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PubMed1996

Effect of blood pressure control and antihypertensive drug regimen on quality of life: the African American Study of Kidney Disease and Hypertension (AASK) Pilot Study.

The African American Study of Kidney Disease and Hypertension (AASK) Pilot Study evaluated the feasibility of carrying out a randomized, multicenter, 7-year clinical trial to determine the effects of two goal levels of blood pressure control and three antihypertensive drug regimens on decline in glomerular filtration rate in African Americans with clinically diagnosed hypertensive nephrosclerosis. Participants were randomized to either a usual mean arterial blood pressure (MAP) goal group (102-107 mm Hg) or a low-MAP goal group (< or = 92 mm Hg) and to a drug regimen (initial therapy with either atenolol, amlodipine, or enalapril). Quality of life was assessed by the Medical Outcomes Short-Form 36 (MOS SF-36) at baseline and the last follow-up visit for 84 of the 94 participants of the AASK Pilot Study. Symptoms were assessed at baseline and throughout the course of therapy by participant self-report. Mean SF-36 scores increased significantly on physical functioning (9.2), role limitations (physical) (19.0), social functioning (9.0), and vitality dimensions (5.6) from baseline to the last follow-up visit in the usual MAP goal group. Scores for the eight health dimensions assessed by the MOS SF-36 did not change significantly during the same time period either in the low-MAP goal group or in any of the drug regimens. The mean score for general health perception was significantly lower at the last follow-up visit in the enalapril drug regimen (49.9) compared to drug regimens with atenolol (65.4) or amlodipine (63.9). Physical functioning, role limitations (emotional), social functioning, mental health, vitality, and general health perception scores were negatively correlated with self-reported symptoms during treatment. We conclude that selected dimensions of quality of life improved during the AASK Pilot Study only in participants randomized to the usual MAP goal group. Significant differences between MAP goal groups and drug regimens at the end of follow-up were observed for only a few health dimensions.

Adult↗

PubMed2000

Etiologies and outcome of acute renal insufficiency in older adults: a renal biopsy study of 259 cases.

Acute renal insufficiency is a common problem, yet one that is frequently reversible with proper diagnosis and treatment. Although it has been argued that a renal biopsy is not needed for diagnosis in most cases of acute renal failure in the elderly, other studies have shown frequent disagreements between clinical and renal biopsy diagnoses in such cases. To investigate the causes of acute renal insufficiency in patients aged at least 60 years who underwent a renal biopsy and possible correlations between biopsy findings and renal survival, we first identified all native renal biopsy specimens from patients aged 60 years or older processed at The University of Chicago Medical Center (Chicago, IL) from 1991 through 1998 and reviewed the clinical records to determine the indication for the biopsy. We then reviewed again the records of those patients who underwent biopsy because of acute renal insufficiency, recorded the primary renal biopsy diagnosis in each of these cases, and obtained follow-up information for patients who underwent biopsy before July 1996. During the study period, 1,065 of 4,264 biopsy specimens (25.0%) received were obtained from patients aged 60 years or older, and acute renal insufficiency was the indication for biopsy in 259 of these patients (24.3%). The most frequent primary diagnoses on these latter biopsy specimens were pauci-immune crescentic glomerulonephritis (GN) with or without arteritis, 31.2% of biopsy specimens; acute interstitial nephritis, 18.6%; acute tubular necrosis (ATN) with nephrotic syndrome, 7.5%; atheroemboli, 7.1%; ATN alone, 6.7%; light chain cast nephropathy (LCCN), 5.9%; postinfectious GN, 5.5%; anti-glomerular basement membrane antibody nephritis, 4.0%; and immunoglobulin A (IgA) nephropathy and/or Henoch-Schönlein nephritis, 3.6%. Eight biopsy specimens (3.2%) showed only benign nephrosclerosis without an apparent cause of acute renal insufficiency, and another six specimens were inadequate. The renal biopsy diagnosis was in agreement with the prebiopsy clinical diagnosis (or differential diagnosis) in 107 of the 161 cases (67%) in which such information was provided. The distribution of diagnoses was similar in patients in the age groups of 60 to 69, 70 to 79, and 80 years or older, although younger age correlated significantly with improved renal and patient survival. The relative risk for progression to end-stage renal disease (ESRD) also increased according to diagnostic categories: LCCN (greatest risk) > GN other than pauci-immune > atheroemboli congruent with pauci-immune crescentic GN > tubulointerstitial diseases other than LCCN (the latter category including ATN with nephrotic syndrome). Development of ESRD correlated significantly with decreased patient survival. In summary, renal biopsy in patients aged 60 years or older with acute renal insufficiency uncovered the cause in greater than 90% of the cases and provided clinically useful information with respect to expectation for renal survival and potential treatment options.

