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Biomedical subjects

M Praga

Publications and source records attributed to M Praga.

At least 55 records · Page 3Linked to original sources
PubMed1999

Absence of hypoalbuminemia despite massive proteinuria in focal segmental glomerulosclerosis secondary to hyperfiltration.

We observed that some patients do not develop hypoalbuminemia despite the presence of massive proteinuria. To investigate whether the absence or presence of hypoalbuminemia could be a marker in the distinction between idiopathic focal segmental glomerulosclerosis (FSG) and FSG secondary to hyperfiltration, we reviewed all our patients with biopsy-proven FSG and persistent nephrotic-range proteinuria (>3.5 g/24 h). Patients who met these conditions were then separated into those with hypoalbuminemia (serum albumin level <3 g/dL; group I; n = 19) and those with normoalbuminemia (>3.5 g/24 h; group II; n = 18). All group I patients had nephrotic edema in contrast with the absence of edema in all group II patients. Serum cholesterol and triglyceride levels were significantly greater in group I. All group I patients had been diagnosed with idiopathic FSG. The diagnoses of group II patients were FSG secondary to massive obesity in eight patients (44%), vesicoureteral reflux in five patients (27%), and renal mass reduction in three patients (16%); only two patients (11%) in this group had idiopathic FSG. The case histories of 19 other patients with nephrotic-range proteinuria associated with hyperfiltering disorders (reflux nephropathy, massive obesity, renal mass reduction), but without renal biopsy, were also reviewed; despite massive proteinuria (5.8 +/- 3.1 g/24 h), serum albumin and total protein levels were always within normal values. In conclusion, patients with FSG secondary to hyperfiltration do not develop hypoalbuminemia or the other characteristic complications of nephrotic syndrome, despite the presence of massive proteinuria values.

Adult↗
PubMed1998

Association of thin basement membrane nephropathy with hypercalciuria, hyperuricosuria and nephrolithiasis.

BACKGROUND: Familial persistent microhematuria with normal renal function is the most common presentation of thin basement membrane nephropathy (TBMN). Gross hematuria episodes and loin pain attacks are other manifestations of the disease. On the other hand, it has been shown that hypercalciuria (HC) and hyperuricosuria (HU) can produce both gross or microscopic non-glomerular hematuria, in addition to their role in renal stone formation. METHODS: We studied the prevalence of HC, HU and nephrolithiasis in a group of 27 biopsy-proven TBMN as well as in 19 non-biopsied first-degree relatives with persistent microhematuria and 25 first-degree relatives without microhematuria. A group of 27 patients with IgA nephropathy (IgAN) and persistent microhematuria, and another group of 20 healthy subjects without known renal diseases were selected as control groups. RESULTS: Ten (37%) patients with TBMN and 8 (42%) relatives with microhematuria showed HC and/or HU at presentation; relatives without microhematuria, IgAN patients and normal controls showed a significantly lower prevalence of HC and HU. The prevalence of previous nephrolithiasis among TBMN patients (25%) was significantly higher than in IgAN patients (3%; P < 0.05). Family history of nephrolithiasis was recorded in 14 (51%) of the 27 TBMN families, in contrast with 2 of 27 (7%) with IgAN and 1 of 20 (5%) in normal controls (P < 0.05). The prevalence of nephrolithiasis, gross hematuria bouts and loin pain episodes among TBMN patients and microhematuric relatives showing HC and/or HU at presentation (44%, 44% and 27%, respectively) were significantly higher than those of TBMN patients and microhematuric relatives with normal calcium and uric acid urinary excretions (10%, 7% and 3%, respectively; P < 0.05). At the end of follow-up (8.8+/-4.1 years in TBMN patients and 9.1+/-4.2 years in relatives with microhematuria), all the cases maintained normal renal function. CONCLUSIONS: We found a high prevalence of HC, HU, and nephrolithiasis among TBMN patients and relatives with microhematuria. Our study also shows a significant relationship between the presence of HC and/or HU and the prevalence of nephrolithiasis, gross hematuria bouts and loin pain episodes.

Adolescent↗
PubMed1997

Membranous glomerulonephritis associated with hepatitis C virus infection in renal transplant patients.

