Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011881 (diabetic nephropathy)
 10,836 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Little research has been conducted into the long-term effects of preeclampsia, despite its frequent occurrence. The aim of this review is to examine the association between preeclampsia and the development of hypertension and kidney diseases later in life. To achieve this aim, we evaluated three retrospective studies conducted in our department. In the first study, 52 women who suffered from preeclampsia during their first pregnancy were followed for 2 years after delivery for any long-term effects upon blood pressure. In the second study, we evaluated HOMA-R, pulse wave velocity and augmentation index in groups of 48 postmenopausal women with a past history of preeclampsia and 204 postmenopausal women without a past history of preeclampsia. In the third study, we examined the association between a past history of preeclampsia and chronic kidney disease based on biopsy in 127 postmenopausal women. From the first study, although there were no significant differences in age, blood pressure at the onset of preeclampsia, the levels of proteinuria and the birth weight of the child between women who remained hypertensive and those who became normotensive, body mass index was significantly larger in women who remained hypertensive compared to those who were normotensive. In the second study, we found that women with a past history of preeclampsia exhibited insulin resistance combined with reduced vascular elasticity. In the third study, of 32 patients with a past history of preeclampsia, 12 patients exhibited focal segmental glomerulosclerosis, 10 exhibited IgA nephropathy and 10 exhibited nephrosclerosis. In contrast, of the women without a past history of preeclampsia, 26 patients exhibited IgA nephropathy, 20 exhibited a minimal change in nephritic syndrome, 6 exhibited nephrosclerosis, 6 exhibited membranous nephropathy, 5 exhibited lupus nephritis, 5 exhibited diabetic nephropathy, and 27 exhibited various nephropathies. None of the women without a past history of preeclampsia exhibited focal segmental glomerulosclerosis. Taken together with previous results, these findings suggest that hypertension and chronic kidney disease in postmenopausal women are closely associated with a past history of preeclampsia.
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PMID:Short- and long-term prognosis of blood pressure and kidney disease in women with a past history of preeclampsia. 1818 Aug 74

Nephrotic syndrome (NS) is an essential clinical problem in the elderly. It may be difficult to recognize NS in the elderly because its symptoms are frequently missed with congestive heart failure or venous insufficiency. Glomerular diseases are not most common in elderly population but they play important role in renal pathology in this group of patients. Many structural and functional changes occur in the kidney with an increasing age. These changes may make, at least in part, the interpretation of renal lesions difficult. Glomerular pathology in this group of patients may be secondary to neoplastic diseases, and, therefore before the kidney biopsy screening for malignancies should be performed. The occurrence of particular forms of glomerular diseases differs between the older and young population. The most common forms of primary glomerular diseases in elderly are membranous nephropathy and focal-segmental glomerulosclerosis, whereas diabetic nephropathy and amyloidosis are common causes of secondary nephropathies. Kidney biopsy in the elderly gives valuable information, just as it is in the other age groups. It is a reasonably safe procedure, although associated with an increased risk of bleedings, when compared to younger population.
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PMID:[Nephrotic syndrome in the elderly. The most frequent causes of the nephrotic syndrome in the elderly (part I)]. 1836 26

On the case of 62 year old patient with diabetes type 2 complicated by diabetic nephropathy, we present diagnostic and therapeutic problems of severe nephrotic syndrome caused by membranous nephropathy confirmed by renal biopsy superimposed on diabetic nephropathy. Special attention was paid to the difficulties in achievement the remission of nephrotic syndrome with typical pharmacological treatment and necessity of using drastic form of treatment which was bilateral embolisation of renal arteries and subsequent continuous renal replacement therapy.
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PMID:[Severe nephrotic syndrome requiring bilateral renal arteries embolisation in patient with membranous and diabetic nephropathy]. 1863 64

