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)

The mode of presentation of renal disease in 44 patients with essential mixed cryoglobulinaemia (EMC) was: acute renal failure (two patients), acute nephritic syndrome (six patients), nephrotic syndrome (eight patients), proteinuria and/or haematuria (28 patients). Renal biopsy, performed in 35 patients showed proliferative lesions in 33, while only minimal glomerular changes were seen in the remaining two. Immunofluorescence studies showed: IgG (85 per cent), IgA (36 per cent), IgM (90 per cent), C3 (90 per cent), C1q (47 per cent), and C4 (33 per cent) deposits, mainly located in subendothelial position. On electron microscopy, crystalloid structure of deposits and monocyte infiltration of capillary loops were the outstanding feature. The survival rate was 75 per cent at 10 years from the onset of clinical symptoms. Thirty-nine patients were followed for three to 146 months (mean 53.8). Twelve patients died, cardiovascular disease and infection being the commonest cause of death. Thirteen patients showed acute renal failure of acute nephritis syndrome: nine recovered completely, whereas the remaining four died during the acute renal episode. Three patients developed chronic renal failure, but only one period required chronic dialysis. The ominous significance of renal impairment in EMC should therefore be revaluated. The high prevalence of hypertension (28/44 patients) which was refractory to treatment in six, may be important to the clinical outcome.
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PMID:Renal disease in essential mixed cryoglobulinaemia. Long-term follow-up of 44 patients. 726 65

Renal function was evaluated before and after intravenous urography (IVU) in 124 randomly selected patients. In cases with renal insufficiency (RI) (serum creatinine level, greater than or equal to 2 mg/dL), the incidence of renal impairment was higher (11 of 20 patients, 55%) than in the group without RI (16 of 104 patients, 15%). In the latter group, high blood pressure (BP) was associated with a higher frequency of renal impairment (28.6% vs 10.5%). Advanced age, mild proteinuria, and a single functioning kidney were not risk factors. The IVU preparation contributed to renal function impairment in ten cases, while in the other 17 cases, the iodinated contrast material was the only factor apparently involved. Renal function returned to its previous level in a mean period of 12 days. One patient suffered progressive and irreversible renal failure, and two others had a slight, persistent impairment of renal function. It was concluded that the incidence of renal function impairment is high, but cases are usually mild and reversible. The most important predisposing factors are RI and high BP.
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PMID:Renal function impairment caused by intravenous urography. A prospective study. 727 1

In an attempt to determine the effects of antihypertensive treatment on proteinuria and renal function, these factors were studied in 155 patients with essential hypertension, before and during antihypertensive therapy. Slight renal impairment tended to increase with the progress of hypertension, as evidenced by a slight but significant increase in the levels of blood urea nitrogen (BUN) and serum creatinine, and by a progressive decrease in creatinine clearance. A decrease in proteinuria appeared as early as one month after initiation of treatment and continued for at least two years during treatment. Apparently the proteinuria was caused by increased glomerular pressure and by vascular damage in the glomerular vessels. In 7 patients, normalization of blood pressure resulted in an elevation of BUN and creatinine concentrations, although initial renal function did not differ significantly from that in other groups who did not show such derangement during treatment. Thus, a reduction of proteinuria seems to be a good criterion for predicting beneficial results from antihypertensive treatment.
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PMID:Proteinuria and renal function during antihypertensive treatment for essential hypertension. 735 3

The role of immunosuppressive drugs in the treatment of IgA nephropathy (IgAN) remains controversial. The effect of treatment with prednisolone and azathioprine on the clinical course of patients with IgA nephropathy is described in this retrospective study. One hundred and fourteen patients, 66 treated (age 13-77 years) and 48 untreated (age 15-64 years), were evaluated. The two groups of patients differed significantly with respect to heavier proteinuria (median 3.6 g/day, range 0.2-18 g/day), lower serum albumin level (< 40 g/l) and more severe renal histopathological involvement in the treated group (P < 0.01). Oral prednisolone 40 mg/day and azathioprine 2 mg/kg BW/day was commenced initially and after gradual tapering was continued at low dose (5 mg/day) for a median duration of 24 months (range 12-98). The median duration of follow-up was 46 months (range 12-180). The clinical course was defined as progressive or non-progressive on the basis of serial serum creatinine (Scr). Of the patients who presented with renal impairment (Scr > 110 mumol/l), a non-progressive course was observed in 79.5% patients of the treated group (n = 39), while only in 36% of the untreated group (n = 22), the difference was statistically significant (P < 0.001). Slopes of reciprocal of Scr versus time were also calculated by linear regression analysis to represent the trend of renal function for patients who had had 3 or more years follow-up (n = 101). An analysis of variance of these trends in patients with renal impairment at presentation (n = 51) showed significant recovery of renal function in the treated group (n = 33) and a decline of renal function in the untreated group (n = 18, P = 0.004). There was no significant effect of the treatment on proteinuria. The histopathological features that favoured response to the treatment were mesangial proliferation, capsular adhesions and interstitial infiltration on light-microscopy, C3 and fibrin deposits on immunofluorescence (P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Can immunosuppressive drugs slow the progression of IgA nephropathy? 747 7

Children with glomerulonephritis may present with acute nephritic or nephrotic features. Glomerulonephritis may be a primary diagnosis or may be secondary to systemic illness. Children with persisting renal impairment, hypertension or proteinuria require careful investigation and assessment by a paediatric nephrologist.
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PMID:Glomerulonephritis in children. 755 96

