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)

Dietary factors may have substantial impact on the clinical manifestations and even the progression of chronic renal failure. Proper dietary management can prevent certain uremic complications, decrease azotemia, and may even prevent the loss of residual renal function. Recent studies indicate that dietary protein may accelerate the normal age-related deterioration of renal function in rats. The extensive ablation of functional renal mass in rats leads to hyperemia and hyperfiltration in remnant nephrons. Continued hyperfiltration theoretically results in glomerular damage, proteinuria, and ultimately glomerular sclerosis. Dietary protein restriction reduces the remnant nephron hyperfiltration and reduces the rate of glomerular sclerosis, at least in the rat. The role of dietary protein in the pathogenesis of human nephrosclerosis remains controversial. Though dietary factors may or may not affect the rate of progression of renal insufficiency, there is no doubt that proper dietary management can limit or forestall uremic symptoms and the need for dialysis. Diets containing about 0.5 gm protein/kg body weight/day usually maintain a neutral or slightly positive nitrogen balance, while lesser amounts usually result in malnutrition. When protein intake exceeds 0.5 gm/kg/day azotemia increases dramatically. The use of nitrogen-free keto- or hydroxy-analogues of amino acids promotes positive nitrogen balance while reducing azotemia in patients with near-end-stage renal disease.
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PMID:The role of dietary protein in the progression and symptomatology of chronic renal failure. 639 62

It has recently been established that the rate of progression of chronic renal failure in man can be slowed by restricting dietary protein. Consequently, the short term and long term effects of a low protein diet on the course of different chronic nephropathies were studied in an attempt to delineate the factors that determine the response to such a diet. When a low protein diet was given for six months renal function improved significantly in nine patients with chronic tubulointerstitial nephritis (p less than 0.025); the diet had a marginally beneficial effect in 12 patients with chronic glomerulonephritis (p less than 0.05) and no effect in nine with hypertensive nephrosclerosis. The heterogeneous functional response in the patients with chronic glomerulonephritis correlated closely with the effect of the diet on these patients' proteinuria (r = 0.76, p less than 0.01). In a short term study (four weeks) of 12 patients with chronic renal failure changes in renal plasma flow were proportional to dietary protein intake. Renal vascular resistance fell during a high protein diet and increased when dietary protein was restricted. The changes in renal plasma flow during the low protein diet correlated well with the patients' long term functional response to the diet (r = 0.76, p less than 0.01). It is concluded that the response to a low protein diet in chronic renal failure is determined, firstly, by the nature of the underlying nephropathy, with maximal benefit being observed in non-glomerular disorders; secondly, by the effect of the diet on the proteinuria in chronic glomerulonephritis; and, thirdly, by the haemodynamic response to the diet, with patients with a reactive renal vascular bed improving with a low protein diet.
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PMID:Selective effect of low protein diets in chronic renal diseases. 643 39

In order to explore immunological features of hypertension, we studied autologous immune complex nephritis (Heymann nephritis) combined with DOCA-NaCl treatment. This combination resulted in hypertension and increased heart weight whereas DOCA-NaCl treatment alone induced only a slight elevation of blood pressure and a moderate increase in heart weight. Nephritic rats without DOCA-NaCl load remained normotensive, their heart weights being comparable to those of controls. This new model of hypertension was neither characterized by azotemia nor by reduced renal excretory capacity. Hypertension was not renin-angiotensin-dependent. DOCA-NaCl treatment accelerated the development of proteinuria. In the hypertensive rats, systolic blood pressure to daily urinary protein excretion. Renal histopathology revealed changes resembling those of malignant nephrosclerosis. Immunohistology and electron microscopy showed a typical membranous glomerulonephritis in all immunized animals. It was concluded that immune complex disease of the Heymann nephritis type may interfere with normal hemodynamic adaptation to hypervolemic sodium load, resulting in hypertension.
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PMID:Autologous immune complex nephritis and DOCA-NaCl load: a new model of hypertension. 644 27

Fetal outcome was evaluated in 157 hypertensive pregnant women whose underlying disease had been established by renal biopsy. The patients had pathologic diagnoses of preeclampsia (95), nephrosclerosis (23), nephrosclerosis with superimposed preeclampsia (13), interstitial and tubular nephropathy (seven), and normal findings (six). Pregnancy outcome in this selected group of patients was extremely poor, with the perinatal mortality rate being 134 per 1,000. There were 21 perinatal deaths; three quarters of these were stillbirths, and most were encountered below the fiftieth weight percentile and before 30 weeks' gestation. In addition 22% of the infants were small for gestational ages, and 40% of the infants were born before term. Most of the perinatal mortality (81%) was in women with preeclampsia. The worst fetal outcome was encountered in multiparous preeclamptic women, over 50% of whom manifested nephrotic-range proteinuria during pregnancy. Despite the presence of hypertension throughout most of their gestation, women with nephrosclerosis alone had the best fetal survival rate.
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PMID:Fetal outcome in hypertensive disorders of pregnancy. 706 13

