Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033687 (proteinuria)
 24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A laboratory model of renal osteodystrophy was developed in rats by a single injection of glycopeptide isolated from renal cortical tissues of rats according to the method used by Shibata et al. to induce glomerulonephritis. Approximately 60-70 days after injection, severe proteinuria appeared and continued for at least 170 days at a rate of more than 1 g/day. Morphological changes in the kidney were typical of chronic glomerulonephritis. The plasma calcium concentration was lowered transiently by the 96th day after injection, but was restored to the normal range thereafter. Plasma parathyroid hormone levels, however, continued to rise in parallel with the degree of proteinuria. Marked secondary hyperparathyroidism was induced which led to severe bone atrophy. Histological examinations showed a marked increase of resorbing cavities, with a quantitatively larger number of osteoclasts in cortical bone tissues compared with the control animals. No spontaneous remission was observed. It is emphasized that all of the biochemical and morphological changes reported here were induced by a single injection of homologous renal glycopeptide, and they were highly reproducible.
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PMID:Osseous changes and abnormalities of mineral metabolism in rats with glycopeptide-induced nephritis. 737 53

A 6-month protocol of oral pulse calcitriol was used in nine uraemic children (2-14 years old) on dialysis who presented with renal osteodystrophy. Calcitriol was administered twice a week, 4 micrograms per dose for patients over 30 kg and 3 micrograms for patients less than 30 kg. Plasma levels of parathyroid hormone, calcium, phosphorus and alkaline phosphatase were carefully controlled during the study. Parathyroid hormone levels decreased by 68% and 56% by the 2nd and 6th months of treatment in seven patients, while they remained unchanged in two patients with focal segmental glomerulosclerosis and massive proteinuria. Eight hypercalcaemic episodes from 77 determinations were observed, all of them recovered after 1 week of vitamin D withdrawal. We conclude that oral calcitriol pulse therapy is a good alternative for renal osteodystrophy in uraemic children. Careful monitoring of plasma parathyroid hormone and calcium is needed during follow-up when using this approach in paediatric patients.
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PMID:Calcitriol oral pulse therapy in children with renal osteodystrophy. 858 20

The prevention of phosphate retention in chronic renal disease may reduce both renal osteodystrophy and disease progression. We evaluated the expression of the sodium-dependent phosphate transporter, NaPi-2, and the response to phosphonoformic acid (PFA) in rats with 5/6 nephrectomy-induced renal failure. Partial nephrectomy resulted in a significant proteinuria and reduced renal function. In addition, there was an approximately 50% reduction in the expression of NaPi-2 mRNA. Treatment of rats for 48 hr with PFA (0.6% in glucose drinking fluid) had no effect on NaPi-2 mRNA; however, PFA resulted in a significant increase in fractional phosphate excretion in both normal (7 +/- 0.5% vs. 3 +/- 0.2%) and uremic (60 +/- 4% vs. 36 +/- 4%) rats. Plasma phosphate concentration was higher in uremic rats (2.5 +/- 0.1 mM) compared with normal rats (1.9 +/- 0.04 mM) but not in uremic rats treated with PFA (2.1 +/- 0.04 mM). These data suggest that PFA can increase renal phosphate excretion independent of changes in phosphate transporter expression and prevent phosphate retention.
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PMID:Phosphate excretion and phosphate transporter messenger RNA in uremic rats treated with phosphonoformic acid. 919 Aug 81

The key messages of these guidelines on chronic kidney disease are: Chronic kidney disease (CKD) is a public health problem due to its wide distribution, high rate of complications and cost. CKD is a common condition, its prevalence being about 10%, and is treatable if it is detected on time. A patient with CKD has a higher risk of cardiovascular mortality than of progression of its underlying renal disease. A new definition of CKD, based on estimated Glomerular Filtration Rate (eGFR) and kidney damage, facilitates its detection and management. CKD is detected with three simple tests: 1) Blood pressure measurement, 2) Detection of proteinuria or albuminuria in an isolated urine sample, and 3) Estimation of renal function (eGFR), based on serum creatinine, age, gender and race. The CKD risk groups are individuals with diabetes, hypertension and a family history of renal disease. The most cost-effective measures are to detect and treat diabetic and hypertensive patients in the community. Therapy must emphasize the maximal reduction of cardiovascular risk. The complications of CKD such as anemia and renal osteodystrophy can be identified and treated on time. Most patients with chronic kidney disease are detected in the community, therefore their initial care must be organized at the level of primary care, along with programs for hypertension and diabetes.
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PMID:[Clinical guidelines on identification, management and complications of chronic kidney disease]. 1940 62

