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)

Nine hundred and forty children with hematuria were admitted to the nephrology service from 1958 to 1973. Percutaneous renal biopsies were performed in all of them. Thirty cases out of this group had recurrent hematuria and constitute the clinical material of this study. The clinical picture was: acute nephrotic syndrome in 19; monosymptomatic hematuria in 8, anaphylactoid purpura nephritis in 2, and hematuria associated with nephrotic syndrome in one patient. All patients with nephritic syndrome showed in their biopsies various types of glomerular lesions; most of the patients with monosymptomatic hematuria had normal glomeruli; at the light microscopy, the immunofluorescence was positive in some of them. Both patients with anaphylactoid nephritis showed diffuse endocapillary and focal extracapillary proliferation and in the only one with nephrotic syndrome, the hematuria was familial and the biopsy showed features of Alport's syndrome. Twenty-four patients who were followed for over two years showed no relationship between the age of onset, sex, initial significant proteinuria, hypertension, frequency of bouts of hematuria and the clinical evolution. At the end of the study, 7 patients had prolonged remission: the light microscopy showed normal glomeruli, endocapillary proliferation and endo and extracapillary proliferation with less than 30% of the glomeruli affected by "crescents". The remaining cases were still active and one of them with endo and extracapillary glomerulonephritis with more than 30% of the glomeruli affected by "crescents", developed chronic renal insufficiency. In conclusion, the prognosis of recurrent hematuria of glomerular origen is related with the type of glomerular lesions and constitutes an indication for renal biopsy. Renal specimens must be studied under light microscopy and immunofluorescence techniques; electromicroscopy is required when hematuria is present in more than one member of the family.
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PMID:[Recurrent hematuria of glomerular origin]. 127 66

We developed an approach in quantifying the risk of developing chronic renal insufficiency (CRI) based on a cohort of 184 patients with idiopathic membranous glomerulonephritis (IMGN), prospectively followed by the Toronto Glomerulonephritis Registry between 1974 and 1988. After a mean follow-up period of 5.8 years, 26% of patients developed CRI (defined as persistent reduction of creatinine clearance (CCr) less than or equal to 60 ml/min/1.73 m2 for greater than or equal to 12 months). We found that when compared to the baseline probability of the unselected patients, the severity of proteinuria at kidney biopsy added only marginally to the prediction of CRI. We introduced a special test condition: persistent proteinuria (PP) (that is, duration of proteinuria, g/day, above different cut-off levels). We examined the positive predictive value (PPV) and sensitivity (SEN) of 15 arbitrarily chosen levels of PP (that is, proteinuria greater than or equal to 4, 6 or 8 g/day persisting for greater than or equal to 6, 9, 12, 18 or 24 months) to select levels with optimal predictive characteristics. We found that PP greater than or equal to 8 g/day for greater than or equal to six months was a simple and useful predictor of CRI with a PPV and SEN of 66%. To further improve our prediction, we tested the following parameters: age, sex, initial SCr and CCr, proteinuria, serum albumin, hypertension, rate of change of CCr over time, and therapy (steroids +/- immunosuppressive drugs) in a multivariate analysis. Proteinuria, initial CCr, and rate of change of CCr were most important in predicting CRI.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Predicting chronic renal insufficiency in idiopathic membranous glomerulonephritis. 145 88

In order to evaluate the prognostic factors concerning the rate of progressive deterioration of renal function, we made an inductive analysis of the behaviour of 456 patients in a multicentre, formal prospective trial aimed at clarifying the possible role of protein restriction in retarding the progression of chronic renal insufficiency (CRI). The main clinical and laboratory findings in patients whose plasma creatinine (PCr) levels doubled in comparison with baseline randomization values or who needed dialysis within 24 months after onset of the study were compared with those of the other patients. In addition, independently of the assigned diet, we tested the main variables that might affect CRI progression (sex, systolic and diastolic blood pressure, change in body weight, hematocrit, calcium-phosphate product, proteinuria, protein catabolic rate, total cholesterol and triglycerides). We used multiple regression analyses and also plotted the mean values of these parameters in each patient against an estimate of the deterioration of chronic renal failure based on the difference between the final and the initial reciprocal of the PCr and the creatinine clearance (CCr) levels. A descriptive analysis of the behaviour of PCr in the three CRI groups and in the four underlying diseases groups was made. PCr levels at entry, underlying disease and proteinuria were prognostic factors for CRI progression. The increase in PCr was 0.0102 mg/dl/month in patients with nephrosclerosis, 0.0203 mg/dl/month in interstitial nephropathy, 0.0360 mg/dl/month in glomerulonephritis and 0.0704 mg/dl/month in polycystic kidney disease.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Factors affecting chronic renal failure progression: results from a multicentre trial. The Northern Italian Cooperative Study Group. 146 79

