Protocol biopsy program after renal transplantation: structure and first results.
Explore the source record for details and available documents.
SEARCH · PubMed Health
Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
BACKGROUND: The goal of the current study was to examine the potential value of p16(INK4a) and p27(Kip1) cyclin-dependent kinase inhibitor (CDKI) genes in the process of human kidney aging in vivo, and in the development of chronic allograft nephropathy (CAN). METHODS: Expression of p16(INK4a) and p27(Kip1) CDKI genes was evaluated and compared in 20 normal human kidney tissues of different ages (range, 21 to 80 years) and in 9 chronically rejected kidney grafts. Age dependency of marker expression was analyzed by the Pearson correlation and linear regression. RESULTS: Expression of p16 in cortical tubular (CTS) and interstitial (CIS) cells of normal kidney was age dependent (correlation coefficients: 0.608 and 0.726, 95% confidence interval [CI]: 0.227 to 0.828 and 0.417 to 0.884, respectively). Cortical tubular expression of p27 was also correlated with increasing age (0.672, 95% CI: 0.327 to 0.859). Linear regression analyses confirmed the linearity of marker relationship with age (coefficient of determination R(2):0.370, 0.452, and 0.527 for CIS p16, CTS p27, and CTS p16, respectively). The mean chronological and predicted graft ages (53 +/- 21 and 76 +/- 8.9 years, respectively) were significantly different (P = 0.0126). The glomeruli, tubules, and interstitial cells of rejected grafts expressed significantly higher levels of p16 and p27 than normal kidneys. Expression of p16 in glomerular and cortical interstitial cells was higher in grade 3 of CAN than in grade 2 (P = 0.013 and 0.004, respectively). CONCLUSION: The results of the current study show that expression of p16(INK4a) and p27(Kip1) CDKI genes is increased in cortical cells of the aging human kidney and in chronic allograft rejection, supporting the senescence theory of CAN.
Three groups consisting of 12 subjects each (continuous ambulatory peritoneal dialysis [CAPD] patients, hemodialysis patients, and healthy controls) matched for age, sex, and body weight were invited to a test meal for the study of hunger, fullness, and food preferences. They were served an excess portion of hash served on a plate placed on a hidden scale ("VIKTOR"), which was connected to a computer registering the eating process on-line. The patients filled in visual analogue scales (VAS) concerning appetite and food preferences before and after the test meal. Mean total intake of food (+/- SD) was significantly higher for healthy controls (357 +/- 175 g) compared with hemodialysis patients (295 +/- 105 g), which in turn was higher than in CAPD patients (206 +/- 70 g). Eating velocity was lower in both dialysis groups compared with controls. CAPD patients experienced less hunger and desire to eat compared with hemodialysis patients and controls. The reason for the low eating drive in CAPD patients despite their great need for protein and calories is unknown, but might be explained by gastric retention, insufficient dialysis, metabolic effects of the high sugar load from the dialysate, or combinations of these factors.
Peritonitis is the most important complication of continuous ambulatory peritoneal dialysis (CAPD). We reviewed our experience with peritonitis over a 2 1/2-year period. Our patients spent 4% of their total time on dialysis in hospital due to peritonitis. Thirty-eight percent of the episodes of peritonitis were treated without hospitalization. We evaluated the dialysate bag change technique as commonly performed with currently available devices (extension tubing and titanium Luerlock Tenckhoff catheter adapter). The aseptic techniques described for dialysis extension tubing changes appear adequate (with no increased incidence of peritonitis demonstrated shortly after an extension tubing set change). Long-term sterility is maintained at the dialysate bag puncture port and at the orifice of the dialysis catheter adapter (no positive cultures from the bag port and orifice of the titanium adapter). Etiologic diagnosis of uremia was not a risk factor predisposing to peritonitis. The incidence of peritonitis was greater among patients with less formal education and lower income. Out data suggest that patients with less formal education and of lower economic status be carefully evaluated before commencing CAPD.
Experimental and clinical evidence are summarized that support the hypothesis that enhanced transmission of systemic hypertension to the adapted glomerulus in the setting of reduced nephron mass may be responsible for accelerated vascular and glomerular damage in the hypertensive stage of parenchymal renal disease in man. In experimental models of hypertension associated with reduced renal mass, the kidney appears to be damaged directly by transmission of pressure rather than primarily through vasoconstriction and ischemia. When hypertension is combined with models of glomerular disease, vascular and glomerular injury are aggravated. It is proposed that adaptive glomerular hemodynamic alterations which occur in parenchymal renal disease magnify the transmission of increased pressure and flows when hypertension supervenes. Accelerated vascular and glomerular damage and functional deterioration result. According to this hypothesis, control of systemic hypertension and minimization of hydraulic stress on the diseased glomerulus become critical to the management of chronic renal disease and the prevention of progressive renal insufficiency.
Many chronic renal diseases lead to the final common state of decrease in renal size, parenchymal atrophy, sclerosis and fibrosis. The ultrasound image show a smaller kidney, thinning of the parenchyma and its hyperechogenicity (reflecting sclerosis and fibrosis). The frequency of renal cysts increases with the progression of the disease. Ultrasound generally does not allow for the exact diagnosis of an underlying chronic disease (renal biopsy is usually required), but it can help to determine an irreversible disease, assess prognosis and avoid unnecessary diagnostic or therapeutic procedures. The main exception in which the ultrasound image does not show a smaller kidney with parenchymal atrophy is diabetic nephropathy, the leading cause of chronic and end-stage renal failure in developed countries in recent years. In this case, both renal size and parenchymal thickness are preserved until end-stage renal failure. Doppler study of intrarenal vessels can provide additional information about microvascular and parenchymal lesions, which is helpful in deciding for or against therapeutic intervention and timely planning for optimal renal replacement therapy option.