Chronic kidney disease is defined by decreased glomerular filtration rate or proteinuria. Diabetic nephropathy and hypertensive renal damage are responsible for the majority of cases. The initiation of therapy has to consider if causal treatment of the underlying disease is possible and indicated. In all patients, even if specific treatment is not possible, therapy should aim at reducing progression of kidney failure. Chronic kidney diseases tend to intrinsic deterioration that persists after cessation of the causative damaging pathomechanism. Progression of disease can be delayed; the most important measures include strict blood pressure control, reduction of proteinuria, and avoidance of further renal harm. Kidney disease induces typical sequelae such as left ventricular hypertrophy, vascular calcification, anemia, and renal osteodystrophy. While these are well understood nowadays therapeutic options are limited. The uremic syndrome is to be avoided by renal replacement therapy.
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PMID:[Diagnosis and treatment of chronic kidney disease]. 2819 76

The risk of cardiovascular death is 10 times higher in patients with CKD (chronic kidney disease) than in those without CKD. Vascular calcification, common in patients with CKD, is a predictor of cardiovascular mortality. Vitamin D deficiency, another complication of CKD, is associated with vascular calcification in patients with CKD. GFR decline, proteinuria, tubulointerstitial injury, and the therapeutic dose of active form vitamin D aggravate vitamin D deficiency and reduce its pleiotropic effect on the cardiovascular system. Vitamin D supplement for CKD patients provides a protective role in vascular calcification on the endothelium by (1) renin-angiotensin-aldosterone system inactivation, (2) alleviating insulin resistance, (3) reduction of cholesterol and inhibition of foam cell and cholesterol efflux in macrophages, and (4) modulating vascular regeneration. For the arterial calcification, vitamin D supplement provides adjunctive role in regressing proteinuria, reverse renal osteodystrophy, and restoring calcification inhibitors. Recently, adventitial progenitor cell has been linked to be involved in the vascular calcification. Vitamin D may provide a role in modulating adventitial progenitor cells. In summary, vitamin D supplement may provide an ancillary role for ameliorating uremic vascular calcification.
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PMID:Role of Vitamin D in Uremic Vascular Calcification. 2828 58

The primary indication for administration of calcitriol or other vitamin D receptor activators (VDRA) in chronic kidney disease (CKD) is secondary hyperparathyroidism (SHPT). Prevention and treatment of SHPT appears important, as imbalances in mineral metabolism are associated with renal osteodystrophy, and higher parathyroid hormone (PTH) levels are associated with increased rates of mortality and morbidity in CKD patients. There is, however, a lack of controlled trial data that show lowering PTH with calcitriol/VDRA equates to improved clinical outcomes. Recent randomized controlled trials have concentrated on potential benefits of calcitriol/VDRA on cardiovascular outcomes and reduction of proteinuria and on possible differences between calcitriol and the various VDRA. Several systematic reviews and meta-analyses have also been published, evaluating the benefits and harms of calcitriol/VDRA. Concerns have been raised about the effectiveness of calcitriol/VDRA for suppression of SHPT in the CKD stages 3-5 population, as well as potential adverse outcomes such as hypercalcaemia and elevation in FGF23 levels, suggesting their routine use to treat SHPT in the pre-dialysis CKD population may not be favourable. Conversely, concerns still exist about the wide PTH range in advanced CKD, and that high values may negatively impact bone quality, result in the progression of parathyroid hyperplasia and decrease the effectiveness of treatments to reduce PTH. We discuss the current controversies relating to the challenges in the management of SHPT in patients with CKD stages 3-5 and the need for more evidence to determine the efficacy or harm of using calcitriol/VDRA in this population.
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PMID:Do the benefits of using calcitriol and other vitamin D receptor activators in patients with chronic kidney disease outweigh the harms? 2842 45