Acute administration of epidermal growth factor (EGF) has been shown to promote recovery from ischemic and nephrotoxic acute renal failure in vivo. The question of whether chronic subcutaneous administration of EGF (19.1 micrograms/day for 3 or 6 wk) could alter the course of chronic renal failure in rats subjected to 5/6 nephrectomy was studied. By week 6, there was no difference in renal function, as assessed by animal survival, BUN, urea and inulin clearances, proteinuria, renal morphometry, or renal size, between EGF- and vehicle-treated rats. This suggests that chronic renal insufficiency differs from acute tubular injury in its sensitivity to exogenous EGF. Unexpectedly, EGF significantly attenuated the rise in systolic blood pressure that occurred by the fourth week after 5/6 nephrectomy. The antihypertensive effect of EGF was still evident at week 5. Urinary flow rate, free water clearance, and excretion of total solutes, Na+, and K+, however, were not significantly altered by EGF at weeks 2, 4, 5, or 6, suggesting a mechanism other than increased natriuresis or diuresis for this antihypertensive effect.
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PMID:Effect of epidermal growth factor in the rat 5/6 renal ablation model. 148 51

Experimental evidence suggests that pharmacological manipulations of glomerular haemodynamics may affect the progression of chronic renal insufficiency and scarring. In this study, we have investigated the short-term (4 weeks) renal haemodynamic effects of nifedipine and nitrendipine (10 mg/thrice daily) in two separate groups of 6 patients with stable chronic renal failure (CRF) (glomerular filtration rate, GFR: 9.7-47.8 ml/min/1.73 m2). Patients were studied on three occasions: (1) before the administration of the calcium antagonist, (2) after 4 weeks of treatment and (3) 4 weeks after the discontinuation of the drug. Mean arterial pressure fell significantly on nifedipine: from 116.33 +/- 12.25 to 107.22 +/- 18.67 mm Hg, p less than 0.05, and on nitrendipine: from 112.22 +/- 10.04 to 102.22 +/- 13.77 mm Hg, p less than 0.05. There was no significant effect of either calcium antagonist on GFR, effective renal plasma flow (ERPF), proteinuria or natriuresis. Consequently, renal vascular resistance (RVR) fell in both experimental groups, nifedipine: from 51.40 +/- 28.77 to 44.97 +/- 30 dyn s cm-5 x 10(3) (mean +/- SD), and nitrendipine: from 37.04 +/- 18.46 to 30.47 +/- 15.56 dyns s cm-5 x 10(3), p less than 0.05. These results show that calcium antagonists reduce systemic blood pressure whilst GFR and ERPF are maintained. The fall in the RVR of patients with CRF treated with calcium antagonists may confer on these agents a therapeutic advantage in the management of progressive renal insufficiency.
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PMID:Short-term effects of calcium antagonists on renal haemodynamics in patients with chronic renal failure. 185 83

The long-term effects of converting enzyme inhibitors and calcium channel blockers on proteinuria and the progression of renal disease in patients with hypertension and chronic renal insufficiency are not well established. We have studied the long-term effects of treating hypertension with an angiotensin-converting enzyme inhibitor, enalapril, and a calcium channel blocker, nicardipine, on urinary albumin excretion (UAE) and on renal function in 16 patients with hypertension and chronic renal insufficiency (creatinine clearance ranging between 17 and 62 ml/min). After 1 year of treatment, these agents caused a similar decrease in blood pressure. Only enalapril, however, caused a significant decrease in UAE (from 641 +/- 98 to 292 +/- 47 mg/24 h, p less than 0.01), whereas UAE did not change in the group treated with nicardipine (675 +/- 78 vs. 601 +/- 75 mg/24 h). Creatinine clearance at the beginning of the study was similar in the group treated with enalapril and in the group treated with nicardipine (35 +/- 3.6 vs. 40 +/- 4.1 ml/min). After 1 year of follow-up, creatinine clearance remained unchanged in both groups of patients. These studies demonstrate that both enalapril and nicardipine can effectively reduce blood pressure in patients with hypertension and chronic renal insufficiency. Enalapril but not nicardipine, however, appears to reduce urinary albumin excretion in these patients. Whether the reduction in UAE has any significant impact on the progression of renal disease remains to be established.
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PMID:Long-term effects of enalapril and nicardipine on urinary albumin excretion in patients with chronic renal insufficiency: a 1-year follow-up. 195 74

