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 protein/creatinine index (p/c) was determined in early morning urine (EMU) samples from available patients with Wilms' tumour who had had a nephrectomy and whose diagnosis had been made between January 1970 and December 1989. Clinical details were obtained by case note review. Results were obtained from 36 boys and 40 girls. The mean interval between nephrectomy and measurement of the EMUp/c was 9.0 years (2-23). Eleven patients had a EMUp/c greater than 20 mg/mmol (normal range less than 20). Of the 11 patients with proteinuria, there were in addition to nephrectomy other adverse features including bilateral tumours, treatment with nephrotoxic drugs, and dysplastic kidneys. Renal dysfunction seems most likely to occur where there are adverse factors in addition to unilateral nephrectomy. There was a significant correlation between the glomerular filtration rate and the EMUp/c, and it is thought that this is a simple tool which can be used for the regular monitoring of renal function in these patients.
Arch Dis Child 1992 Dec
PMID:Urinary protein/creatinine index in follow up of patients with Wilms' tumour after nephrectomy. 133 53

27 patients with hypertension and persistent proteinuria were investigated by renal biopsy. The 13 patients without structural glomerular abnormalities were younger and had less proteinuria than the other 14, but otherwise the two groups had similar clinical features. 6 of the 14 had diffuse glomerular abnormalities; the other 8 had segmental sclerosing lesions, which were mainly in the hilum of the glomeruli, as seen in states of glomerular overload. Glomeruli in all groups were larger than those in normotensive people. It is possible that hypertension causes glomerular enlargement, proteinuria, and segmental glomerular lesions because of loss of functioning glomeruli due to ischaemia.
Lancet 1992 Dec 12
PMID:Renal biopsy findings in hypertensive patients with proteinuria. 136 May 61

In the F1 hybrid of phenotypically normal NZW (H-2z) and systemic lupus erythematosus (SLE)-prone BXSB mice (H-2b), features of the disease became more severe than those seen in the BXSB mice, regardless of the presence or absence of the Yaa (Y-chromosome-linked autoimmune acceleration) mutant gene. To determine whether the gene(s) linked to the major histocompatibility complex (MHC) of NZW mice is involved in this event, we developed the H-2-congenic NZW.H-2d strain and compared the severity of autoimmune disease between (NZW x BXSB) F1 (H-2z/b) and (NZW.H-2d x BXSB) F1 mice (H-2d/b). The H-2z/b, but not H-2d/b, heterozygous F1 mice of both sexes showed an accelerated, higher incidence of proteinuria and a more severe thrombocytopenia than did the BXSB mice. In NZW x (NZW x BXSB) F1 backcross mice, the H-2z/b heterozygous progeny showed more severe disease than did the H-2z/z homozygotes. Thus, disease-accelerating events in (NZW x BXSB) F1 mice are linked to the H-2z/b heterozygosity. Because H-2d/z heterozygosity plays a crucial role for SLE in (NZB x NZW) F1 mice, in which SLE features differ from those in (NZW x BXSB) F1 mice, the present observations may imply that the different but related MHC heterozygosity acts as a predisposing genetic element in these different SLE syndromes.
Clin Immunol Immunopathol 1992 Dec
PMID:Heterozygosity of the major histocompatibility complex controls the autoimmune disease in (NZW x BXSB) F1 mice. 145 34

Low-protein diets supplemented with keto-analogues and essential amino acid (KA-EAA) mixtures or with EAA have been widely used to retard renal deterioration without affecting nutrition. These assumptions have recently been challenged in clinical studies and rest on little or no experimental data. The effects of EAA and KA-EAA supplementations have not been compared. We compared three groups of rats with subtotal nephrectomy that were fed (1) a 16% casein reference (R) diet, (2) a 6% casein plus EAA (A) diet, or (3) a 6% casein plus KA-EAA (K) diet with KA as amino acid salts. The three diets had the same energy and mineral contents, and they induced comparable growth. The two supplements had the same nitrogen content. The only difference found until month 3 was higher proteinuria and plasma urea levels in group R rats. Renal biopsies performed at month 3 showed more severe glomerular sclerosis and tubular changes in R rats than in A and K rats. From months 3 through 7, R rats developed higher plasma creatinine levels than did A and K rats (final median values: 167, 106, and 83 mumol/L; p < 0.04), had more proteinuria (232, 56, and 84 mg/day), and showed greater mortality rates. At the time the rats were killed, 2 R, 6 A, and 5 K rats had survived while receiving the diets. Examination of the remnant kidneys, regardless of time of death, showed that renal lesions were significantly worse in R than in A and K rats, with sclerosis affecting more than 50% of the glomeruli in 7 of 13 R, 4 of 14 A, and 4 of 15 K rats, and less than 25% glomeruli in 2 of 13 R, 10 of 14 A, and 10 of 15 K rats (A and K vs R: p < 0.03). In conclusion, restriction of nonessential amino acids compensated by EAA or by KA-EAA mixtures retards renal damage without affecting growth, but no real benefit of KA or EAA has been observed.
J Lab Clin Med 1992 Dec
PMID:Supplemented low-protein diets protect the rat kidney without causing undernutrition. 145 98