Acute Kidney Injury↗

PubMed2001

Transjugular renal biopsy in patients with liver disease.

Although transjugular renal biopsy has been used extensively in Europe, experience with its use in the United States has been limited. We report 25 patients who underwent both transjugular liver and renal biopsies in the same sitting and 4 patients who underwent only a transjugular renal biopsy. All 29 patients had both liver disease and renal abnormalities. Each patient was also believed to have a relative or absolute contraindication to a percutaneous renal biopsy (usually in the form of a bleeding abnormality). Transjugular renal biopsy yielded a quantity of tissue sufficient for diagnosis in all but 1 patient. The mean number of glomeruli obtained per biopsy was 19.4 +/- 12.2 (SD). Pathological diagnoses found were tubular injury in 5 patients, membranoproliferative glomerulonephritis in 5 patients, nephrosclerosis in 3 patients, diabetic nephropathy in 2 patients, immunoglobulin A (IgA) nephropathy in 2 patients, minimal change disease in 2 patients, end-stage renal disease in 2 patients, nonspecific changes in 1 patient, early glomerulosclerosis in 1 patient, tubular atrophy only in 1 patient, and normal renal histological characteristics in 4 patients. One patient with suspected IgA nephropathy had no histological diagnosis established because of a lack of glomeruli in the biopsy specimen. There were no instances of major bleeding from the perirenal area; however, a small perirenal hematoma was identified in 3 patients by postbiopsy computed tomography or sonography. Thus, based on our experience, transjugular renal biopsy appears to be a safe and effective procedure for establishing a histological diagnosis and is an attractive alternative biopsy method for patients with advanced liver disease and contraindications to conventional percutaneous renal biopsy.

Adult↗

PubMed1994

Clinical documentation of end-stage renal disease due to hypertension.

Hypertensive end-stage renal disease (ESRD) purportedly accounts for 25% of new ESRD patients each year in the United States, but remains poorly understood. Clinical features include normal renal function at diagnosis of hypertension, family history of hypertension, left ventricular hypertrophy, and minimal proteinuria. We evaluated clinical and historic data documenting the diagnosis of hypertensive ESRD in 43 patients with ESRD attributed to hypertension who were referred to our center for renal transplantation. Hypertensive ESRD patients were more likely to be black patients with left ventricular hypertrophy compared with our overall population. Few of the hypertensive ESRD patients had undergone kidney biopsy, none of whom had classic features of benign nephrosclerosis. Less than 5% of patients had hypertension documented at any time with normal renal function. Based on our review, it is clearly possible that the number of patients reaching dialysis and transplantation with renal failure attributed to hypertensive ESRD may be overestimated.

Adult↗

PubMed1990

Mortality on dialysis--on the influence of early start, patient characteristics, and transplantation and acceptance rates.

We compared changes from 1965 to 1987 in patients accepted to chronic dialysis, in a Swedish and a US dialysis center, by medical and clinical parameters at the start of dialysis and by duration of the dialysis. We also studied cause of death, outcome, and cumulative survival and tried to relate them to changes in patients and procedures. Finally, we studied how cumulative survival of dialysis patients was dependent on acceptance rates and transplant rates in five European regions and the United States. At both centers, the number of patients accepted grew, but since 1980, the only patient group that has increased has been older patients with many other diseases; these comorbid conditions have increased from approximately 1.2 to 1.4. In both centers, the number of patients with systemic disease, diabetes, and nephrosclerosis doubled. Cause of death showed a decrease in cardiovascular deaths and an increase in deaths due to stopping dialysis. The hemoglobin level increased from 70 to 90 g/L (7.0 to 9.0 g/dL) and the diastolic blood pressure decreased from 100 to 90 mmHg. The creatinine level decreased 30%, with an unchanged urea. Cumulative 3-year survival for patients without complications increased from 60% to approximately 90% and in patients with complications, it improved from 20% to 60% in Sweden and remained at approximately 60% in the US center. In the United States, many more patients were accepted to dialysis and the transplant rate was high. Cumulative survival on dialysis was inversely correlated both to the acceptance rates to dialysis and to the percent of patients transplanted. These factors explained over 90% of the differences in dialysis survival.