Renal injury associated with the intrarenal reflux (IRR) of urine that is either infected, under high pressure, or both, is a major cause of severe hypertension during childhood and adolescence and of chronic renal insufficiency in patients less than 30 years of age. Many, but not all, adolescent and adult patients with reflux nephropathy (RN) give a history of urinary tract infection (UTI) or unexplained fevers in infancy or early childhood, when the kidney is thought to be at greatest risk of injury. Although vesicoureteric reflux (VUR) is observed more commonly in infants than children with UTI, it is rare in uninfected patients at any age and should never be considered a normal finding during human development. Renal scarring may not be obvious in radiographic or radionuclear studies to medical management alone, no definite benefit of one over the other was observed, regardless of the grade of VUR. Moreover, progressive renal injury in scarred kidneys has been noted even after VUR had been corrected, when infection had been prevented, and while hypertension had been controlled satisfactorily. Focal glomerular sclerosis, a lesion found in patients with proteinuria and RN, has been identified not only in scarred kidneys, but also may be seen in contralateral, unscarred kidneys without VUR, which might suggest a humoral factor or, perhaps, a hyperfiltration phenomenon. RN is one of the most frequent causes of end-stage renal disease (ESRD) in children, adolescents, and young adults, which is potentially preventable. However, prevention will depend on early identification of patients at risk--infants and young children after the first UTI and siblings of patients with VUR--aggressive and effective treatment of UTI, minimizing intravesical pressure, and education of patients, parents, and physicians.
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PMID:Vesicoureteric reflux and renal injury. 202 50

Chronic renal insufficiency is a progressive, self-perpetuating process which is influenced in part by activation of the intrarenal renin-angiotensin system. Oral angiotensin-converting enzyme inhibitors are being studied in animals and humans to determine whether they slow the decline in renal function characteristic of progressive renal disease. In animals that have reduced renal mass, streptozotocin-induced diabetes mellitus, or puromycin aminonucleoside nephrosis, these agents can reduce proteinuria, decrease the frequency of sclerotic glomeruli, and normalize intrarenal hemodynamics. They also may decrease glomerular hypertrophy that occurs after renal ablation. In human trials, angiotensin-converting enzyme inhibitors decrease proteinuria by altering the glomerular capillary permeability. The effect of these agents on progressive disease may be influenced by how soon therapy is begun and how long it is continued.
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PMID:Use of angiotensin-converting enzyme inhibitors in chronic progressive renal disease. 202 23

We performed a retrospective chart analysis on 449 AIDS patients admitted to Bellevue Hospital Center from 1983-1986 to characterize the etiologies and clinical course of acute renal failure (ARF) and to define the incidence and clinical course of AIDS-associated nephropathy (AAN) in an unselected hospitalized AIDS population. Defining ARF as a rise from baseline serum creatinine of at least 2.0 mg%, we found 88 cases (a prevalence of almost 20%) or 14.5 cases per 100 admissions. Volume depletion was the most common etiology and was as severe a cause of ARF as other etiologies. There were 21 cases of ARF in 17 patients with a peak serum creatinine greater than or equal to 6.0 mg%. Volume depletion accounted for 7/21 of these cases. Baseline renal insufficiency existed in 9/17 patients (12/21 cases) and volume depletion was the cause of ARF in 3 of these cases. Only 4 cases required dialysis. There were 34 patients (prevalence of 7.6% or 3.0 cases per 100 patient-years) with otherwise unexplained chronic renal insufficiency and/or persistent qualitative or quantitative proteinuria and thus were defined on clinical grounds to have AIDS-associated nephropathy. Thirty-two of these patients (94%) had evidence of AAN at or within 1 year of presentation. Eleven patients (32%) reached ESRD (serum creatinine greater than or equal to 6.0 mg%); 9 patients did so within 1 year of presentation and 3 required dialysis. In those with adequate follow-up (9 cases), the mean survival from time of ESRD was 25.5 days and all cases died within 6 months of reaching ESRD.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Acute and chronic renal disease in hospitalized AIDS patients. 160 80

The authors deal with the clinicopathology of the renal, alterations in light-chain disease in connection with 6 cases. The disease was recognized by the monotype (in 5 cases kappa, in 1 case lambda) immunoreactivity of the light-chain paraprotein deposited in the basal membranes of the renal tissue. Electron microscopic examinations proved the fine-granulated, electrodense character of the paraprotein. Multiple myeloma was found in 3 cases and plasma cell dyscrasia of non-tumorous characteristic in 3 cases in the background of the deposition. The renal involvement appeared clinically in the picture of proteinuria without nephrosis syndrome and in progressing azotemia. Chronic renal insufficiency developed during some months in 5 patients. Morphologically renal impairment manifested in interstitial fibrosis, tubular atrophy and ateriolar hyalinosis was seen. These were associated with different glomerular alterations, for instance in 3 cases with nodular glomerulosclerosis. In 1 patient with plasma cell dyscrasia of non-tumorous characteristic nodular glomerulosclerosis and semilunar formation was observed in 56% of the glomeruli. In an other patient with myeloma the simultaneous existence of cylinder nephropathy and light-chain nephropathy was demonstrated. Both observations are unusual phenomena in plasma cell dyscrasia.
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PMID:[Light-chain nephropathy]. 211 26


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