Diabetic nephropathy is a major microangiopathic complication of diabetes mellitus. Its features are represented by: proteinuria and renal function decrease. The etiology of proteinuria in diabetic patients is assessed in this study. The study was performed on 30 patients with diabetes mellitus (11 type 1, 19 type 2) and proteinuria (19 males and 11 females), at the mean age of 42.1+/-7.72 years. Renal biopsies were done with Vim-Silverman needle, using hematoxylin-eosin and PAS staining. Diabetic retinopathy was found in 26 patients (86.66%). The values of proteinuria were: 0.62+/-0.07 g/24 hours in 4 (13.33%), 2.41+/-1.26 g/24 hours in 10 (33.33%) and 4.68+/-2.11 g/24 hours in 16 patients (53.33%). 18 patients presented elevated blood pressure (170.11+/-6.25/97.12+/-4.44 mmHg). Reduced creatinine clearance (48.01+/-7.25 ml/min) was found in 7 patients (23.33%). Histological analysis showed: diffuse diabetic glomerular lesions in 14 patients (46.66%), nodular diabetic glomerular lesions associated with diffuse glomerular lesions in 12 patients (40%) and membranous glomerulonephritis, without diabetic lesions in 4 patients (13.33%). Appearance of proteinuria in diabetic patients is not synonymous with diabetic nephropathy, requiring further investigations. including renal biopsy.
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PMID:The etiology of proteinuria in diabetic patients. 1892 63

Selectivity index (SI) has been reported to reflect the selectivity of proteinuria, and it has a relationship with tubulointerstitial damage. Moreover it has a predictive value on functional outcome. However, it is necessary to measure serum IgG, serum transferrin, urinary IgG, and urinary transferrin to calculate SI. We measured urinary micro-cholesterol (mCHO) levels in sixty-three patients with proteinuria (urinary total protein > or = g/gCr) and compared urinary mCHO/total protein(uTP) ratio and SI. The patients' diseases were minimal change nephrotic syndrome (MCNS, n = 12), focal and segmental glomerular sclerosis (FSGS, n = 12), membranous nephropathy (MN, n = 17), and diabetic nephropathy (DMN, n = 22). Urinary mCHO levels were measured by the ECC method using cholesterol ester hydrolase (CEH) and cholesterol dehydrogenase, and this method was performed conveniently by automatic analyzer. No correlation was observed between urinary mCHO/gCr and serum lipid levels. There was no difference of urinary protein levels among each disease group. We found urinary mCHO/uTP ratio has a good positive correlation with SI(R = 0.722, p < 0.001). Although the difference between ROC curves of SI and urinary mCHO/uTP ratio in distinguishing MCNS from other diseases (FSGS+MN+DMN) did not reach the statistical significance, the area under the curve was larger for mCHO/uTP ratio. These results suggest that measurement of urinary mCHO by ECC method can be a simple and useful tool for predicting selectivity of proteinuria and lipoprotein-loading tubulopathy.
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PMID:[Clinical significance of urinary cholesterol/total protein ratio as a marker of selectivity of proteinuria: comparison with selectivity index]. 1931 16

Endoplasmic reticulum (ER) stress refers to physiological or pathological states that result in accumulation of misfolded proteins in the ER. To handle misfolded proteins, the ER has in place quality control mechanisms, including the unfolded protein response and ER-associated degradation (ERAD). ER stress in renal pathophysiology is a relatively new area of research. Mice heterozygous for a mutation in the ER chaperone, BiP, develop glomerulosclerosis and tubulointerstitial disease. Induction of ER stress in glomerular cells has been described in experimental models of membranous nephropathy and membranoproliferative glomerulonephritis, and exogenous induction of ER stress ('preconditioning') reduced proteinuria. In human kidney biopsies, markers of ER stress in glomeruli have been identified in various noninflammatory and inflammatory glomerulopathies. A tubulointerstitial ER stress response, in some cases associated with tubular cell apoptosis, may occur in glomerular diseases associated with proteinuria, including puromycin aminonucleoside nephrosis, protein overload, and experimental and human diabetic nephropathy. Certain missense mutations in nephrin and podocin, as well as underglycosylation of nephrin, result in misfolding and retention in the ER, and eventually ERAD. Understanding the various aspects of ER stress will provide an opportunity for development of novel therapeutic strategies for proteinuric diseases.
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PMID:Endoplasmic reticulum stress in proteinuric kidney disease. 1981 38