Aged↗

PubMed1993

The familial risk of end-stage renal disease in African Americans.

African Americans have higher overall incidence rates of end-stage renal disease (ESRD) compared with American whites. Hypertensive nephrosclerosis (HN), nephropathy secondary to diabetes mellitus types I and II, and chronic glomerulonephritis (CGN) all occur more frequently in African Americans. To explore the possibility that hereditary factors may play a role in the increased risk of ESRD in African Americans, the family history of 131 African American hemodialysis patients (cases) was compared with 115 age-, sex-, and race-matched non-ESRD controls. Odds ratios (ORs) were calculated to define the prevalence of a relative with ESRD among cases versus controls. Chi-square values were estimated from a log-linear model, while controlling for gender, to test for significance of ORs. Forty percent (12/30) of HN cases, 35% (18/51) of type II diabetes mellitus-induced renal failure cases, and 13% (5/38) of CGN cases had a first-, second-, or third-degree relative with ESRD. The presence of a first-degree relative with ESRD increased an African American's risk for developing ESRD ninefold (OR, 9.13; 95% confidence interval [CI], 2.6 to 31.8; P < 0.001). The presence of a first- or second-degree relative increased the risk fivefold (OR, 5.23; 95% CI, 2.2 to 12.3; P < 0.0002). First-, second-, or third-degree relatives with ESRD were more prevalent among cases with ESRD due to hypertension and type II diabetes mellitus compared with CGN (P < or = 0.05). Gender differences among the ORs were nonsignificant (P > 0.2) and socioeconomic class (level of education and income) did not differ markedly between cases and controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1997

Short-term effects of blood pressure control and antihypertensive drug regimen on glomerular filtration rate: the African-American Study of Kidney Disease and Hypertension Pilot Study.

The African-American Study of Kidney Disease and Hypertension pilot study randomized 94 nondiabetic black men and women (mean age, 53 years; 75% male) with presumed hypertensive nephrosclerosis and a baseline glomerular filtration rate (GFR) of 25 to 70 mL/min/1.73 m2 (mean, 52.3 mL/min/1.73 m2) to blood pressure control at either a low mean arterial pressure (MAP) goal of < or = 92 mm Hg or a usual MAP goal of 102 to 107 mm Hg and an antihypertensive drug regimen that included either a calcium antagonist (amlodipine), a beta-blocker (atenolol), or an angiotensin-converting enzyme (ACE) inhibitor (enalapril). After 3 months of follow-up (n = 90), the mean GFR was similar (53.0 mL/min/1.73 m2 v 53.7 mL/min/1.73 m2) to the baseline levels in participants randomized to the low MAP group (n = 44), whereas the mean GFR increased by 3.9 mL/min/1.73 m2 (P = 0.02) in participants randomized to the usual MAP group (n = 46). During the same period of time, the mean GFR increased significantly in participants randomized to the calcium channel blocker regimen (n = 28) (5.7 mL/min/ 1.73 m2; P = 0.01) but not in participants randomized to the beta-blocker regimen (n = 31) (1.7 mL/min/1.73 m2; P = 0.10) or the ACE inhibitor regimen (n = 31) (1.1 mL/min/1.73 m2; P = 0.52). Changes in GFR at 3 months were significantly different among the three treatment groups (P = 0.04). We conclude that the magnitude of short-term effects of blood pressure control and antihypertensive drug regimens on GFR should be considered when estimating sample size for clinical trials designed to evaluate the effects of these interventions on long-term changes in GFR slope.

Adolescent↗

PubMed1997

Improved preservation of residual renal function in chronic hemodialysis patients using polysulfone dialyzers.

