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Query: UMLS:C0011881 (diabetic nephropathy)
 10,836 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Increased signal intensity in the cerebrospinal fluid (CSF) on magnetic resonance imaging due to the presence of gadolinium is rarely observed, but has been seen in patients with brain or spinal pathology or underlying renal impairment. We report this phenomenon in a 66-year-old woman with diabetic nephropathy and discuss the possible pathogenesis of the scan findings. Recognition of this unusual finding, and features distinguishing it from other causes of high CSF signal intensity, such as subarachnoid haemorrhage and protein in the CSF, are emphasised to help prevent diagnostic errors.
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PMID:High signal in the cerebrospinal fluid following prior gadolinium administration in a patient with renal impairment. 1797 81

Diabetic nephropathy, the most common etiology for end-stage renal disease, complicates approximately 5% of insulin-dependent diabetic pregnancies. Assessment for vasculopathy is important before pregnancy because nephropathy can increase perinatal risks including potential for preeclampsia and preterm birth. Counseling women receiving renoprotective medications including angiotensin converting enzyme inhibitors has recently become complicated in light of new information suggesting a teratogenic risk for these agents. Most reproductive age women with overt diabetic nephropathy have preserved renal function and do not seem to have the progression of their disease affected by pregnancy. Perinatal outcomes are excellent for these women who have received care in tertiary institutions. However, there are relatively few women with significant renal impairment included in case series of pregnancies complicated by diabetic nephropathy. For these women, adverse perinatal outcomes are more common, and the effect of pregnancy on the course of their disease is less certain.
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PMID:Diabetic nephropathy and pregnancy. 1798 43

Chronic kidney disease (CKD) is a world-wide public health problem, the causes of which differ in children from that reported in adult patients. There is an increased incidence of congenital and hereditary diseases causing chronic renal failure in the pediatric age-group and virtually no diabetic nephropathy. To determine the major causes, clinical expression, course, and outcomes of CKD in Syrian children we conducted a prospective study from February 2002 to February 2003 in the pediatric nephrology department at the Kidney Hospital in Damascus, Syria. Fifty-five patients with varying degrees of renal impairment were involved in the analysis. A total of 31 children (56%) had obstructive nephropathy (ON) as the cause of chronic renal insufficiency and 24 children (44%) had non-obstructive nephropathy (Non-ON). Neurogenic bladder was the commonest cause of ON, seen in 15 patients (27%), nephrolithiasis was seen in 10 patients (18%), urethral stenosis in three (5%), Uretro-Pelvie Junction (UPJ) stenosis in two (3%), and posterior urethral valves in one case (2%). Chronic glomerulonephritis and renal hypoplasia were the commonest causes of non-ON seen in six patients each (11%). Reflux nephropathy was seen in four patients (7%), hereditary nephritis in three (5%), polycystic kidney, nephrocalcinosis and Prune Belly syndrome in one case each (2%), and the cause was unknown in two patients (3%). The study is still ongoing and will be reviewed after two years with a bigger sample and possibly more reliable results.
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PMID:The major causes of chronic renal insufficiency in Syrian children: a one-year, single-center experience. 1820 63

Diabetes as the dominant cause of ESRD is also the major cause of renal anaemia. However, most patients with diabetic kidney disease will succumb to co-morbid vascular disease or heart failure before developing severe renal impairment. In these patients, anaemia is also common finding, with a 2-3 times greater prevalence and earlier onset than in patients with renal impairment from other causes. We have recently shown that at least one in five outpatients with type 1 or type 2 diabetes in tertiary referral clinics have anaemia, in whom it constitutes a significant additional burden. Impaired renal erythropoietin release in response to declining haemoglobin levels appears to be the major contributor to anaemia in diabetes. This may be due to the predominance of damage to cells and vascular architecture of the renal tubulointerstitium associated with diabetic nephropathy that may be apparent, like albuminuria, before demonstrable changes in renal function. In addition, systemic inflammation, autonomic neuropathy and reduce red cell survival may also compound anaemia in diabetes. While anaemia may be considered a marker of diabetic kidney disease, reduced haemoglobin levels, even within the normal range, identify diabetic patients with an increased risk of hospitalisation and mortality. Anaemia may also be significant in determining the outcome of heart failure and hypoxia-induced organ damage in patients with diabetes. Upcoming studies will determine whether correction of anaemia in diabetes will lead to improved outcomes in these patients.
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PMID:Anaemia in diabetes: an emerging complication of microvascular disease. 1822 May 87

