Search PubMed⌕ Search

Biomedical subjects

A Lupo

Publications and source records attributed to A Lupo.

At least 73 records · Page 4Linked to original sources

Hypertension in primary immunoglobulin A nephropathy (Berger's disease): hemodynamic alterations and mechanisms.

Twenty-two patients with primary IgA nephropathy (Berger's disease), 12 with normal and 10 with high blood pressure, were studied. The mean intra-arterial pressure was 88 +/- 6 mm Hg in the normotensive group and 113 +/- 10mm Hg in hypertensive patients; plasma renin activity was high in normotensives and normal in hypertensives. The glomerular filtration rate was 83 +/- 23 and 73 +/- 26 ml/m in 1.73 m2 in normotensive and hypertensive patients, respectively (p = n.s.). Blood volume was high in IgA nephropathy patients: 82 +/- 12 ml/kg body weight in normotensives and 96 +/- 7 ml/kg body weight in hypertensives. Mean arterial pressure was significantly correlated with blood volume (r = 0.541, p less than 0.01), but not with plasma renin activity and glomerular filtration rate. The cardiac index was high in both groups: 4.20 +/- 0.88 liters/min/m2 in normotensive and 3.95 +/- 0.87 liters/min/m2 in hypertensive patients. The total peripheral resistance index was significantly lower than normal in normotensives (1,659 +/- 387 dyn/s/cm-5/m2) and significantly higher (2,419 +/- 562 dyn/s/cm-5 m2) in hypertensives. The cardiac index did not correlate with blood volume and mean arterial pressure; a positive correlation was found between mean arterial pressure and peripheral vascular resistance (r = 0.630, p less than 0.01). No correlation was observed between blood volume and plasma renin activity. Our study indicates that hypertension in IgA nephropathy is primarily volume dependent, and that this increase in blood volume is not related to the deterioration of renal function. The role of the renin-angiotensin system in the maintenance of the hypertension is not well-defined.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Renal histological lesions and clinical syndromes in multiple myeloma. Renal Immunopathology Group.

This retrospective multicenter study, based on 42 patients affected by renal damage due to multiple myeloma, analyzes the renal biopsy results, the clinical data at the time of biopsy and the subsequent renal outcome in order to clarify the correlations existing between clinical and histological changes. Plasmocytoma components were Bence Jones alone in 55% of the patients and light-chain excretion was present in over 90%. Rapidly progressive renal failure was the most frequent clinical presentation (27 cases). The histological lesions directly attributable to multiple myeloma were subdivided into 3 basic categories: related to light-chains, direct tumor involvement of renal parenchyma and attributable to systemic effects of neoplastic disease. Light-chains seemed to cause renal lesions in 59.4% of the cases. Myeloma cast nephropathy was the prominent bioptic diagnosis established (20 cases). Among the clinical, laboratory and histological parameters studied, only the degree of tubular-interstitial damage was significantly correlated to the renal outcome in the 32 patients who had an adequately documented follow-up period.

Acute Kidney Injury↗

Prognostic factors and effectiveness of treatment in acute renal failure due to multiple myeloma: a review of 50 cases. Report of the Italien Renal Immunopathology Group.

We studied 50 patients with myeloma acute renal failure to investigate possible prognostic factors and to evaluate the effectiveness of the various treatment schedules used. Renal failure was reversible 1 month after the onset in 50% of the patients considered. The patients treated with chemotherapy and plasma exchange recovered renal function more frequently (61% of the cases) than those treated only with chemotherapy (27%). The most important clinical prognostic factors were total proteins, serum creatinine values and myeloma type. Considering the histological findings, the prognosis correlated with the severity of the lesions and number of tubular casts. Survival at 1 year was higher in the patients who regained renal function than in those in whom renal function did not improve.

Acute Kidney Injury↗

Clinical features of patients with solitary kidneys.

A clinical study was performed in 2 groups of patients with solitary kidneys, followed for 11-146 months. Group 1 had 9 patients (7 males and 2 females, aged between 23 and 68 years) with unilateral renal agenesis. Group 2 had 13 patients (9 females and 4 males, aged between 27 and 70 years) who underwent unilateral nephrectomy for the following reasons: hydronephrosis secondary to ureteropelvic junction stenosis, 7 patients; renal trauma, 4 patients; benign neoplasia, 2 patients. During the follow up, urinary protein excretion of more than 300 mg/day was observed in 9 patients, 3 in group 1 and 6 in group 2. Eleven patients, 8 in group 1 and 3 in group 2, were hypertensive (diastolic blood pressure higher than 95 mm Hg). Hyperuricemia was observed in 14 patients, 10 in group 1 and 4 in group 2. Seven patients, 4 in group 1 and 3 in group 2, had a significant deterioration of renal function. Neither proteinuria nor renal failure were observed before at least 10 years had elapsed since the anatomic condition of solitary kidney had been established. A surgical renal biopsy was performed in 1 patient with unilateral renal agenesis and showed focal glomerular sclerosis. This study adds support to the view that the reduction of 50% of the renal tissue may be a risky situation in humans as well as in animals.