The development of renal dysfunction in experimental glomerulonephritis (GN) is mediated in part by enhanced leukotriene (LT) formation. In our studies the pathophysiological role of LTs was investigated through pharmacological inhibition of LT biosynthesis in a rat model of nephrotoxic serum nephritis. MK-0591, an indirect inhibitor of 5-lipoxygenase activity, was co-administered to rats injected with nephrotoxic rabbit serum, followed by assessment of renal function, morphology and microsomal LTC4 synthase activity on day 7. A significant improvement in glomerular function was noted (p < 0.05), together with a 50% reduction in proteinuria (p < 0.01) in animals receiving MK-0591 (60 mg kg-1 day-1). In addition, the fall in renal LTC4 synthase activity which occurred in nephritic rats (to 74% of control values, p < 0.01) was prevented in drug-treated animals. Based on these results, it appears that inhibition of LT biosynthesis protects against both renal impairment and alterations in LTC4 synthase activity during the development of experimental GN, and may provide a useful therapeutic adjunct in the treatment of this disease.
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PMID:Inhibition of leukotriene biosynthesis improves renal function in experimental glomerulonephritis. 755 79

The mechanisms of renal injury that result in proteinuria in active Heymann nephritis (AHN) remain unclear, though data suggest that in analogy of the passive form of the disease the membrane attack complex C5b-9 may be involved. AHN was induced in an inbred strain of PVG/c-rats that are totally deficient in the C6 component of complement and are unable to form the lytic C5b-9 complex, as well as in non-complement deficient PVG/c+ rats that are immunologic identical to the deficient strain. In both groups of animals comparably high titers of anti-Fx1A autoantibodies were found after three weeks and persisted at 40 weeks. Proteinuria was also similar in both groups, and was first evident at six weeks. High levels of urinary protein, ranging from 200 mg/24 hr to 500 mg/24 hr, were found after 10 weeks and persisted up to one year. Renal biopsy findings at various times post-immunization were identical in both groups, including immunofluorescence staining for Ig and C3 deposits, and also EM findings of subepithelial electron-dense deposits were not different. The injection of heterologous rabbit complement, that partially and temporarily restored the CH50 activity in PVG/c- rats did not alter or hasten the disease. Long-term follow-up showed that all rats in both groups continued to have severe proteinuria and that most animals died between 8 to 12 months after disease induction, without renal impairment. EM findings in serial biopsies demonstrated that the growth of the subepithelial deposits as measured by surface area occurred between weeks 4 and 12. A positive correlation (r = 0.94) between the size of the deposits and the level of proteinuria was found. These studies demonstrate that the membrane attack complex of complement does not play a major role in AHN. The relationship of the size of the immune deposits to the level of proteinuria suggests that the growth of the immune deposits on itself initiate secondary mechanisms that damage the permselective characteristics of the glomerular membrane.
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PMID:Active Heymann nephritis in complement component C6 deficient rats. 764 29

A 34-year-old female patient was admitted to our hospital with a 1-year history of chronic congestive heart failure, massive proteinuria and tibial edema. On admission, she presented with hemolytic anemia, hepatomegaly, splenomegaly and renal impairment. Furthermore, the skin of her face, hand, forearm, lower extremities showed crust and bulla. Laboratory examination revealed a large amount of protoporphyrin in her blood and feces, but no increase in urine. Light microscopy of renal biopsy showed moderate chronic tubulointerstitinal disease and mild proliferation of mesangial cells. The prophyians are a group of compounds associated with involving the disturbance of various biosynthetic heme pathwas. Until now, the regulation of porphyrin and heme metabolism in the kidney have received relatively little attention as compared with those in liver and erythropoietic tissue. However, some recent reports have confirmed that proximal tubular cells may contribute to heme biosynthesis. It was strongly suggested that chronic tubulointerstitinal injury in this case might be directly induced by the disturbance of the biosynthetic heme pathway in the tubules.
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PMID:[A case of erythropoietic protoporphyria associated with tubulointerstitial disease and dilated cardiomyopathy]. 773 Nov 9

Survival of patients with increasingly complex congenital heart disease has produced a population of children and adolescents who are susceptible to subacute bacterial endocarditis (SBE). We report a child whose endocarditis went unrecognised, and who developed amyloidosis. Asymptomatic proteinuria, haematuria and renal impairment are occasionally seen in SBE and usually indicate glomerulonephritis. Amyloidosis should also be suspected in children with long-standing bacterial endocarditis with proteinuria or other evidence of renal impairment, especially if associated with organomegaly. The diagnosis is made by renal biopsy.
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PMID:Secondary amyloidosis from long-standing bacterial endocarditis. 774 18

Overt proteinuria is often accompanied by hypercholesterolemia and is associated with increased lipoprotein(a) levels. These lipid abnormalities are probably involved in the high incidence of macrovascular complications associated with diabetic nephropathy and possibly other kinds of non-diabetic proteinuric renal disease. Over the last decade many studies have shown that ACE inhibitors can reduce urinary protein excretion but little attention was paid to the impact of this form of therapeutic intervention on the lipid profile. In this article we review our recent data showing that fosinopril administration was associated with significant decreases in both urinary protein excretion, serum total cholesterol levels, and plasma lp(a) levels. The use of ACE inhibitors in patients with renal impairment can result in the development of hyperkalemia as a result of suppression of angiotensin II-driven aldosterone secretion by the adrenal gland. Inhibition of aldosterone secretion may depend on the degree of inhibition of angiotensin II formation in the circulation and also locally in the adrenal gland. Because the various ACE inhibitors exhibit different degrees of ACE inhibition at the tissue level, we have postulated that angiotensin II-dependent aldosterone production will be inhibited to a lesser degree by agents that have low tissue affinity for the adrenal gland. The implication of this theoretical concept for the development of hyperkalemia in patients with impaired renal function treated with ACE inhibitors is discussed.
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PMID:Selected aspects of ACE inhibitor therapy for patients with renal disease: impact on proteinuria, lipids and potassium. 775 17


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