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

Nutritional factors, especially calcium, calorie and fat intakes may be important in the treatment with active vitamin D, so that the effect appears more efficient. Incidence of bone changes, due to hyperparathyroidism in diabetic nephropathy, was less than that in non-diabetic patients under hemodialysis. No effect of control status of diabetes mellitus was demonstrated, regarding incidence of subperiosteal resorption of finger bones. Bone mass was decreased in diabetic patients in whom the control of blood glucose was inadequate.
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PMID:Nutrition and renal osteodystrophy. 383 19

The first study compared two groups on dialysis: 25 patients with diabetes mellitus and 25 matched non-diabetic patients, in relation to the presence of signs of hyperparathyroidism, to assess the reported low incidence of hyperparathyroidism in these patients. The diabetic group showed significantly lower values of PTH, Alk phosphatase, percentage of patients requiring vitamin D treatment, and less evidence of hyperparathyroidism on X-ray and in bone histomorphometry. In the second study 16 patients with chronic renal failure due to diabetic nephropathy were compared to 27 patients with the same degree of renal failure of other origin, the diabetic nephropathy group showed no increase in PTH, with falling creatinine clearance. Despite this low PTH, the phosphaturia was higher in the diabetic nephropathy group (Tm PO4/C Cr: 1.94 +/- 0.43 vs 2.5 +/- 0.68). In conclusion, patients with diabetes mellitus are less prone to develop hyperparathyroidism in progressive renal failure. This could be due to a relative increase in phosphaturia during declining function.
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PMID:Low incidence of hyperparathyroidism in diabetic renal failure. 399 89

A significant loss of bone has been observed in diabetes mellitus. The pathogenesis is unknown, but an impairment of vitamin D metabolism might be involved. Consequently, we have studied vitamin D metabolism in five groups of insulin-dependent diabetic patients. Significantly reduced levels of serum 25(OH)D were seen only in patients with diabetic nephropathy. The serum levels of 1,25 (OH)2D were reduced only in diabetic ketoacidosis but normalized during recovery. It is concluded that vitamin D metabolism is largely normal in adult insulin-dependent diabetes, and it seems unlikely that a disturbance of the vitamin D metabolism can explain the bone loss in the ordinarily controlled diabetics.
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PMID:Vitamin D metabolism in insulin-dependent diabetes mellitus. 642 48

Besides defining the appropriate doses of frusemide in uraemic patients, A. Heidland's contribution to the treatment of hypertension in chronic renal failure consisted in the following demonstrations: (1) In patients on chronic haemodialysis, calcium antagonists have a beneficial effect on their glucose intolerance and decreased plasma levels of 25OH vitamin D while their effect on blood lipids is neutral. (2) In 5/6 nephrectomized rats, captopril, verapamil, and metoprolol have the same protective effect on their GFR and tubular secretion of protons, at equal blood-pressure-lowering effect. (3) In rats with streptozotocin-induced diabetes, atrial natriuretic peptide does not play a role in their hyperfiltration. (4) Severe retinopathy is observed in patients with uraemic nephropathies at a much smaller elevation of their blood pressure than in patients with essential hypertension. This article reviews the following points: (1) The role of hypertension in the loss of renal function is convincingly demonstrated only in a few experimental models, and in man only in malignant hypertension and diabetic nephropathy but not in essential hypertension nor in non-diabetic nephropathy. However, preliminary results suggests that antihypertensive treatment may retard the progression of renal disease in normotensive patients (DBP <90 mmHg) with either microalbuminuric diabetes and normal renal function or non-diabetic uraemic nephropathy. (2) Only the ACE inhibitors have been proved to have a specific renal protective effect, independent of their diurnal blood-pressure-lowering effect, both in diabetic nephropathy and in non-diabetic uraemic nephropathy.
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PMID:Hypertension and progression of renal insufficiency. 807 21