To test the effect of converting enzyme inhibition (CEI) on diabetes, with or without renal insufficiency, we studied streptozotocin-induced diabetic rats, with or without reduced renal mass, which were treated with insulin in sufficient amounts to maintain glucose values in the mild to moderately hyperglycemic range. We found that diabetes increased glomerular filtration rate (GFR) (inulin clearance, 2.3 +/- 0.5 ml/min vs 1.9 +/- 0.1 ml/min; p < 0.05) and blood pressure (137 +/- 15 mm Hg vs 116 +/- 6 mm Hg; p < 0.05) but did not increase plasma atrial natriuretic peptide (ANP) values, when compared with control rats (72 +/- 38 vs 68 +/- 24 pg/ml). CEI decreased GFR and blood pressure to control values. In rats with diabetes and concomitantly reduced renal mass, hypertension, elevated ANP values, proteinuria, and glomerulosclerosis were prominent features. CEI was associated with reduced blood pressure (172 +/- 17 mm Hg vs 138 +/- 15 mm Hg; p < 0.05), without a concomitant decrease in GFR (1.1 +/- 0.1 ml/min vs 1.1 +/- 0.1 ml/min). Further, CEI reduced the elevated ANP values (140 +/- 34 pg/ml vs 66 +/- 19 pg/ml; p < 0.05) to those of control rats. CEI reduced proteinuria by 50% and ameliorated the histopathologic changes. In separate experiments, rats with 5/6th nephrectomy and hypertension but without diabetes were also found to have elevated ANP levels that decreased to control values with CEI. The data speak for a renal protective effect of angiotensin I-converting enzyme inhibition in this model but do not support a specific role for ANP in the model of diabetes with concomitantly reduced renal mass.
J Lab Clin Med 1992 Dec
PMID:Effects of angiotensin-converting enzyme inhibition in diabetic rats with reduced renal function. 145 98

Two types of lupus mice, NZB/NZW F1 female hybrids and mice with graft-versus-host disease (GVHD), were studied. Histones H3 and H2A were detected by immunofluorescence in glomeruli of 22/22 proteinuric GVHD and 8/12 proteinuric NZB/W F1 female mice; in non-proteinuric animals, 3/5 GVHD and 2/27 NZB/W F1 female were positive. Using antibodies to histone peptides it was shown that mainly the N-terminal regions of histones H3 and H2A were exposed in glomerular deposits. Western blot analysis revealed antibodies to histone subfractions in sera of 33/34 lupus mice that developed proteinuria. This study provides evidence that histones are involved in the pathogenesis of lupus nephritis.
Clin Exp Immunol 1992 Dec
PMID:Glomerular immune deposits in murine lupus models may contain histones. 145 82

Angiotensin-converting enzyme (ACE) inhibitors decrease albuminuria in patients with diabetic nephropathy. To study the change in albuminuria in relation to changes in systemic and renal hemodynamics, nine normotensive patients with type 1 (insulin-dependent) diabetes mellitus and persistent proteinuria were given a single oral dose of 25 mg of the ACE inhibitor captopril. Blood pressure, glomerular filtration rate (GFR), effective renal plasma flow (ERPF), and albumin excretion rate (AER) were measured in two periods of 40 minutes before and in four periods of 40 minutes after administration of captopril. A constant water diuresis was maintained. Blood pressure did not decrease significantly (130/79 +/- 4/3 v 124/74 +/- 4/3 mm Hg; mean +/- SEM), median AER decreased from 403 (interquartile range [IQR], 812) micrograms/min to 333 (707) micrograms/min (P < 0.01). GFR did not change (123 +/- 13 v 117 +/- 14 mL/min), but ERPF increased significantly from 609 +/- 56 to 714 +/- 55 mL/min (P < 0.01). Consequently, the filtration fraction (FF; quotient of GFR and ERPF) decreased from 0.20 +/- 0.014 to 0.17 +/- 0.014 (P < 0.01). A strong correlation was found between the decrease of AER and the decrease of FF (rs = 0.75; P < 0.02). No correlation was found between the decrease in AER and changes in GFR or blood pressure. In the normotensive patient with diabetic nephropathy, captopril causes an acute reduction of AER, which is probably mediated by a lowering of the intraglomerular pressure.
Am J Kidney Dis 1992 Dec
PMID:Captopril acutely lowers albuminuria in normotensive patients with diabetic nephropathy. 146 82