Microalbuminuria is an important risk factor for cardiovascular disease and progressive renal impairment. This holds true in the general population and particularly in those with diabetes, in whom it is common and marks out those likely to develop macrovascular disease and progressive renal impairment. Understanding the pathophysiological mechanisms through which microalbuminuria occurs holds the key to designing therapies to arrest its development and prevent these later manifestations. Microalbuminuria arises from the increased passage of albumin through the glomerular filtration barrier. This requires ultrastructural changes rather than alterations in glomerular pressure or filtration rate alone. Compromise of selective glomerular permeability can be confirmed in early diabetic nephropathy but does not correlate well with reported glomerular structural changes. The loss of systemic endothelial glycocalyx--a protein-rich surface layer on the endothelium--in diabetes suggests that damage to this layer represents this missing link. The epidemiology of microalbuminuria reveals a close association with systemic endothelial dysfunction and with vascular disease, also implicating glomerular endothelial dysfunction in microalbuminuria. Our understanding of the metabolic and hormonal sequelae of hyperglycaemia is increasing, and we consider these in the context of damage to the glomerular filtration barrier. Reactive oxygen species, inflammatory cytokines and growth factors are key players in this respect. Taken together with the above observations and the presence of generalised endothelial dysfunction, these considerations lead to the conclusion that glomerular endothelial dysfunction, and in particular damage to its glycocalyx, represents the most likely initiating step in diabetic microalbuminuria.
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PMID:What is the mechanism of microalbuminuria in diabetes: a role for the glomerular endothelium? 1834 77

The correlations co-exist among diabetes mellitus, hypertension and the kidney. Renal injury will develop in 35% type 1 and type 2 diabetes mellitus patients. Diabetic nephropathy is the key factor for the occurence of hypertension in type 1 diabetes mellitus. In case of type 2 diabetes mellitus with prevalent essencial hypertension the diabetic nephropathy is supporting factor for the development of hypertension. Untreated or inadequately treated hypertension accelerates the progression of diabetic renal impairment. The presence of diabetes mellitus as well as hypertension or proteinuria is significant cardiovascular risk factor. The goal of treatment with angiotensin converting enzyme inhibitors or AT1 receptor of angiotensin II blockers is both slowing-down of renal injury progression and reduction in risk of cardiovascular complications.
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PMID:[Diabetes mellitus, hypertension and kidney]. 1863 Jun 36

The UK Prospective Diabetes Study is the largest study in Type 2 diabetes with pre-specified renal outcomes. The study showed that the natural history of nephropathy in newly diagnosed Type 2 diabetic patients was similar to that described previously in those with Type 1 diabetes. Around 2% per annum progress from normo- to micro-albuminuria [urinary albumin concentration (UAC) > 50 mg/l] and a further 2% from microalbuminuria to clinical grade proteinuria (UAC > 300 mg/l). Mortality rates for those with nephropathy are high, increasing from 1.4% per annum (normoalbuminuria) to 4.6% per annum (clinical grade proteinuria), and to 19.2% per annum for those with renal impairment. More intensive blood glucose control resulted in both a 33% reduction in relative risk of development of microalbuminuria or clinical grade proteinuria at 12 years, and a significant reduction in the proportion doubling their plasma creatinine (0.91 vs. 3.52%, P = 0.0028). Tighter blood pressure control also reduced microalbuminuria and clinical grade proteinuria; but at 6 years there was no effect on plasma creatinine levels. These data underline the importance of glycaemic and blood pressure control in Type 2 diabetes in order to prevent diabetic nephropathy. Those patients unlucky enough to develop nephropathy need intensive surveillance and correction of cardiovascular risk factors.
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PMID:Microvascular disease: what does the UKPDS tell us about diabetic nephropathy? 1871 75