The less rigorous attention to the management of the complications of chronic renal insufficiency (CRI) and its comorbid conditions has potentially tragic consequences. In fact, with early recognition and intervention, many of the complications of CRI and its comorbid conditions can be ameliorated or prevented. We review here the most prevalent, troublesome, and potentially preventable complications and comorbidities of CRI with a view toward developing high-quality, cost-effective strategies for delivering early interventional care. Complications of CRI include malnutrition, anemia, disorders of divalent ion metabolism and osteodystrophy, metabolic acidosis, and dyslipidemia. Important comorbid conditions of CRI are hypertension, diabetes mellitus, and cardiovascular disease. Clinical intuition suggests that early intervention will avert morbidity related to the hypoalbuminemia and other nutritional disorders of CRI, the metabolic acidosis, and the dyslipidemias, but prospective data are lacking at present. Correction of anemia, usually with recombinant human erythropoietin, may be key to the prevention of cardiac disease and other comorbidities of CRI. Incipient disorders of bone and mineral metabolism are managed prospectively using such measures as protein restriction to reduce phosphorus intake, phosphate binders, calcium supplementation, and vitamin D analogues. Hypertension, whatever its original etiology, is clearly an important risk factor for the progression of kidney failure and for the development of diffuse vascular disease; appropriate and aggressive treatment is essential. In patients with diabetic nephropathy, the principles of both primary and secondary prevention have been validated in several large trials of glycemic and blood pressure control. The seeds of these insidious, challenging, and costly comorbid conditions are sown very early in CRI, at a time when they are-in theory-most amenable to intervention. We therefore must be as proactive as possible in the timely implementation of relatively simple therapies that have the potential to prevent some of these adverse outcomes of CRI.
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PMID:Complications of chronic renal insufficiency: beyond cardiovascular disease. 1111 56

Vitamin D has been used for topical treatment of psoriasis, and 22-oxacalcitriol (OCT), shown to be less calcemic, was developed for the topical treatment of psoriasis in Japan. Recently, we treated a psoriatic patient with diabetic nephropathy who developed severe hypercalcemia with exacerbation of chronic renal failure by the use of topical OCT. Analysis of the reported cases demonstrated that both the severity of psoriasis and renal dysfunction are critical factors in the induction of hypercalcemia in the topical treatment of psoriasis. Therefore, we must pay attention to the severity of psoriasis, especially when complicated by renal function impairment. Regular monitoring of Ca and renal function is essential to avoid life-threatening hypercalcemia from the topical treatment with vitamin D analogues.
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PMID:Topical treatment with 22-oxacalcitriol (OCT), a new vitamin D analogue, caused severe hypercalcemia with exacerbation of chronic renal failure in a psoriatic patient with diabetic nephropathy; a case report and analysis of the potential for hypercalcemia. 1471 59

The db/db mouse develops features of type II diabetes mellitus as the result of impaired signaling through its abnormal leptin receptor. In spite of accurate metabolic features of diabetes, renal disease manifestations in these mice are not as severe as in humans suggesting the presence of protective genes. There is a growing body of evidence in humans for the relevance of vitamin D in diabetes. Here we followed a large cohort of db/db mice and their non-diabetic db/+ littermates. Transcriptional profiling revealed significant upregulation of 23 genes involved in Ca2+ homeostasis and vitamin D metabolism in db/db glomeruli relative to db/+ glomeruli. Increased glomerular expression of vitamin D3 1alpha-hydroxylase, vitamin D binding protein, calbindins D9K and D28K, and calcyclin mRNA was confirmed by quantitative reverse transcription-polymerase chain reaction in 20-, 36-, and 52-week-old db/db glomeruli. Although vitamin D3 1alpha-hydroxylase protein was primarily expressed and upregulated in db/db renal tubules, it was also expressed in glomerular podocytes in vivo. Serum 1,25-dihydroxyvitamin D3 and urinary Ca2+ excretion were increased >3-fold in db/db mice compared to db/+ mice. Cultured glomerular podocytes had mRNA for vitamin D3 1alpha-hydroxylase, vitamin D receptor, and calbindin D28K, each of which was increased in high glucose conditions. High glucose also led to enhanced production of fibronectin and collagen IV protein, which was blocked by 1,25-dihydroxyvitamin D3. These results show that vitamin D metabolism is altered in db/db mice leading to metabolic and transcriptional effects. The podocyte is affected by paracrine and potentially autocrine effects of vitamin D, which may explain why db/db mice are resistant to progressive diabetic nephropathy.
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PMID:Altered vitamin D metabolism in type II diabetic mouse glomeruli may provide protection from diabetic nephropathy. 1682 Jul 93