Arterial hypertension is the most common chronic medical condition requiring office visits to physicians and is a major contributing factor to the development of myocardial infarction and stroke. Its importance as a cardiovascular risk factor is at least as significant in women as in men; however, the ever-growing literature on hypertension shows surprisingly little data concerning sex differences. Large clinical trials of antihypertensive treatment have not clearly demonstrated gender differences in blood pressure response and outcome, but the majority of patients in these trials were men. Even so, some evidence indicates that white women treated for hypertension obtain less benefit than men. The pathophysiology of hypertension in men and women is similar in many aspects, but important gender differences are now emerging. Studies designed to clarify these differences are required, as a better knowledge of the underlying mechanisms will allow for a more precise stratification of risk and a more accurate approach to both nonpharmacologic and pharmacologic treatment.
The D allele of the angiotensin-converting enzyme (ACE) gene has been linked with diabetic nephropathy and IgA glomerulonephritis and with faster renal disease progression. The association of this allele with nephroangiosclerosis has been scarcely investigated. We have tested this association in 45 hypertensive patients (all whites) with well defined nephroangiosclerosis (diagnosis established on the basis of renal biopsy in all cases) and moderate to severe renal failure. As studies of genetic association of small size often produce conflicting results, besides a control group of 343 Italian patients with essential hypertension and normal renal function, we elected to use also a very large control group of race-matched subjects taken from a meta-analysis of 27,565 whites. The proportion of patients with the D allele (64%) was higher in patients with nephroangiosclerosis than that in Italian hypertensives (54%) and in whites (54%). DD and DI genotypes were more prevalent in patients than in control groups. The dominant model (DD and DI v II: nephroangiosclerosis v Italian controls: chi2 = 6.19, P = .012; nephroangiosclerosis v whites chi2 = 6.86, P = .009) fitted the data better than the codominant and the recessive model (P < or = .022). The D allele is associated with nephroangiosclerosis with a dominant effect in the sample of patients studied. Although intervention studies are needed to see whether these findings imply a causal association, our data suggest that this allele may at least act as disease marker in nephroangiosclerosis.
The aim of this study was to assess the grade of heterogeneous disturbance in the renal cortical circulation using dynamic computed tomography and to investigate the relationship between the heterogeneity of renal cortical circulation and hypertension. We studied 125 patients who underwent dynamic computed tomography (CT) for various abdominal diseases and had no serious hemodynamic abnormalities. In dynamic computed tomography under appropriate conditions, each pixel (image element), less than 1 mm2, has a CT number that is in proportion to the concentration of contrast media, which reflects the blood volume in the pixel. The image was constructed at the hilus level about 50 s after the start of a continuous infusion of contrast medium. The mean and standard deviation were calculated from the CT numbers in the renal cortex. The coefficient of variation, ie, the standard deviation divided by the mean value, was used as the index of the heterogeneity of renal cortical circulation. The coefficient of variation was significantly (P < .001) greater in the hypertensive patients (n = 48, 0.174 +/- 0.006 [mean +/- SE]) than in normotensive subjects (n = 77, 0.140 +/- 0.004). The coefficient increased in parallel with the patient's age and with the grade of renal surface irregularity. In the patients whose serum creatinine levels were normal, this parameter also had a significant relationship (r = 0.367, P < .0001) with serum creatinine. These results suggest that the heterogeneity of renal cortical circulation is increased in hypertension and is also associated with aging. This parameter may become a sensitive indicator to detect slight deterioration in the renal cortical circulation.
Explore the source record for details and available documents.
The effects of oral sulindac on renal hemodynamics were studied in normal subjects, elderly persons with mild renal failure, and patients with chronic renal disease. Renal function was measured before dosing and 24 hours and 28 days after oral sulindac. Effective renal plasma flow was reduced in all subjects after 24 hours. Effective renal plasma flow and the glomerular filtration rate were not altered after 28 days in control subjects, whereas effective renal plasma flow, but not glomerular filtration rate, was lower after 1 month in subjects with renal disease. None of these changes are likely to be of major clinical significance.
Explore the source record for details and available documents.
Renal biopsy specimens of 16 adult patients with nephrotic syndrome and focal glomerular sclerosis were examined by light and electron microscopy. Particular attention was paid to alterations of podocytes. Except for loss of foot processes, five patients had no podocyte changes, five had mild changes and six had severe changes. Of the last group (group III), four patients were heroin addicts, the fifth had infectious mononucleosis and the sixth, an apparent idiopathic disease; five patients were males, 16 to 25 yr old. Podocyte changes consisted of cytoplasmic degeneration, detachment of epithelial cells from basement membranes, with filling of resulting space by cell debris and new membranes. Underlying capillaries were often collapsed. Repeat biopsies in three patients in group III revealed progression of lesions, paralleling rapid clinical deterioration. It is concluded that some cases of focal glomerular sclerosis are associated with severe damage to podocytes which may be caused by drugs, infection or unknown factors and may contribute to the development and progression of the glomerular lesions.
A study of renal disease in familial dysautonomia identified excess glomerulosclerosis in 10 or 13 autopsied and biopsied patients. Sympathetic nerve terminals could not be found on renal vessels in biopsied tissue; they were invariably demonstrable in controls. Altered renovascular responsivity to systemic hypotension in familial dysautonomia may lead to ischemia and subsequent sclerosis of glomeruli. Review of 79 living outpatients showed that clinically overt renal disease was rare in familial dysautonomia. Nevertheless, frequent observations of elevations of serum creatinine concentrations (32% of patients) and blood urea concentrations (76% of patients) indicated a high prevalence of abnormality. An association was found between hypotension and renal dysfunction.