Our objective was to determine whether patients with chronic renal failure requiring maintenance hemodialysis retain intrinsic renal function longer when using reprocessed polysulfone (PS) membrane hemodialyzers or single-use cellulose acetate (CA) membrane hemodialyzers. Fifty consecutive patients with residual renal function (urea clearance > 2.0 mL/min) using PS dialyzers were compared with a retrospective, disease- and time-matched population of patients using CA dialyzers. Endogenous urea clearance was measured every 3 months in all patients with remaining residual function. Other data collected included age, sex, cause of chronic renal failure, use of angiotensin-converting enzyme inhibitors or calcium channel blockers, and hemodynamic stability during hemodialysis. All patients were observed for at least 6 months while using a single type of dialyzer. Study end points included loss of residual renal function (urea clearance < 1.0 mL/min), death, transplant, transfer to peritoneal dialysis, or change of dialyzer. The PS and CA groups of patients were well matched for sex, age, initial renal clearance, predialysis blood pressure, and hemodynamic stability during hemodialysis. The PS patients had a higher delivered Kt/V (1.34 +/- 0.30 [mean +/- SD]) than the CA patients (1.06 +/- 0.20). The PS group had a higher average urea clearance than the CA group after 4 to 9 months of dialysis (2.8 +/- 2.6 mL/min v 1.7 +/- 1.6 mL/min, respectively), after 10 to 15 months of chronic dialysis (2.0 +/- 2.4 mL/min v 1.1 +/- 1.5 mL/min, respectively), and after 16 to 21 months of dialysis (1.3 +/- 1.9 mL/min v 0.5 +/- 1.1 mL/min, respectively; all P < 0.03, t-test). After 22 to 24 months of dialysis, the difference between the two groups was not significant. When comparing patients with identical causes of chronic renal failure, there were no differences between the PS and CA groups for those with diabetes mellitus, tubulointerstitial disease, or polycystic disease. Patients with parenchymal renal disease (glomerulonephritis or nephrosclerosis) had markedly better retention of intrinsic renal function with PS than with CA dialyzers (all P < 0.01). Kaplan-Meier analysis for retention of intrinsic renal function showed that PS patients with parenchymal renal disease had a mean of 23 months before loss of intrinsic renal function, whereas for CA patients the mean was 11 months before loss of intrinsic renal function (P = 0.0005). Cellulose acetate patients lost renal function at an average rate of 0.27 +/- 0.22 mL/min/mo, whereas for PS patients the rate was 0.14 +/- 0.56 mL/min/mo (P = 0.06, rank sum). CA patients with parenchymal renal disease lost renal function at a rate of 0.29 +/- 0.22 mL/min/mo, whereas for PS patients the rate was 0.0 +/- 0.8 mL/min/mo (P = 0.004, rank sum). Age, sex, and the use of either angiotensin-converting enzyme inhibitors or calcium channel blockers did not have an effect on the loss of intrinsic renal function. Patients with nondiabetic parenchymal renal disease receiving chronic hemodialysis with hydrogen peroxide/peroxyacetic acid-reprocessed PS dialyzers and a higher Kt/V lose residual renal function at a slower rate than disease-matched patients using single-use CA dialyzers. Our findings provide further evidence that the choice of dialyzer membrane may have an effect on intrinsic renal function.

Biocompatible Materials↗

PubMed1999

Evaluation of markers on human chromosome 10, including the homologue of the rodent Rf-1 gene, for linkage to ESRD in black patients.

There is abundant evidence supporting the contribution of genetic factors to the development of end-stage renal disease (ESRD) in blacks. Two renal failure susceptibility genes, Rf-1 and Rf-2, have been identified in the fawn-hooded rat, an animal model of hypertension and nephrosclerosis. The human homologous region containing the rodent Rf-1 gene has been localized to chromosome 10q. We tested for genetic linkage between 21 polymorphic markers on human chromosome 10 and chronic renal failure in 129 black sibling pairs concordant for ESRD. Two adjacent markers on 10p, D10S1435 and D10S249 (4 centiMorgans from D10S1435), approached significance for linkage to ESRD in sibling pairs with nondiabetic causes of ESRD (P = 0.035 pairwise, P = 0.082 multipoint for D10S1435; P = 0.074 pairwise, P = 0.063 multipoint for D10S249). The markers spanning the homologous region of Rf-1 did not show evidence for linkage to ESRD in sibling pairs concordant for diabetic ESRD, sibling pairs concordant for nondiabetic causes of ESRD, or in the entire family set. These results suggest that the human homologue of Rf-1 is unlikely to contribute substantially to renal failure susceptibility from the common causes of kidney disease in blacks.

Animals↗

PubMed1996

MR angiography of the renal arteries.