Adult↗

Clinical status and acid-base balance during biofiltration in patients with acetate dialysis intolerance.

Nine patients intolerant to acetate hemodialysis were treated with biofiltration. This consisted in a 4-h acetate hemodialysis during which an additional 2 liters of ultrafiltrate were replaced by a bicarbonate solution (100 mEq/l). Hypotensive episodes disappeared and six out of nine patients were symptom-free during the session. Compared to standard hemodialysis, arterial blood bicarbonate and pO2 did not drop during biofiltration. The anion gap did not change during standard hemodialysis, but was significantly reduced during biofiltration (24.5 +/- 2.9 vs 19.9 +/- 1.4 mEq/l). In our conditions clinical results were positive with biofiltration. On the basis of anion gap changes and preliminary results of plasma acetate determinations, it is suggested that a better cellular metabolism of acetate may be induced by bicarbonate infusion.

Acetates↗

Effects of nadolol on systemic and renal hemodynamics in patients with renoparenchymal hypertension and various degrees of renal function.

It has been shown that renal hemodynamic changes following the decrease in cardiac output (CO) after therapy with beta-blockers may affect glomerular filtration rate (GFR), therefore limiting the effectiveness of these drugs; obviously more serious effects might be expected in nephropathic patients with previously reduced renal function. Recent clinical studies have demonstrated that nadolol, a non-cardioselective beta-blocker, preserves the renal blood flow (RBF) and the GFR. In this study, the drug was administered alone (80 mg once daily) for 2 months to 9 male renal parenchymal hypertensive patients with normal or moderately reduced renal function. Systemic and renal hemodynamics, plasma volume (PV), plasma renin activity (PRA) and urinary aldosterone excretion (UA) were evaluated before and after treatment. As blood pressure (BP) fell so did the cardiac index (4.27 +/- 1.05 l/min/m2 to 3.14 +/- 0.48 p less than 0.01), while the peripheral resistance index (TPRI) rose slightly (2257 +/- 658 to 2459 +/- 498 p = NS). No change in PV, RBF, GFR and renal vascular resistance was observed. An increasing trend in PRA (0.81 +/- 0.56 to 1.27 +/- 0.95 ng/ml/h) and no change in UA were observed. Our data show that nadolol was both well tolerated and effective in lowering BP, that it caused systemic hemodynamic alterations similar to those described for other beta-blockers, and preserved RBF and GFR also in renal hypertensive patients with reduced non-azotemic renal function.

Adult↗

Biofiltration in the treatment of patients with acetate dialysis intolerance.

Nine patients with intolerance to acetate hemodialysis were treated with biofiltration. It consisted of a 4 hour acetate hemodialysis during which an additional 2 liters of ultrafiltrate was replaced by a bicarbonate solution (100 mEq/l). Hypotensive episodes disappeared and six out of nine patients were symptomless during the session. Compared to standard hemodialysis, arterial blood bicarbonate and pO2 did not drop during biofiltration. Serum acetate levels, which were abnormally high in patients during standard hemodialysis, were reduced during biofiltration to the levels of a control group of acetate tolerant patients. Our data show that positive clinical results are obtained with biofiltration and suggest that they can be due to a better cellular metabolism of acetate induced by the bicarbonate infusion.

Acetates↗

Progression of renal failure in patients with renal disease of diverse etiology on protein-restricted diet.