A statistical survey of 3932 nationwide hemodialysis (hereafter, dialysis) facilities was carried out at the end of 2004, and 3882 facilities (98.73%) responded. The population undergoing dialysis at the end of 2004 was 248 166, an increase of 10 456 patients (4.4%) from that at the end of 2003. The number of dialysis patients per million people was 1943.5. The crude death rate of dialysis patients from the end of 2003 to the end of 2004 was 9.4%. The mean age of patients who underwent dialysis in 2004 was 65.8 years, and that of the total dialysis population was 63.3 years. The percentage distribution of patients who underwent dialysis according to a newly underlying disease showed that 41.3% of patients had diabetic nephropathy and 28.1% had chronic glomerulonephritis. The frequency of calcium carbonate use for dialysis patients was 75.1% and that of sevelamer hydrochloride use was 26.2%. The frequency of sevelamer hydrochloride use does not necessarily have a strong correlation with the dose of calcium carbonate. Patients who received high doses of sevelamer hydrochloride tended to have a low concentration of arterial blood HCO(3-). Approximately 15% of dialysis patients used an intravenous vitamin D preparation, generally maxacalcitol. The longer the patients had been on dialysis, the higher the frequency of use of an intravenous vitamin D preparation. When the concentration of serum intact parathyroid hormone (PTH) was more than 200 pg/mL, the frequency of use of an orally administered vitamin D preparation decreased; but that of intravenous vitamin D preparation increased. The percentage of dialysis patients who received percutaneous ethanol injection therapy (PEIT) was 1.4%. The percentage was more than 50% in the patients who had been on dialysis for more than 10 years. The percentage of patients who received PEIT again was 35.0%. The percentage of patients who had been on hemodialysis for more than 10 years and received PEIT again was more than 50%.
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PMID:An overview of regular dialysis treatment in Japan (as of 31 December 2004). 1719 80

1,25-Dihydroxyvitamin D3 negatively regulates the renin-angiotensin system (RAS), which plays a critical role in the development of diabetic nephropathy. We tested if mice lacking the vitamin D receptor (VDR) are more susceptible to hyperglycemia-induced renal injury. Diabetic VDR knockout mice developed more severe albuminuria and glomerulosclerosis due to increased glomerular basement membrane thickening and podocyte effacement. More fibronectin (FN) and less nephrin were expressed in the VDR knockout mice compared to diabetic wild-type mice. In receptor knockout mice, increased renin, angiotensinogen, transforming growth factor-beta (TGF-beta), and connective tissue growth factor accompanied the more severe renal injury. 1,25-Dihydroxyvitmain D3 inhibited high glucose (HG)-induced FN production in cultured mesangial cells and increased nephrin expression in cultured podocytes. 1,25-Dihydroxyvitmain D3 also suppressed HG-induced activation of the RAS and TGF-beta in mesangial and juxtaglomerular cells. Our study suggests that receptor-mediated vitamin D actions are renoprotective in diabetic nephropathy.
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PMID:Renoprotective role of the vitamin D receptor in diabetic nephropathy. 1816 10

Zhang and co-workers report on the renoprotective role of the vitamin D receptor (VDR) in diabetic nephropathy using the method of streptozotocin-induced hyperglycemia in wild-type and VDR(-/-) mice. Also, experiments with cultured mesangial cells and podocytes confirm the effect of the active vitamin D metabolite 1,25(OH)(2)D(3) on inhibition of the renin-angiotensin system (RAS) in vitro. The authors conclude that the higher activation of the intrarenal RAS is the key factor to induce more severe diabetic nephropathy in VDR(-/-) mice.
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PMID:Renoprotection with vitamin D: specific for diabetic nephropathy? 1792 26


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