MR angiography (MRA) has shown considerable promise as a noninvasive tool in the evaluation of renal vascular morphology. There are two fundamental approaches to MRA of the renal arteries: time of flight and phase contrast imaging. Recently, three-dimensional, gradient-echo, gadolinium-enhanced MRA using breath-hold techniques also has been introduced. These techniques have made MRA of the renal arteries a very promising, noninvasive tool in the detection of main renal artery stenosis, with sensitivities between 90% and 100%. MRA is used most often in the evaluation of renal arteries of patients with abdominal aortic aneurysms or allergies to iodinated contrast media, or when other noninvasive screening examinations have been inconclusive. One of the most helpful and unique applications of MRA is in patients who have accelerating hypertension and accelerating renal insufficiency. These patients often have preexisting unilateral renal artery stenosis with a new contralateral renal artery stenosis. Conventional angiography is risky in these patients because of possible contrast nephropathy. MRA, in such cases, is very helpful for differentiating between bilateral renal artery stenosis and end-stage nephrosclerosis.

Humans↗

PubMed2003

Differential regulation of osteopontin expression in the clipped and nonclipped kidney of two-kidney, one-clip hypertensive rats.

BACKGROUND: Osteopontin (Opn) is highly upregulated in many different animal models of renal disease, where it is suspected to participate in progression of the disease. In some models, angiotensin II (Ang II) seems to induce the elevated Opn production. Therefore, we examined the regulation of Opn in two-kidney, one-clip (2K1C) hypertensive rats, in which Ang II mediates the elevated blood pressure. METHODS: At days 7, 14, and 28, the clipped and nonclipped kidneys of hypertensive or sham-operated rats were analyzed for osteopontin protein, mRNA expression and mononuclear cell infiltration by imumunohistochemistry, in situ hybridization, and Northern blot analysis. Rats were treated with the Ang II type 1 receptor antagonist Valsartan starting 14 days after clipping. RESULTS: In sham-operated rats, Opn was mainly localized to cells of the thin ascending limbs of the outer medulla. No significant Opn staining was observed in cortical tubules. Focally defined tubular cortical Opn staining was observed in clipped and contralateral kidneys of hypertensive animals at days 14 and 28. Osteopontin protein expression correlated with the mRNA expression detected by in situ hybridization and Northern blot. Treatment with Valsartan reduced osteopontin staining by 51%, mRNA by 47%, and mononuclear cell number by 97% in nonclipped kidneys compared to untreated two-kidney, one-clip animals. In clipped kidneys, however, Opn protein and mRNA expression was not reduced, but a 240% increase in interstitial mononuclear cell number was observed. CONCLUSIONS: Osteopontin is involved in the induction of nephrosclerosis in renovascular hypertension, probably by a mechanism augmenting monocyte infiltration. Angiotensin II appears to be an important inducer of Opn in the nonclipped kidney. Ischemic conditions may regulate Opn expression in the clipped kidney.

Angiotensin Receptor Antagonists↗

PubMed1997

Renovasculopathies in elderly normotensives of Bombay, India.

In essential hypertension, specific vasculopathies distinguish the kidney of nephrosclerosis. The severity of renovasculopathy can be measured histologically at autopsy. A previously determined equation uses the measurements to calculate mean blood pressure levels. That equation did not encompass elderly subjects with minimal vasculopathy, because they were deficient in the previous data set. Such subjects were abundant in a series of 86 autopsies conducted at the J.J. Hospital in Bombay. That newly reviewed series now provides many instances of normotension accompanying minimal vasculopathy at ages greater than 40-50 years. These conditions are seldom observed in the U.S.A. The newly examined elderly normotensives manifest degrees of renovasculopathy equivalent to those of youthful normotensives with comparable blood pressure levels. The elderly subjects who escaped a rise of blood pressure with age were those with long delayed progression of renovasculopathy; this may be the explanation for avoidance of hypertension in old age. The outcome places the J.J. Hospital patients among the populations of the world with the slowest rates of progression of hypertension.

Adult↗

PubMed2001

Spectrum of renal diseases in the elderly: single center experience from a developing country.