The rate of progression of early renal failure was evaluated in three groups of adult patients with renal disease of diverse etiology on dietary protein and phosphorus restriction (about 0.6 g/kg of protein, 700 mg of phosphorus) and in a control group of 22 patients with the same renal disease, retrospectively studied, on a free diet. Group 1 had 33 patients with chronic glomerulonephritis (CG), initial serum creatinine (Scr) of 1.4 to 4.3 mg/dl (mean, 2.20), followed for 5 to 94 months (mean, 44). Group 2 had 17 patients with polycystic kidney disease (PKD), Scr 1.3 to 4.7 mg/dl (mean, 2.40), followed for 8 to 81 months (mean, 42). Group 3 had 28 patients with primary chronic pyelonephritis (CP), Scr of 1.5 to 4.5 mg/dl (mean, 2.57), followed for 9 to 92 months (mean, 41). The control group had 22 patients (11 with CG, five with PKD, and six with CP), with Scr 1.7 to 4.1 mg/dl, followed for 6 to 72 months (mean, 24). In the regression analysis between reciprocal creatinine and time, the slopes were -0.0017, -0.0025, and -0.00016 dl/mg/month in the three patient groups on a protein-restricted diet, respectively. The difference between both groups 1 and 2 and group 3 was statistically significant (P less than 0.05). The slopes in patients on a free diet were significantly greater than those found in patients on a protein-restricted diet. The actuarial survival probability at 72 months, assuming as "renal death" a Scr of 10 mg/dl, was 45% in patients with CG, 44% in those with PKD, and 67% in those with CP on a protein-restricted diet.(ABSTRACT TRUNCATED AT 250 WORDS)

Actuarial Analysis↗

Hypertension of polycystic kidney disease: mechanisms and hemodynamic alterations.

32 polycystic kidney disease (PKD) patients, 16 with normal 16 with variably decreased renal function, were studied; 12 were normotensive, 20 were hypertensive. Mean arterial pressure (MAP) was 90 +/- 8 mm Hg in the normotensive group and 117 +/- 17 in hypertensive patients; plasma renin activity (PRA) was similar. The glomerular filtration rate (GFR) was lower, but not significantly, in the hypertensive group and plasma volume (PV) was higher in hypertensive patients (normotensive 40.25 +/- 3.47 ml/kg body weight; hypertensive 46.30 +/- 3.54). No correlation was found between MAP, and PRA or GFR but MAP correlated with PV. Cardiac output was higher in hypertensive patients (normotensive 3.48 +/- 0.70 l/min/m2; hypertensive 3.89 +/- 1.47), also total peripheral resistance was higher in the hypertensive group (normotensive 2,035 +/- 503 dyn/s/cm-5/m2; hypertensive 2,577 +/- 808). Cardiac output and PV showed a high degree of correlation, but no correlation was seen between total peripheral resistance and PV, or PRA. The hypertensive patients were divided into two groups: one with hypertension of less than 2 years duration and one with more than 2 years but with similar GFR, PRA, PV and hemodynamic pattern. Our data indicate that hypertension in PKD is volume-dependent; that the increase in PV was not related to the loss of GFR, and that the role of the renin-angiotensin system in maintaining the hypertensive state is not well defined. Hemodynamically hypertension is characterized by high cardiac output and total peripheral resistance independent of the duration of hypertension.

Adult↗

Renal acidification defects in patients with recurrent calcium nephrolithiasis.

The frequency of renal tubular acidosis was evaluated in 28 adult patients with recurrent calcium nephrolithiasis (19 with 'renal' hypercalciuria, 9 with normocalciuria and no metabolic abnormality) and no evidence of obstruction or infection of the urinary tract. Eight patients with hypercalciuria (42%) had a defective renal reabsorption of bicarbonate, based on a fractional excretion of bicarbonate higher than 7% and a TmHCO3/GFR lower than 2.2 mEq/dl; 2 of them had an associated distal defect of acidification, as judged by a U-B pCO2 lower than 18 mm Hg in maximally alkaline urine. One patient with hypercalciuria had distal tubular acidosis, based on a urine pH higher than 5.3 during acidosis. Only 1 patient with normocalciuria had associated proximal and distal acidification defects. The remaining 8 patients displayed a normal renal acidifying capacity. The bicarbonate wastage was independent of serum PTH levels, vitamin D status and hypercalciuria and was associated with a defective tubular reabsorption of phosphate, increased random urinary pH and more active nephrolithiasis, with a prevalence of mixed calcium oxalate and phosphate stones. Our study shows a high incidence of defective tubular reabsorption of bicarbonate in patients with calcium nephrolithiasis and 'renal' hypercalciuria and suggests that the proximal acidification defect plays a pathogenetic role in promoting calcium nephrolithiasis.

Acidosis, Renal Tubular↗

Bone histology and calcium metabolism in patients with nephrotic syndrome and normal or reduced renal function.