Urinalysis is a simple, efficient, and accurate guide in the diagnosis of renal disease. By determining a patient's history and obtaining a physical examination, the physician is very often able to diagnose a patient's renal lesion. Heavy proteinuria and a microscopic sediment containing red cells and red cell casts strongly suggest acute glomerulonephritis. The causes of this nephropathy are legion. On the other hand, mild proteinuria and a lack of microscopic findings suggest nephrosclerosis, interstitial nephritis, or acute tubular necrosis in the proper clinical setting. When glomerular disease produces nephrotic syndrome, the various types of glomerular disease can be diagnosed accurately without biopsy in a high percentage of cases.
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PMID:Urinalysis and clinical renal disease. 721 37

Proteinuria may be an independent risk factor for nephrosclerosis. One potential mechanism has emerged with the finding that lipoproteins, including albumin, modulate the biology of mesangial cells and proximal tubular epithelial cells when internalized. Consequent alterations in renal-cell lipid metabolism may underlie some of these effects.
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PMID:Renal toxicity of albumin and other lipoproteins. 755 6

The kidney can be considered as both culprit and victim in the hypertensive process. Deranged renal function contributes to the development of arterial hypertension and of secondary vascular damage at the glomerular and arteriolar level and accounts for the development of progressive nephrosclerosis. The most common alteration of renal function observed in humans from the early stages of essential hypertension is the presence of renal vasoconstriction. This can be accompanied by hyperuricaemia and increased urinary excretion of enzymes such as N-acetyl-beta-glucosaminidase and proteins such as albumin and beta 2-microglobulin. Later, a progressive fall in glomerular filtration rate, sometimes accompanied by proteinuria, can be observed if high blood pressure persists.
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PMID:Renal damage in hypertension. 760 39

Between April 1985 and April 1992, 25,672 men (age 47 +/- 9 years, mean +/- SD) and 9,791 women (48 +/- 9 years) underwent mass urinalysis in the Center for Adult Complete Physical Examination in our hospital. The results revealed proteinuria in 6.3% of the men and 4.4% of the women and hematuria in 17.4% of the men and 37.8% of the women. Thirty-five subjects with asymptomatic persistent proteinuria and/or hematuria identified as a result of follow-up testing by the nephrologists at our hospital underwent renal biopsy. All of the biopsy specimens obtained were examined by light microscopy, fluorescence microscopy and electron microscopy. Histopathological findings in the biopsy specimens from these 35 subjects were as follows: One case (3%) of chronic pyelonephritis, 11 cases (31%) of IgA nephropathy, 4 cases (11%) of IgA nephropathy (severe type), 5 cases (14%) of membranous nephropathy, 4 cases (11%) of thin basement membrane disease (TMD), 7 cases (28%) of benign nephrosclerosis and 3 cases (9%) of minor glomerular abnormality. Light microscopy, fluorescence microscopy and electron microscopy for histopathological assessment of renal specimens, especially for the diagnosis of TDM, which was not uncommon, were indispensable tools in our study. Moreover, it is essential for proteinuria and hematuria to be tested simultaneously using the same standard method in all the urine specimens collected.
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PMID:[Histopathological assessment of renal biopsy specimens of subjects with urine abnormality]. 760 27

The paper provides evidence and results of using new therapeutical treatment of glomerulonephritis, such as pulse-therapy with cyclophosphane, therapy with angiotension-converting enzyme (ACE) inhibitors or that with antihyperlipidemic agents. Based on much experience with pulse-therapy with cyclophosphane (over 100 patients with chronic glomerulonephritis (CGN) and lupus nephritis), it is concluded that this method is highly effective. Treating 57 patients with ACE inhibitors has shown that in CGN these drugs should be used only when taking into account their antihypertensive effect and capacity of lowering intraglomerular hypertension, as evidenced by the renal functional reserve, and diminishing proteinuria. The long-term (7-12 month) antihyperlipidemic therapy (diet and lovastatin) in 20 patients with CGN accompanied by the nephrotic syndrome caused a significant reduction in the concentration of serum cholesterol and proteinuria, a significant increase in serum albumin levels; remission of the nephrotic syndrome occurred in 9 patients; but better effects were observed in non-inflammatory nephropathies, such as membranous nephropathy, focal segmental glomerulosclerosis, and nephrosclerosis.
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PMID:[New approaches to the treatment of nephritis]. 762 87

Ischemic nephropathy encompasses renal insufficiency due to 3 different diseases, namely renal artery stenosis, so-called benign nephrosclerosis, and renal cholesterol embolism. All 3 disease entities may lead to a progressive loss of renal excretory function. If a patient presents with renal failure of unknown origin, renal artery stenosis should be looked for by color-coded duplex scanning or arteriography. The clinical presentation of benign nephrosclerosis in caucasians has no typical clues. Usually, a renal biopsy identifies this renal disorder in a patient with long-standing hypertension, moderate proteinuria and renal insufficiency. Cholesterol embolism typically affects several arterial trees, and is induced by arteriography in patients with arteriosclerosis of the aorta. The best treatment for ischemic nephropathy due to renal artery stenosis [conservative, angioplasty, surgery] is unknown because appropriately controlled trials are lacking. Invasive therapy should be considered in patients with bilateral renal artery stenosis or stenosis of a single functioning kidney, particularly if the affected kidney is not contracted. Arguments in favor of invasive therapy include the progressive nature of renal artery stenosis and the poor outcome of dialysis patients with this diagnosis as underlying renal disease.
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PMID:[Ischemic nephropathy]. 778 95


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