From November 1998 to March 2000, two hundred patients over the age of 60 years (Elderly) with clinical renal disease were studied. 144 patients were between ages of 60-69 years, 46 between 70-79 years and 10 were above 80 years. The elderly patients (Male 165; Female 35) with renal disease constituted 11% (200/1816) of the total nephrology consultation during the study period. The clinical presentation included chronic renal failure (42.5%); acute renal failure (28%); nephrotic syndrome (14.5%); acute glomerulonephritis (7.5%); renal vascular disease (5%) and renal cystic disease (2.5%). Diabetic nephropathy, obstructive uropathy and hypertensive nephrosclerosis were the major causes of CRF, accounting for 80% of total CRF in the elderly. Chronic glomerulonephritis and chronic pyelonephritis (CPN) were less common and etiology of CRF was uncertain in 5.9% of cases. However, diabetic nephropathy was the commonest (49.4%) cause of chronic renal failure. We did not see a single case of ischemic nephropathy causing CRF in the present study. Prerenal ARF, obstructive uropathy and sepsis were contributing factors for ARF in 82% of the cases. Volume depletion due to gastrointestinal fluid loss and urinary tract obstruction on account of enlarged prostate were the leading causes of ARF in 20 (35.7%) and 8 (14.3%) cases respectively. Sepsis with or without multiorgan failure was the major (46.7%) cause of mortality in patients with ARF and overall mortality was 26.8%. The commonest (31%) cause of nephrotic syndrome was the idiopathic membranous nephropathy. Diabetic nephropathy related to type-2 diabetes mellitus was the second most common (24.1%) cause of nephrotic syndrome. Diffuse endocapillary proliferative GN of post infectious etiology was the commonest (73.3%) type of acute GN in our elderly patients. Renal cystic diseases were noted in 5 (ADPKD 3; Simple cyst-2) patients. Thus, overall spectrum of renal disease in our elderly patients is similar to that of developed nations except in two ways: (i) Endocapillary proliferative GN of post infectious origin was the commonest type of acute GN and (ii) Rarity or absence of ischemic nephropathy and atherosclerotic renal artery occlusive disease.

Aged↗

PubMed1999

HLA-identical sibling renal transplantation--a 21-yr single-center experience.

Human lymphocyte antigen (HLA)-identical sibling organs offer the best long-term outcomes for recipients of a renal transplant apart from an identical twin. Unlike cadaveric transplants, however, factors that affect long-term survival of these immunologically privileged grafts are not well described. We reviewed 108 HLA-identical transplants performed at our institution between January 1977 and February 1993. Variables chosen for graft survival analysis were: gender, age and ABO blood type of donors and recipients, panel reactivity antibodies (PRA), blood transfusions prior to transplant, pregnancies, and the underlying renal disease. Additionally, incidence of acute rejection (AR), timing of AR, serum creatinine levels at 1 wk and at 1 yr, and presence of hypertension were included in the analysis. Mean follow-up was 130.9 +/- 58.2 months (range 38-250 months). Actual 5-yr patient and graft survivals were 92 and 88%, respectively. Thirty-eight grafts were lost, and 22 recipients died during the observation period. Death was the main cause of graft failure. Cardiac events accounted for the majority of deaths. AR occurred in 46% and repeated rejections in 11% of recipients. Actuarial graft survival at 10 yr was poorer for patients with any AR (69%), and significantly worse with repeated AR (33%), compared to patients without AR (86%), p = 0.001). Sixty percent of all rejections and 88% of the first rejections occurred in the first 60 d post-transplantation. The first AR that occurred after 60 d was associated with poor graft survival (49 vs. 70%, p = 0.04). Recipients with renal diseases with potential to recur (membranous glomerulonephritis (MGN), membrano-proliferative glomerulonephritis (MPGN), focal and segmental glomerulonephritis (FSGN), polyarteritis nodosa (PAN), rapid progressive glomerulonephritis (RPGN), Henoch-Schoenlein purpura (HSP), diabetes mellitus (DM), interstitial nephritis, systemic lupus erythematosus (SLE) and chronic glomerulonephritis (CGN)) faired worse as a group than recipients with hypertensive nephrosclerosis (HTN), autosomal dominant polycystic kidney disease (ADPKD), Alport's, reflux or congenital dysplasia (68 vs. 96% at 10 yr, p = 0.0009). Poor patient survival was seen in diabetics (71 vs. 88% at 10 yr, p = 0.01). There was a trend to poorer graft survival in diabetic recipients when compared to non-diabetics (65 vs. 81% at 10 yr, p = 0.054). Elevated creatinine at 1 yr was associated with worse graft survival. Likewise, the magnitude of creatinine increase during the first year directly correlated with the risk of graft loss. Hypertensive patients were more likely to lose their grafts than normotensive recipients (72 vs. 86%, p = 0.04). Pre-transplant blood transfusion, pregnancy, and PRA level were not associated with increased graft failure or AR. Graft survival was not affected by gender, age, or ABO blood type of donors or recipients. In conclusion, better prevention and treatment of AR, hypertension, and cardiac disease should improve graft and patient survival. Close attention to recurrence of disease and subtle changes in the creatinine level during the first year might dictate early diagnostic and, hopefully, therapeutic interventions.