BACKGROUND: Hepatitis C virus (HCV) infection has been described in association with various types of glomerular diseases, usually type I membranoproliferative glomerulonephritis and rarely membranous glomerulonephritis (MGN). In this article, we describe the first series of MGN exhibited in renal transplant patients and associated with HCV infection. METHODS: From January 1980 to December 1994, 2045 kidney transplantations were performed in our renal transplant units. A retrospective analysis demonstrated an overall 20% prevalence of HCV virus-positive patients; 409 transplanted patients were HCV positive (ELISA and RIBA). RESULTS: Fifteen patients developed an allograft MGN (3.66%) 24 months after renal transplantation. MGN appeared in the form of significant proteinuria (>1.5 g/24 h) with stable renal function. In all cases, graft biopsy demonstrated a thickening of the capillary wall, subepithelial electron-dense deposits, and IgG and C3 diffuse granular deposits along the basal membrane. Ten cases were considered de novo, two cases were considered recurrent MGN, and three cases were considered undetermined because the primary renal disease was chronic glomerulonephritis. All patients showed negative antinuclear antibodies and cryoglobulins, normal complement, and negative rheumatoid factors. During follow-up (an average of 2 years), 12 patients developed a progressive worsening of renal function, with increased serum creatinine and persistent proteinuria; 8 of the 12 patients returned to dialysis. Of the remaining three cases, two patients showed partial remission of nephrotic syndrome after high doses of steroids, and one patient persisted with stable renal function and proteinuria (<2 g/24 h.). CONCLUSIONS: In summary, HCV is preferentially associated with MGN in renal transplant patients, rather than with membranoproliferative glomerulonephritis as in the normal adult population. MGN associated with HCV infection has a similar clinical picture and outcome to posttransplant idiopathic de novo MGN, with persistent massive proteinuria and progressive deterioration of renal function.

Adult↗
PubMed1997

Elevation of von Willebrand factor levels in patients with IgA nephropathy: effect of ACE inhibition.

The von Willebrand factor (vWF) has been used as a marker of endothelial dysfunction in several diseases. We measured plasma vWF in patients with immunoglobulin A nephropathy (IgAN). In a group of 10 IgAN patients with normal renal function, normal blood pressure, and no proteinuria, vWF plasma levels were significantly higher than in a group of 21 healthy volunteers (134% +/- 38% v 80% +/- 22%; P < 0.01). In another group of 16 IgAN patients with normal renal function and proteinuria ranging between 0.3 and 3.8 g/d, vWF levels were also significantly higher than in the control group (148% +/- 63% v 80% +/- 22%; P < 0.001). Afterward, we studied the effects of enalapril administered for 4 weeks on vWF levels and proteinuria in a group of 11 IgAN patients with normal renal function and proteinuria > or = 1 g/d. After 2 weeks on enalapril treatment, both vWF levels and proteinuria had significantly decreased (vWF: 158% +/- 122% to 117% +/- 72%, P < 0.05; proteinuria: 1.6 +/- 0.7 g/d to 0.9 +/- 0.4 g/ d, P < 0.05). After enalapril withdrawal, both vWF and proteinuria significantly increased. A significant correlation between the variations in vWF levels and proteinuria was observed (r = 0.6; P < 0.05). No correlations between blood pressure and changes in vWF or proteinuria were found. We conclude that endothelial dysfunction is observed in patients with IgAN. This abnormality is already present in some patients with normal blood pressure, normal renal function, and absence of proteinuria. Angiotensin-converting enzyme inhibition induced a significant decrease in both vWF levels and proteinuria.

Adult↗
PubMed1997

Antiproteinuric effect of angiotensin-converting enzyme inhibition and C5b-9 urinary excretion in membranous glomerulonephritis.

BACKGROUND: Angiotensin-converting enzyme (ACE) inhibitors have an antiproteinuric effect in membranous glomerulonephritis (MGN). However, no studies have investigated whether this antiproteinuric effect is influenced by urinary C5b-9 excretion, a marker of immunological activity in this disease. METHODS: Eleven patients with biopsy-proven MGN were treated with captopril for 8 weeks. The evolution of several clinical and biochemical parameters, including 24-h urinary protein excretion was evaluated every 4 weeks. Urinary C5b-9 excretion was measured at the onset and at the end of captopril treatment. RESULTS: Patients with MGN had significantly higher C5b-9 excretions than a group of 14 healthy controls (89 +/- 23 vs 3.7 +/- 1.4 ng/mg UCr; P < 0.001). A significant correlation was found between urinary C5b-9 and the magnitude of proteinuria, both at the onset and at the end of treatment. After 8 weeks of captopril treatment, proteinuria had decreased from 8 +/- 1.8 to 5.2 +/- 1.3 g/day (P < 0.05). Four weeks after captopril discontinuation, proteinuria rose to 7.3 +/- 1.7 g/day (P < 0.05). A marked variability in the antiproteinuric response was observed, ranging from 0 to 85% with respect to baseline values. No correlation between decrease in proteinuria and baseline urinary C5b-9 levels was observed. Several patients with elevated urinary C5b-9 levels had captopril-induced decrease in proteinuria. CONCLUSIONS: ACE inhibition induces an antiproteinuric effect in patients with MGN. The urinary C5b-9 excretion does not predict the magnitude of this response.

