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Biomedical subjects

M Praga

Publications and source records attributed to M Praga.

At least 19 recordsLinked to original sources
PubMed2001

Clinical features and long-term outcome of obesity-associated focal segmental glomerulosclerosis.

BACKGROUND: Several cases of obesity-associated focal segmental glomerulosclerosis (OB-FSG) have been reported but little is known about the clinico-pathological features of this entity and its long-term outcomes. METHODS: We studied 15 obese patients (BMI 35+/-5.2 kg/m(2)) with biopsy-proven FSG. They were compared with a control group of 15 non-obese patients with idiopathic FSG (I-FSG). RESULTS: Mean proteinuria at the time of renal biopsy was 3.1+/-2 g/24 h in OB-FSG; it reached the nephrotic range (> or =3.5 g/24 h) during follow-up in 12 patients (80%), but none of them had oedema, hypoproteinaemia, or hypoalbuminaemia. Proteinuria was more marked amongst I-FSG (6.5+/-4.2 g/24 h) and most of them developed oedema and biochemical nephrotic syndrome. Glomerulomegaly was observed in all renal biopsies from OB-FSG patients (mean glomerular diameter 256+/-24 microm in OB-FSG vs 199+/-26 microm in I-FSG, P<0.001). Twelve OB-FSG patients (80%) were treated with ACE inhibitors (ACEI) and proteinuria significantly decreased within the first 6 months of treatment but showed a later increase. None of the obese patients achieved a sustained weight loss. Seven (46%) patients with OB-FSG experienced a progressive renal insufficiency and five of them started intermittent dialysis. Kaplan-Meier estimated probabilities of renal survival after 5 and 10 years were 77 and 51%, respectively, in OB-FSG patients, and 52 and 30% in I-FSG (P<0.05). The risk of developing progressive renal failure among OB-FSG patients was statistically correlated with serum creatinine and creatinine clearance at presentation. CONCLUSIONS: OB-FSG indicates a poor prognosis with almost one-half of patients developing advanced renal failure. Knowledge of the clinico-pathological features of this entity (obesity, FSG lesions with glomerulomegaly, absence of nephrotic syndrome despite nephrotic-range proteinuria) should be helpful in establishing an accurate and early diagnosis.

Adult↗
PubMed2000

Double versus single renal allografts from aged donors.

BACKGROUND: The age limit of the cadaver kidney donors is increasing in response to the growing demand for renal transplantation. Simultaneous double kidney transplantation (SDKT) with kidneys obtained from elderly adults has been proposed to increase the transplantation number and improve its results. However, if SDKT is performed when there are no clear indications, a negative effect could be produced on the total number of transplanted patients as both kidneys would be used for only one recipient. MATERIAL AND METHODS: In December 1996 we designed a transplantation protocol to be able to extend the selection of cadaver kidney donors with normal serum creatinine levels without establishing any age limit. A pregraft renal biopsy was always performed to analyze the glomerulosclerosis (GE) percentage whenever the donors were 60 years of age or older. A SDKT was performed in a single recipient when the donor age was 75 years or older or when the donors between 60 and 74 years old had a GE rate of more than 15%. On the contrary, a single kidney transplantation was performed in two different recipients for kidneys from donors between 60 and 74 years of age with a GE rate of less than 15%. Kidneys having GE rates of more than 50% were discarded for transplantation. Donor kidneys from subjects younger than 60 years of age were always used for a single kidney transplantation. RESULTS: Based on the above mentioned protocol, from December 1996 to May 1998, 181 patients received a kidney transplantation in our hospital. These patients were divided into three groups: group I which included the SDKT recipients (n=21), group II or single kidney recipients from 60- to 74-year-old donors (n=40), and group III or recipients from <60-year-old donors (n=120). The mean follow-up time was 15+/-5 months (range 6-24). Mean donor age was 75+/-7 years in group I, this was significantly higher than in group II (67+/-4, P<0.001) and group III (37+/-15, P<0.001). The primary nonfunction rate was low in the three groups, there being no statistically significant differences (5, 5, and 4%, respectively). A significantly greater percentage of patients from group I (76%) presented immediate renal graft function as compared with group II (43%, P<0.01) and III (50%, P<0.05). The acute rejections rate was very low in all three groups (9.5, 7.5, and 22%, respectively) with significant differences between groups II and III (P<0.05). No significant differences between the different groups were observed for one year actuarial patient survival (100, 95, and 98%, respectively) or graft survival rates (95, 90, and 93%, respectively). The 6-month serum creatinine levels were excellent in the three groups, although there were significant differences between groups I and II (1.6+/-0.3 vs. 1.9+/-0.6 mg/dl, P<0.05), II and III (1.9+/-0.6 vs. 1.4+/-0.4 mg/dl, P<0.001), and I and III (P<0.05). CONCLUSIONS: Simultaneous double kidney transplantations make it possible to use kidneys from extremely elderly donors (>75 years) or those whose GE>15%. In addition, kidneys from donor 60-74 years old in which the GE<15% can be used for single kidney transplantations in two different recipients with excellent results.

Adult↗
PubMed2000

Secondary (AA-type) amyloidosis in patients with polymyalgia rheumatica.