The onset of diabetic nephropathy is characterised by a rise in albumin excretion rate (AER) and/or a transient rise in glomerular filtration rate (GFR) (hyperfiltration). Without intervention AER increases exponentially and there is a linear decrease in GFR after onset of overt nephropathy. In overt nephropathy, AER is a predictor of decline in GFR and the early AER response to antihypertensive therapy correlates with long-term decline in GFR. AER can be measured by immunoassay or by other techniques including HPLC. However, HPLC assays result in higher levels of AER in normal subjects compared with immunoassayable AER. Recent data suggest that there are distinct albuminuric and non-albuminuric pathways to renal impairment in type 1 and type 2 diabetes. In type 2 diabetes, the non-albuminuric pathway may explain a decline in GFR to <60 ml/min/1.73 m(2) in approximately one in four subjects after accounting for the use of renin angiotensin system inhibitors. In established nephropathy (chronic kidney disease (CKD) stages 3 and 4), plasma cystatin C based estimates of GFR are marginally superior to creatinine based estimates. However, cystatin C clearly outperforms creatinine based estimates of GFR decline at GFR levels >60 ml/min/1.73 m(2) (CKD stages 1 and 2). Other potential markers of progression of diabetic nephropathy include transforming growth factor beta (TGFbeta) and connective tissue growth factor (CTGF). However, long-term studies are needed to define their roles as markers of progression. Diabetic nephropathy is likely to be more susceptible to intervention at an early stage and accurate estimation of GFR is already possible with cystatin C. However, improved formulas for estimating GFR based on using creatinine or other markers are still required, because this may still provide the most cost effective approach applicable to existing clinical practice.
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PMID:New and old markers of progression of diabetic nephropathy. 1893 92

Diabetic nephropathy (DN) is the leading cause of end-stage renal disease in the western world. Increased number of interstitial macrophages has been observed in biopsies from patients with DN. Monocyte chemo-attractant protein-1 (MCP-1) is the strongest known chemo-tactic factor for monocytes and is upregulated in DN. We examined urinary levels of MCP-1 in patients with type-2 diabetes mellitus (DM) to assess its possible correlation with other para-meters of renal injury. The urinary MCP-1 level was assessed in 75 patients with type-2 DM (25 patients each with no microalbuminuria, with macroalbuminuria and, with renal impairment) and compared them with matched healthy control subjects. The HbA1c and estimated glomerular filtration rate (eGFR) derived from the abbreviated Modification of Diet in Renal Disease (MDRD) equation were examined in the study groups in relation to the urinary MCP-1. The urinary MCP-1 level was significantly higher in patients with micro and macroalbuminuria (167.41 +/- 50.23 and 630.87 +/- 318.10 ng/gm creatinine respectively) as compared with normoalbuminuric patients and healthy controls (63.85 +/- 21.15 and 61.50 +/- 24.81 ng/gm creatinine, p p 0.001), HbA1c (r= 0.55, p 0.001) and inversely with eGFR (r=-0.60, p< 0.001). Our findings suggest that hyperglycemia is associated with increased urinary levels of MCP-1 that is closely linked to renal damage as reflected by proteinuria and eGFR levels. Collectively, these findings suggest that MCP-1 is involved in the pathogenesis of diabetic nephropathy through its various stages.
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PMID:Correlation of urinary monocyte chemo-attractant protein-1 with other parameters of renal injury in type-II diabetes mellitus. 1897 75

Urinary excretion of lipocalin-type prostaglandin D synthase (L-PGDS) has been suggested to be a useful biomarker of early diabetic nephropathy. We studied whether L-PGDS is also a marker of gentamicin (GM)-induced renal damage in the "creatinine-blind" range. A prospective study was conducted in 6 patients who were given long-term intravenous administration of GM (18-42 days in combination with a beta-lactam/carbapenem antibiotic or vancomycin) for the treatment of infective endocarditis. Urinary excretions of L-PGDS, beta2-microglobulin, and N-acetyl-beta-D-glucosaminidase were measured in the early (within 10 days from commencement) and late (thereafter) phases of GM therapy. Systemic clearance of GM (CLGM) and creatinine clearance (CLcr) was also measured concomitantly. CLGM was reduced significantly (P < 0.05) by 10% from the early to late treatment phase, whereas urinary L-PGDS excretion showed a significant (P < 0.05) increase (from 7.3 +/- 4.6 to 8.7 +/- 5.0 mg/g creatinine, mean +/- SD) concomitantly. In contrast, no significant changes were observed for urinary beta2-microglobulin and N-acetyl-beta-D-glucosaminidase concentrations. In conclusion, urinary L-PGDS may be a promising biomarker for the early phase of GM-induced renal impairment.
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PMID:Urinary lipocalin-type prostaglandin D synthase: a potential marker for early gentamicin-induced renal damage? 1912 50


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