Bone histology and its relationship with calcium metabolism was evaluated in adult patients with nephrotic syndrome: 29 had normal renal function (GFR 103 +/- 4 ml/min/1.73 m2) (group 1) and 20 had renal insufficiency (GFR 31 +/- 4 ml/min/1.73 m2) (group 2). In group 1, serum PTH, 1.25-HCC and 24.25-HCC levels were normal, while 25-HCC values were reduced. Bone histology was normal in 76% of the patients, while 17% had isolated osteomalacia and 7% an associated bone resorption. Group 2 showed a higher incidence of bone resorption when compared with a matched group of patients with renal failure and no proteinuria (40% vs. 13%) and a comparable frequency of isolated mineralization defect (25% vs. 34%). PTH levels were definitely increased and serum total calcium and all the vitamin D metabolites were reduced. A significant correlation between the apparent duration of the disease and the severity of osteodystrophy was found only in group 2. In conclusion, no constant derangement of calcium metabolism and bone histology is evident in patients with nephrotic syndrome and normal renal function, while patients with persistent proteinuria are at high risk of osteodystrophy even in the early phases of renal failure.

Adolescent↗

Carbohydrate metabolism in patients with nephrotic syndrome and normal renal function.

The effects of a standard oral glucose tolerance test (OGTT) on the serum concentrations of glucose, insulin, growth hormone (GH) and cortisol were evaluated in 38 adult patients with primary nephrotic syndrome and with normal renal function, and in 10 normal subjects. 14 patients had a diabetic-like response and 24 were not different from controls. In both groups of patients an increase in insulin pool secretion, probably due to elevated serum GH levels, was observed. The increased GH values were not related to serum albumin nor to urinary protein losses. No significant difference in serum cortisol values was observed in patients with nephrotic syndrome as compared to controls. There was no strict correlation between the various histologic lesions and the metabolic abnormalities. However, patients with a diabetic-like response to OGTT had a higher frequency of membranous glomerulopathy or focal glomerular sclerosis.

Adult↗

Early dietary protein and phosphorus restriction is effective in delaying progression of chronic renal failure.

A diet containing about 40 kcal/kg, 0.6 g/kg of protein, 700 mg of phosphorus, and 1,000 to 1,500 mg of calcium (orally supplemented) was prescribed to three groups of patients with chronic renal failure for 6 to 76 months. The mean serum creatinine values were 2.18 mg/dl in group 1 (25 patients), 4.24 mg/dl in group 2 (20 patients), and 6.10 mg/dl in group 3 (8 patients). An additional group of 30 patients (group 4) who had followed no specific dietary treatment for 3 to 72 months was taken as control. The plots of reciprocal serum creatinine against time gave slopes of -0.0008, -0.0010, and -0.0041 in the three groups of patients on the protein-restricted diet, and a slope of -0.020 in the patients on the free diet. The differences between the slopes in patients in groups 1, 2, and 3 versus that in patients in group 4 are statistically significant (analysis of variance and F ratio: P less than 0.01). During the follow-up period a decline in reciprocal serum creatinine greater than the mean values in the whole group was observed in 37.5% of patients in group 3, in 20% of those in group 2, and in only 12% of those in group 1. Thus, the degree of functional renal deterioration is critical in modulating the effects of dietary protein and phosphorus restriction. Several nonimmunologic factors, including hypertension, infection, electrolyte abnormalities, and low-calorie intake, appeared to play an important role in influencing the rate of progression of renal failure in patients on dietary protein restriction.

Adolescent↗

Effects of dietary protein and phosphorus restriction on the progression of early renal failure.

Three groups of patients with chronic renal failure were studied. Group 1 comprised 25 patients with a mean serum creatinine of 2.18 mg/dl and a mean arterial pressure of 117 mm Hg. Group 2 had 20 patients with a mean serum creatinine of 4.24 mg/dl and a mean arterial pressure of 119 mm Hg. All these patients were kept for 18 to 76 months on a diet containing about 40 kcal/kg, 0.6 g/kg of protein, 700 mg of phosphorus, and 1,000 to 1,500 mg of calcium (orally supplemented). Group 3 comprised 30 patients with a mean serum creatinine of 2.28 mg/dl and a mean arterial pressure of 116 mm Hg. They had followed no specific dietary regimen for 3 to 72 months, and their dietary calorie, protein, phosphorus, and calcium intakes averaged 35 kcal/kg, 70 g, 900 mg, and 800 mg, respectively. The plots of reciprocal creatinine against time gave slopes of -0.0008 and -0.0010 in patients in groups 1 and 2, and a slope of -0.020 in group 3 patients. The slopes of both groups 1 and 2 were statistically different (analysis of variance and "F" test, P less than 0.01) from that of group 3. No evidence of progressive protein and phosphorus depletion was observed in groups 1 and 2 patients. We conclude that a moderate dietary restriction of protein and phosphorus is an acceptable and effective regimen for delaying progression of functional deterioration in early renal failure.

Adolescent↗