Several cases of systemic amyloidosis associated with polymyalgia rheumatica (PMR) or giant-cell arteritis (GCA) have been described. Nevertheless, the type of amyloid deposit has not been characterized in most of them. Here we report on two patients with PMR (one with associated GCA) who developed nephrotic syndrome and end-stage renal failure caused by massive amyloid deposition. Immunohistochemical analysis showed that the amyloid deposits were of AA type (secondary amyloidosis) in both cases.

Aged↗
PubMed2000

Familial microscopic hematuria caused by hypercalciuria and hyperuricosuria.

We report 12 patients belonging to five different families in whom persistent isolated microhematuria was associated with hypercalciuria and/or hyperuricosuria. Four patients had episodes of gross hematuria, three patients had passed renal stones, and a history of nephrolithiasis was obtained in four of the families (80%). Calcium oxalate and uric acid crystals were commonly observed in the urine sediments. Urinary erythrocytes had a normal appearance on phase-microscopic examination. Reduction of calciuria and uricosuria by thiazide diuretics, allopurinol, forced fluid intake, and dietetic measures led to a persistent normalization of urine sediment with complete disappearance of hematuria. Determination of calcium and uric acid urinary excretions should be included in the study of familial hematuria.

Adolescent↗
PubMed2000

Influence of obesity on the appearance of proteinuria and renal insufficiency after unilateral nephrectomy.

BACKGROUND: Some patients develop proteinuria and progressive renal failure after unilateral nephrectomy, although the majority of patients maintain normal renal function. Reasons to explain this different evolution are not known. METHODS: A cross-sectional study was performed in 73 patients who had undergone unilateral nephrectomy 13.6 +/- 8.6 years before. Patients with morphologic abnormalities in the remaining kidney, systemic disorders, or abnormal renal function at the time of nephrectomy were excluded. All of the 73 included patients showed normal renal function and negative proteinuria at nephrectomy. The patient's medical records were reviewed, and clinical and analytical data throughout follow-up were obtained. RESULTS: Fifty-three out of the 73 patients (group I) showed a normal renal function and negative proteinuria at the cross-sectional study. The remaining 20 patients (group II) showed proteinuria (3.4 +/- 3.1 g/day). The time elapsed between nephrectomy and proteinuria appearance was 10.1 +/- 6.1 years. Thirteen patients of group II had developed renal insufficiency (serum creatinine at the cross-sectional study of 3.9 + 3.2 mg/dL) in addition to proteinuria. The time elapsed between proteinuria appearance and the onset of renal insufficiency was 4.1 +/- 4.3 years. Renal insufficiency showed a slowly progressive course in most of these patients. There were no significant differences between group I and group II patients in age, gender, renal function, or blood pressure at the time of nephrectomy. In contrast, group II patients showed a body mass index (BMI) that was significantly higher than group I at nephrectomy (31.6 +/- 5.6 vs. 24.3 +/- 3.7 kg/m(2), P < 0.001), at cross-sectional study (33.3 +/- 6.6 vs. 25.1 +/- 3.5 kg/m(2), P < 0.001), and throughout follow-up. Among the 14 obese (BMI > 30 kg/m(2)) patients at the time of nephrectomy, 13 (92%) developed proteinuria/renal insufficiency. In contrast, among the 59 patients with BMI < 30 kg/m(2), only 7 (12%) developed these complications (P < 0.001). Kaplan-Meier estimated probability of negative proteinuria and normal renal function 10 years after nephrectomy was 40 and 70%, respectively, in obese patients at nephrectomy. At 20 years after nephrectomy, these percentages were 8 and 35%, respectively. In contrast, in nonobese patients, the probability of negative proteinuria and normal renal function was 93 and 98%, respectively, at 10 years (P < 0.001) and 77 and 91%, respectively, at 20 years (P < 0.001). Multiple logistic regression analysis showed that the risk of developing renal disease was only statistically correlated with BMI at the time of unilateral nephrectomy (odds ratio 1.34, 1.03 to 1.76 CI). CONCLUSIONS: Obese patients are at risk for developing proteinuria and chronic renal failure after unilateral nephrectomy. Regular and long-term follow-up are recommended in these patients.

Acute Kidney Injury↗
PubMed1999

Paracellin-1, a renal tight junction protein required for paracellular Mg2+ resorption.

Epithelia permit selective and regulated flux from apical to basolateral surfaces by transcellular passage through cells or paracellular flux between cells. Tight junctions constitute the barrier to paracellular conductance; however, little is known about the specific molecules that mediate paracellular permeabilities. Renal magnesium ion (Mg2+) resorption occurs predominantly through a paracellular conductance in the thick ascending limb of Henle (TAL). Here, positional cloning has identified a human gene, paracellin-1 (PCLN-1), mutations in which cause renal Mg2+ wasting. PCLN-1 is located in tight junctions of the TAL and is related to the claudin family of tight junction proteins. These findings provide insight into Mg2+ homeostasis, demonstrate the role of a tight junction protein in human disease, and identify an essential component of a selective paracellular conductance.

Amino Acid Sequence↗