in the formation of low-molecular weight degradation products incorporating AGE modifications (LMW-AGEs). In addition to being biomarkers of AGE modification, LMW-AGEs may have a high toxic potential, being free to interact with AGE receptors at distant sites via the circulation. Several free AGEs have been identified, including pentosidine, N(epsilon)-(carboxymethyl)lysine (CML), and free-imidazole AGEs. In addition, fluorescence (370 nm [excitation]/440 nm [emission]) in the LMW phase of serum correlates with tissue fluorescence, an established marker for AGE modification. In experimental diabetes, LMW fluorescence increases with duration of disease and is normalized with the AGE inhibitor aminoguanidine. LMW fluorescence is also higher in patients with diabetes, in whom it is associated with glomerular filtration rate and hemoglobin. Patients with hyperfiltration have lower LMW fluorescence than those with normal renal function, which may protect them from AGE accumulation in the short term. These findings provide clinical support for the association between AGEs and progressive renal injury in diabetes.
Biomarkers↗
The burden of anaemia in type 2 diabetes and the role of nephropathy: a cross-sectional audit.
BACKGROUND: Anaemia is a common finding in patients with diabetes and constitutes an additional burden in patients with advancing age and comorbid vascular disease. This study examines the prevalence and predictors of anaemia in long-term outpatients with type 2 diabetes from three large clinical centres. METHODS: A full blood count was obtained in addition to routine testing in a cross-sectional survey of all patients with type 2 diabetes in long-term follow-up at the Austin Medical Centre, Melbourne (n = 670) and the Royal Prince Alfred Hospital (n = 915) and the Royal North Shore Hospital (n = 540), Sydney, Australia. The prevalence and correlates of anaemia (haemoglobin < 130 g/l in men and < 120 g/l in women) were identified using multivariate logistic regression. RESULTS: Roughly, one in five patients in each centre had anaemia. Patients at greatest risk could be readily identified by the presence of renal disease, manifested as impaired renal function and/or albuminuria in > 75% of patients with anaemia. Patients with diabetes and mild renal impairment [creatinine clearance (CCr) 60-90 ml/min/1.73 m(2)] were twice as likely to have anaemia as those with normal renal function (CCr > 90 ml/min/1.73 m(2)). Diabetics with moderate renal impairment (CCr < 60 ml/min/1.73 m(2)) were also twice as likely to have anaemia as those with mild renal impairment. Patients with anaemia were also more likely to have macrovascular disease, reflecting the high prevalence of nephropathy in these patients. CONCLUSIONS: Anaemia is a prevalent finding in patients with type 2 diabetes and represents a significant unrecognized burden. Patients at greatest risk can be identified by the presence of renal disease, either in the form of renal impairment and/or albuminuria.
Aged↗
Differences in urinary albumin detected by four immunoassays and high-performance liquid chromatography.
OBJECTIVES: To compare the analysis of urinary albumin from diabetic patients by four conventional immunoassays including radioimmunoassay (RIA), immunonephelometry (IN), and two different methods of immunoturbidimetry (IT), as well as by high-performance liquid chromatography (HPLC). DESIGN AND METHODS: Urines were collected over a 24-h period and stored at -20 degrees C until assay. Urinary albumin concentration was determined by an in-house RIA, by IN using a Beckman Array Analyser with reagents from Beckman Diagnostics (Sydney, Australia), by IT using a Dade-Behring Turbitimer with reagents from Dade-Behring (Marburg, Germany), by IT using a Dade-Behring Dimension R x L Chemistry Analyser with reagents from DiaSorin (Stillwater, OK, USA), and by HPLC using a Zorbax Bio series preparative GF-250 column. Regression lines were calculated using a least squares method to determine the correlation between the assays studied. Bland-Altman bias plots including limits of agreement were also calculated. RESULTS: The correlation coefficients calculated were high (>0.85) indicating a strong linear relationship between all assays studied. The slopes calculated for the comparisons demonstrate that each assay can vary from one another (up to threefold) and have a slope significantly different from an ideal slope of 1 (P < 0.001). These results were confirmed by Bland-Altman bias plots and calculation of the limits of agreement that were all large. CONCLUSIONS: At this time, there is no global standard by which urinary albumin assays may be standardized. This study suggests the need for such standards.
Albumins↗
Renal processing of serum proteins in an albumin-deficient environment: an in vivo study of glomerulonephritis in the Nagase analbuminaemic rat.