Iron, which has been shown to accumulate within proximal tubule lysosomes in proteinuric models of renal disease, may play a role in the progression of chronic renal disease by the generation of reactive oxygen species. Therefore, renal biopsies from humans with proteinuria and/or chronic renal failure were examined at an ultrastructural level for iron by energy dispersive analysis and compared with normal biopsies. Iron accumulated in proximal tubular lysosomes in renal disease (P < 0.05 v normals), accompanied in some cases by phosphorus and silicon. Both the number of iron-containing lysosomes per tubular cross-section (1.86 +/- 0.41 v 0.66 +/- 0.22, P < 0.05) and the mean concentration of lysosomal iron (254.5 +/- 73.4 mg/dL v 81.2 +/- 23.8, P < 0.001) was greater in patients with nephrotic syndrome (n = 12) than in those without (n = 8). Iron accumulation (number of iron-containing lysosomes/tubule) correlated with protein excretion (r = 0.68, P = 0.003, n = 20), but not with glomerular filtration rate. Damaged tubules contained greater amounts of iron than tubules with less damage (288.5 +/- 68.5 mg/dL v 80.4 +/- 13.9, P < 0.01). Further studies are needed to define the possible role of iron in causing tubular damage and progression of renal disease.
Am J Kidney Dis 1992 Dec
PMID:Iron accumulation in human chronic renal disease. 146 86

We investigated the value of cytodiagnostic urinalysis in detecting and scoring the severity of the four types of renal lesions (glomerular, interstitial, tubular, and vascular). Both cytodiagnostic urinalysis and concurrent renal biopsy were performed in 77 patients (47 from native kidneys and 30 from transplants) and the scoring and findings assessed in a double-blinded fashion. Evaluation of the reproducibility for the counting of renal cells showed a low intraobserver and interobserver variation. Cytodiagnostic urinalysis correlated with the renal biopsy with respect to primary lesions in 42 (89%) of the native kidney cases, and in 23 (77%) of the transplant kidney cases. The accuracy of diagnosis of glomerular lesions in both native and transplanted kidneys was 0.91, and for acute rejection in transplanted kidneys, the accuracy of diagnosis was 0.73. Severity scores showed good correlation between cytodiagnostic urinalysis and renal biopsy in both transplanted and in native kidneys and cytodiagnostic urinalysis correlated well with the increase in creatinine levels. The most important components of cytodiagnostic urinalysis for the diagnosis of glomerular lesions were dysmorphic erythrocytes and proteinuria. The specificity and sensitivity of dysmorphic erythrocytes for a glomerular lesion were 0.89 and 0.88, respectively. In cases with biopsy-proven glomerular lesions, more severe changes were found by cytodiagnostic urinalysis when the biopsy showed proliferative lesions in the glomeruli than when normal glomeruli were found by light microscopy. Cytodiagnostic urinalysis has the advantage over renal biopsy that it can be repeated as often as necessary and thus allows observation of the development or regression of the renal lesion over time. We conclude that cytodiagnostic urinalysis is well correlated with the renal biopsy and that it provides valuable and quantitative information regarding the disease process in the kidney.
Am J Kidney Dis 1992 Dec
PMID:Analysis of cytodiagnostic urinalysis findings in 77 patients with concurrent renal biopsies. 146 92

In a population-based study in Taiwan, 11,478 subjects aged 40 years or older were screened for diabetes in one urban and five rural areas. Among the 715 subjects proven to have diabetes, 527 subjects underwent ophthalmoscopy. Diabetic retinopathy was present in 184 of the 527 subjects (35.0%), including background diabetic retinopathy in 157 subjects (30.0%), preproliferative diabetic retinopathy in 15 subjects (2.8%), and proliferative diabetic retinopathy in 12 subjects (2.2%). Diabetic retinopathy was correlated with the duration of diabetes and age at onset of diabetes, type of diabetes treatment, higher serum creatinine levels, and lower serum cholesterol levels. Several other factors, including gender, age, residential area, family income, educational level, control and family history of diabetes, body mass index, physical activity, exercise, cigarette smoking, stroke, ischemic heart disease, leg vessel disease, hypertension, and proteinuria, had no significant association with retinopathy. By multiple logistic regression analysis, duration of diabetes was the most important risk factor related to retinopathy. Diabetic subjects treated with insulin had a higher risk of developing retinopathy than those treated with dietary control (relative risk, 1.57; .05 < P < .10). The univariate analysis disclosed that proliferative diabetic retinopathy was related to older age at examination, older age at onset of diabetes, type of diabetes treatment, and presence of leg vessel disease. Insulin-treated diabetic subjects also had a higher risk of proliferative diabetic retinopathy than patients in whom diabetes was controlled by diet, with a relative risk of 2.51 (.05 < P < .10) in the multiple logistic regression analysis.
Am J Ophthalmol 1992 Dec 15
PMID:Prevalence and risk factors of diabetic retinopathy among noninsulin-dependent diabetic subjects. 146 42


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