Adult↗
PubMed1997

L-arginine reverses the antinatriuretic effect of cyclosporin in renal transplant patients.

BACKGROUND: Cyclosporin has been shown to facilitate renal vasoconstriction and to have an antinatriuretic effect. The existence of an interference of cyclosporin with the vasodilating properties of endothelium mediated by nitric oxide production could mediate these effects. On the other hand, the infusion of the nitric oxide precursor L-arginine has been shown to induce renal vasodilatation and to facilitate natriuresis in normal volunteers. We have investigated the renal effects of the administration of an infusion of L-arginine in renal transplant patients chronically treated with cyclosporin. To facilitate the analysis of the data the effects of the administration of a similar dose of cyclosporin on renal function during the infusion of a vehicle were also investigated during the administration of a vehicle of L-arginine. DESIGN: Ten male renal transplant patients, chronically treated with cyclosporin and with a stable renal function were studied during 2 consecutive days after the administration of the usual morning dose of cyclosporin. The first day they received an intravenous infusion of vehicle and the second the infusion of graded doses of L-arginine (50, 100, 150 mg/kg/h) during 3 consecutive h. RESULTS: The first day, after cyclosporin administration a significant fall (P < 0.01) was observed in natriuresis and kaliuresis in the absence of changes in renal plasma flow and glomerular filtration rate. After the administration of L-arginine significant (P < 0.01) increases of renal plasma flow, glomerular filtration rate, and natriuresis were seen. The increase in blood levels of cyclosporin after its administration did not differ between days 1 and 2. CONCLUSION: These results indicate that L-arginine facilitates renal vasodilatation and natriuresis in renal transplant patients. Furthermore, the observed increase in sodium excretion could indicate that L-arginine counteracts the antinatriuretic effect of cyclosporin.

Adult↗
PubMed1996

Lipoprotein(a) and vascular access survival in patients on chronic hemodialysis.

Lipoprotein(a) [Lp(a)] is an independent risk factor for atherosclerotic and cardiovascular complications in the general population and in hemodialysis patients. Increased Lp(a) levels have been also described as a possible predictor of vascular access occlusion in patients on chronic hemodialysis. We have studied prospectively the relationship between vascular access survival and Lp(a) levels in 40 hemodialysis patients. The Lp(a) plasma concentrations were measured by enzyme-linked immunosorbent assay in all patients in April 1993. Throughout the following year, evolution and survival of their vascular accesses were analyzed. Failure of vascular access was established when there were complications requiring surgical repair or transluminal angioplasty. Fourteen patients showed failure of vascular access, and the cumulative survival of vascular accesses after 1 year of follow-up was 63.8%. The Lp(a) levels were higher in patients with failure of vascular access than in the others (35.2 +/- 31 vs. 22.4 +/- 25 md/dl), but this difference did not reach statistical significance (p = 0.064). The vascular access survival in patients with Lp(a) levels > 75th percentile (52.5 mg/dl) was significantly lower than in the remaining patients (40 vs. 72%; p = 0.045). This difference increased when we analyzed the patients with Lp(a) levels > 90th percentile (76 md/dl; 25 vs. 68%; p = 0.002). Our results suggest that patients with the highest levels of Lp(a) are at risk of developing complications in their vascular accesses, and they also have lower vascular access survival.

Adult↗
PubMed1996

Cyclosporine nephrotoxicity and rejection crisis: diagnosis by urinary enzyme excretion.

The urinary enzymes alanine aminopeptidase (AAP; EC 3.4.11.2) and N-acetyl-B-D-glucosaminidase (NAG; EC 3.2.1.30) were measured daily in 35 renal transplant recipients during the early postoperative period. Each peak value of fractional excretion was corrected for its baseline value (CFE). CFE values above normal for both NAG and AAP were more frequently found in episodes of acute rejection than in cyclosporine acute nephrotoxicity episodes (76 vs. 0%; p < 0.001). Consequently, a rise in CFE levels for both NAG and AAP is strongly suggestive of acute rejection crisis.

Acetylglucosaminidase↗