BACKGROUND: Plasma albumin has been considered as important for governing glomerular permselectivity as well as being tubulotoxic in proteinuric states. The purpose of this study was to examine glomerular permselectivity and protein clearance of plasma albumin-deficient Nagase analbuminaemic rats (NAR) in normal and proteinuric states associated with puromycin aminonucleoside nephrosis (PAN) and anti-glomerular basement membrane glomerulonephritis (anti-GBM GN) and to compare the results with those of previous studies using Sprague-Dawley rats. METHODS: Glomerular permselectivity was measured using tritium-labelled polydisperse Ficoll. In vivo fractional clearance (FC) of albumin, transferrin and immunoglobulin G was measured to include both intact and degraded forms of filtered material. Endogenous protein clearance was analysed using two-dimensional electrophoresis in combination with matrix-assisted laser desorption ionization (MALDI) mass spectrometry. RESULTS: FCs of proteins and Ficoll in control NAR were similar to those found in Sprague-Dawley rats. Despite the lack of serum albumin in NAR, proteinuria and morphological changes observed were also similar to those found in Sprague-Dawley rats, with total protein excretion increasing 6-fold in PAN rats and 4-fold in anti-GBM GN rats with respect to controls. Two-dimensional electrophoresis in combination with MALDI mass spectrometry identified the major proteins being excreted as transferrin and a group of mildly acidic proteins in the MW range 40-50 kDa, namely antithrombin III, kininogen, alpha-1-antiproteinase, haemopexin and vitamin D-binding protein. CONCLUSIONS: Both diseases exhibited similar effects to those observed in Sprague-Dawley rats despite the lack of serum albumin, including inhibition of renal protein degradation. The net changes in protein FC, particularly in the range of radii of 36-55 A, could not be accounted for by changes in size selectivity as Ficoll FC was little affected by the disease states. This emphasizes the need to reassess the relative importance of changes in renal tubular handling vs changes in glomerular capillary barrier in proteinuric states. These studies also demonstrate that albumin is not a critical factor in governing glomerular permselectivity or proteinuria.
Acetylglucosaminidase↗
New insights into the significance of microalbuminuria.
PURPOSE OF REVIEW: This review summarizes recent work that has explored the association between microalbuminuria and adverse clinical outcomes in the presence and absence of diabetes. RECENT FINDINGS: Recent investigations have documented the prevalence of microalbuminuria in the general community and have also highlighted the continuous relationship between the level of urinary albumin excretion and clinical endpoints. Even below traditional microalbuminuria thresholds, urinary albumin levels appear to correlate with clinical outcomes. Microalbuminuria is becoming increasingly recognized as an independent risk factor for cardiovascular morbidity and mortality. At least for subjects with type 2 diabetes and microalbuminuria, intensive, multifactorial interventions can reduce the risk of cardiovascular events by about 50%. Although several studies have found an association between microalbuminuria and surrogate measurements of vascular disease, the exact molecular mechanisms linking an increase in urinary albumin excretion and vascular disease are still unknown. Microalbuminuria also has a well-documented association with progressive diabetic renal disease but recent studies have suggested that the prognostic significance of microalbuminuria in this regard may not be as powerful as originally reported. SUMMARY: Aggressive, multifactorial interventions, including the use of drugs that interrupt the renin-angiotensin system are strongly recommended for patients with diabetes and micro-albuminuria to ameliorate the progression of renal and vascular complications. This approach should also possibly apply to microalbuminuric subjects without diabetes. The relationship between microalbuminuria and progressive diabetic renal disease requires re-evaluation given temporal trends in the prevention and treatment of diabetic complications.
Albuminuria↗
Interactions between angiotensin II and NF-kappaB-dependent pathways in modulating macrophage infiltration in experimental diabetic nephropathy.
NF-kappaB-dependent pathways play an important role in macrophage infiltration and kidney injury. NF-kappaB is regulated by angiotensin II (AII). However, the role of this pathway in diabetic nephropathy has not been clearly delineated. First, the activation of NF-kappaB, monocyte chemoattractant protein-1 (MCP-1), and macrophage infiltration in the diabetic kidney were explored, in a temporal manner. The active subunit of NF-kappaB, p65, was elevated in the diabetic animals in association with increased MCP-1 gene expression and macrophage infiltration. Second, the effects of treatment for 4 wk with the AII type 1 receptor antagonist valsartan, the AII type 2 receptor antagonist PD123319, or pyrrolidine dithiocarbamate, an inhibitor of NF-kappaB and on these parameters were assessed. These treatments were associated with a reduction in p65 activation, MCP-1 gene expression, and macrophage infiltration. These findings demonstrate a role for activation of NF-kappaB, in particular the p65 subunit, in the pathogenesis of early renal macrophage infiltration in experimental diabetes. In the context of the known proinflammatory effects of AII, it is postulated that the renoprotection conferred by angiotensin II receptor antagonism is at least partly related to the inhibition of NF-kappaB-dependent pathways.
Angiotensin II↗
Elevated iron indices in patients with diabetes.
AIMS: Excess iron has been implicated in the pathogenesis of diabetes and its complications. This study documents the assessment of plasma iron indices and the correlation between transferrin saturation with biochemical and clinical parameters in a cross-sectional survey of 820 patients with diabetes in long-term follow-up in a single clinic. METHODS: Plasma iron indices, together with the biochemical and clinical profile of all patients, were recorded over a 2-year period. Predictors of the transferrin saturation were identified using multiple and logistic regression analysis. RESULTS: Eighty per cent of patients had Type 2 diabetes. The prevalence of elevated transferrin saturation (> 35%) was 3-4-fold higher in patients with diabetes, compared with historical prevalence described in the general population. Independent associations with elevated transferrin saturation were male gender, low C-reactive protein, and increased fasting plasma glucose (all P < 0.0001). Patients with Type 1 diabetes were also more likely to have an elevated transferrin saturation [odds ratio 3.9 (95% CI 1.9-8.0), P < 0.001]. Patients with an elevated transferrin saturation were younger, but had a similar duration of diabetes, possibly suggesting an earlier age of onset. There was no correlation between the presence of diabetic complications and the presence of elevated iron indices. CONCLUSIONS: Elevated iron indices are more common in patients with diabetes. Excess iron may have a role in the development of diabetes and subsequently in glycaemic control. This should be balanced by the strong association between iron indices and anaemia in patients with diabetes.