Adolescent patients who require the care of a nephrologist present with a variety of challenges. For the treating physician, it is important to be competent in relevant principles of adolescent physiology, such as somatic growth and puberty. It is also essential to be familiar with the stages of adolescent emotional and intellectual development, and their influence on behavior and adherence. Patients transitioning from pediatric nephrology may experience difficulties adjusting to the adult care system. Although the renal pathology of adolescents has more in common with that of adults than that of prepubertal children, there are unique epidemiological, diagnostic, and treatment approaches to these patients that should be considered. Membranous glomerulonephritis and diabetic nephropathy are rare in adolescents, whereas IgA and systemic lupus erythematosus are often important differential diagnoses. Despite all of the challenges posed by adolescents, there is a real prospect of intervening early in the course of chronic kidney disease with the potential to alleviate long-term morbidity.
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PMID:Caring for adolescent renal patients. 2001 May 45

The glomerular basement membrane (GBM) is a kind of net that remains in a state of dynamic equilibrium. Heparan sulfate proteoglycans (HSPGs) are among its most important components. There are much data indicating the significance of these proteoglycans in protecting proteins such as albumins from penetrating to the urine, although some new data indicate that loss of proteoglycans does not always lead to proteinuria. Heparanase is an enzyme which cleaves beta 1,4 D: -glucuronic bonds in sugar groups of HSPGs. Thus it is supposed that heparanase may have an important role in the pathogenesis of proteinuria. Increased heparanase expression and activity in the course of many glomerular diseases was observed. The most widely documented is the significance of heparanase in the pathogenesis of diabetic nephropathy. Moreover, heparanase acts as a signaling molecule and may influence the concentrations of active growth factors in the GBM. It is being investigated whether heparanase inhibition may cause decreased proteinuria. The heparanase inhibitor PI-88 (phosphomannopentaose sulfate) was effective as an antiproteinuric drug in an experimental model of membranous nephropathy. Nevertheless, this drug is burdened by some toxicity, so further investigations should be considered.
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PMID:The role of heparanase in diseases of the glomeruli. 2004 46

There is a paucity of high quality clinical trials in glomerular disease, particularly in non-diabetic kidney disease. The aims of this review include quantifying the extent of this problem and exploring reasons for the scarcity of such trials in primary glomerular disease, with an emphasis on immunoglobulin A nephropathy, minimal change disease, focal segmental glomerulosclerosis, and membranous nephropathy in comparison with the more common diseases of diabetic nephropathy and lupus nephritis. Reasons for the dearth of high quality clinical trials in primary glomerular disease include (1) low prevalence of disease; (2) variability in clinical presentation; (3) variability in treatment response; (4) lack of consensus in definitions; (5) difficulty in recruiting patients; (6) high costs of randomized controlled trials; and (7) lack of collaborative efforts. To facilitate greater numbers of high quality clinical trials in glomerular disease, practice guidelines should establish common classification systems of disease and common clinical end points, industry and non-industry sponsored research should find common ground and work together toward advancing science, and national registries should be created to encourage collaborations across institutions and across nations.
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PMID:Glomerular disease: why is there a dearth of high quality clinical trials? 2378 34

Injury to the podocytes is the initiating cause of many renal diseases, leading to proteinuria with possible progression to end-stage renal disease. Podocytes are highly specialized cells, with an important role in maintaining the glomerular filtration barrier and producing growth factors for both mesangial cells and endothelial cells. With their foot processes they cover the glomerular basement membrane, and form slit diaphragms with neighboring podocytes. Human podocytopathies include focal and segmental glomerulosclerosis, minimal change disease, membranous nephropathy, collapsing glomerulopathy and diabetic nephropathy. Research in the last two decades has demonstrated great progress in understanding the molecular mechanisms leading to podocytopathies. These include single gene defects in slit diaphragm proteins, but also discovery of apoptotic, enzymatic and other pathways involved in podocyte injury. With this progress, a great number of animal models is now available to study either specific podocytopathies, e.g. in mouse models with single gene mutations, or more general podocyte injury patterns, such as the lipopolysaccharide or protamine sulfate model of foot process effacement. In this review, the morphology of the glomerulus will be discussed, with a focus on the podocyte, its interactions with surrounding cells, and the highly differentiated slit diaphragm separating the apical from the basal membrane. We also provide an overview of human podocytopathies and animal models to study these diseases. In the last part we discuss targeted therapies addressing pathways and proteins affected in podocyte injury.
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PMID:Targeting podocyte-associated diseases. 2082 90


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