Adolescent↗
Earlier detection of microalbuminuria in diabetic patients using a new urinary albumin assay.
BACKGROUND: Microalbuminuria is regarded as the most important predictor of high risk for the development of diabetic nephropathy. Early detection may allow treatment to prevent progression to persistent albuminuria and renal failure. Recent studies have shown that conventional immunoassays underestimate urinary albumin concentration, as albumin in urine may exist in two forms, immuno-reactive and immuno-unreactive. The present study examines the differential lead-time for the development of microalbuminuria as measured by both conventional radioimmunoassay (RIA; measures immuno-reactive) and high-performance liquid chromatography (HPLC; measures total albumin = immuno-reactive plus immuno-unreactive) analysis in both type 1 and type 2 diabetic patients. METHODS: Analysis was performed on 511 stored urine samples collected over the last 13 years from type 1 diabetic patients who either progressed from normo- to microalbuminuria (progressors, N= 17), or who remained normoalbuminuric (nonprogressors, N= 25) as defined by RIA, and on 634 urine samples collected from patients with type 2 diabetes defined as either progressors (N= 24) or nonprogressors (N= 25). RESULTS: For type 1 progressors, the mean lead-time for the HPLC assay versus the RIA was 3.9 years, with a 95% CI of 2.1 to 5.6 years. For type 2 progressors, the mean lead-time was 2.4 years with a 95% CI of 1.2 to 3.5 years. There was no significant difference between the lead-time analysis between type 1 and type 2 diabetic patients. CONCLUSION: These results demonstrate that measurement of total albumin may allow earlier detection of microalbuminuria associated with diabetic nephropathy.
Adult↗
Low-molecular-weight AGEs are associated with GFR and anemia in patients with type 2 diabetes.
BACKGROUND: Advanced glycation end products (AGEs) are implicated in the development and progression of diabetic nephropathy. We examined the predictors of low-molecular-weight (LMW) AGEs in a cross-sectional survey of 604 patients with type 2 diabetes in a single clinic. METHODS: A clinical history and results of routine blood and urine testing were obtained for all patients over a 2-year period. Fluorescent LMW AGEs were estimated in serum samples taken concurrently, using an established flow injection method. Predictors of LMW AGEs were identified using multiple regression analysis. RESULTS: LMW AGEs were 34% higher in patients with diabetes than nondiabetic volunteers from the same community (P < 0.001). Independent predictors for LMW AGEs in patients with diabetes were glomerular filtration rate (GFR) and hemoglobin (both P < 0.001). While patients with renal impairment and anemia had the highest levels of LMW AGEs, both GFR and hemoglobin remained predictive when patients with a serum creatinine or hemoglobin within the "normal range" were analyzed separately. Patients with hyperfiltration had significantly lower LMW AGEs than those with normal renal function. Gender was also a significant independent predictor of LMW AGEs in patients without anemia. However, LMW AGEs were not associated with metabolic control or the presence of macrovascular disease. CONCLUSION: Circulating levels of LMW AGEs are elevated in patients with diabetes, especially those with impaired renal function or anemia. These findings extend the evidence for an association between AGEs and progressive renal injury in patients with type 2 diabetes. Whether LMW AGEs contribute to, or are a marker of, renal damage needs to be established by prospective studies.
Adult↗
Anemia in patients with type 1 diabetes.
Anemia is a common finding in diabetes, although most patients in these studies have type 2 disease. This study examines the prevalence and predictors of anemia in outpatients with type 1 diabetes. A full blood count was obtained in addition to routine testing in patients with type 1 diabetes at the Austin Medical Centre (n = 135), Melbourne, the Royal Prince Alfred Hospital (n = 42), and the Royal North Shore Hospital (n = 135), both in Sydney, Australia. One in seven patients had anemia (14%). Patients at greatest risk could be identified by the presence of diabetic kidney disease. More than half (52%) of patients with macroalbuminuria had anemia, compared with 24% of patients with microalbuminuria and less than 8% of normoalbuminuric patients. Patients with diabetes and renal impairment were more than six times more likely to have anemia than those with normal renal function. Patients with anemia were more likely to have retinopathy and macrovascular complications than were patients with a normal hemoglobin level, independent of comorbid renal disease. Anemia is a prevalent finding in patients with type 1 diabetes and represents a significant unrecognized burden. Patients at greatest risk can be identified by the presence of renal disease, in the form of albuminuria and/or renal impairment.
Adult↗