ABO Blood-Group System↗

PubMed1992

Demographic factors influencing cyclosporine pharmacokinetic parameters in patients with uremia: racial differences in bioavailability.

The impact of several demographic and blood biochemistry factors on the pharmacokinetics of the immunosuppressive drug cyclosporine were studied in 187 patients with uremia. All patients underwent a pharmacokinetic evaluation including a 3 mg/kg intravenous dose of cyclosporine and a 14 mg/kg oral dose of cyclosporine. Cyclosporine was analyzed by specific monoclonal radioimmunoassay on whole blood samples. Statistical analysis included univariate analyses and stepwise multiple regression analysis. Major findings were as follows: The bioavailability (F) of cyclosporine was significantly lower in black patients than in white patients (mean values of 30.9% +/- 12.3% and 39.5% +/- 16.5%, respectively; p < 0.001). This difference was noted both before transplant and at 1 week after kidney transplantation, at which time the corresponding mean values were 28.6% +/- 15.5% and 36.1% +/- 15.5%, respectively (p < 0.01). Other factors that correlated with F were serum triglyceride (positively) and blood hemoglobin concentrations (inversely). Patients with diabetes displayed a longer mean absorption time than other patients and a larger volume of distribution of cyclosporine at steady state (VSS). Other factors that correlated with VSS were serum albumin concentration and patient height. Cyclosporine clearance (CL) decreased with patient age and also with increasing concentrations of serum triglycerides and blood hemoglobin. It was lower in patients with the pretransplant diagnosis of nephrosclerosis than in patients with other diseases. Several pharmacokinetic parameters correlated with the level of substances that can potentially bind cyclosporine in the blood. Serum triglycerides correlated with maximum concentration, time to maximum concentration, F, and CL. Blood hemoglobin concentration and blood hematocrit correlated with F, CL, and intravenous mean residence time. Although several relationships were observed between demographic factors and cyclosporine pharmacokinetics, the racial difference in F is of great clinical significance and may contribute to the poorer outcome observed after kidney transplantation in black patients.

Adult↗

PubMed1991

Circulating anti-entactin antibodies in patients with glomerulonephritis.

Sera from 305 consecutive patients in a renal biopsy series were analyzed for the presence of anti-entactin antibodies by ELISA. Of these patients, 59% had primary glomerulonephritis, 21% had secondary glomerulonephritis, while 20% had other nephropathies (noninflammatory conditions like amyloidosis, diabetic nephropathy, nephrosclerosis, etc.). Forty-one of these patients (13.4%) were positive for IgG/IgM antibodies against entactin: 60% of them had primary glomerulonephritis, 35% had secondary glomerulonephritis, while the remaining 3 patients had other nephropathies. Fifteen (70%) of the 23 patients with primary glomerulonephritis had proliferative glomerulonephritis (PGN), whereas 13 (87%) of the 15 patients with secondary glomerulonephritis were due to systemic connective tissue diseases (SCTD): 7 due to SLE, 4 due to SLE like SCTD and two due to other SCTD. There was a peak of incidence corresponding to the group aged 18 to 30 years. A majority of these patients (12 of the total 17) had primary glomerulonephritis and were associated with nephrotic or subnephrotic grade proteinuria, poorly or nonresponsive to immunosuppressive treatment and associated, in several cases, with progressive deterioration of renal function. In addition, there was a tendency to another peak in the age group 51 to 60 years. Most of these patients (6 of the total 8) had glomerulonephritis secondary, mainly, to SLE or SLE like SCTD with milder degree of proteinuria and better preserved renal functions. Anti-entactin antibodies were not found in certain glomerulonephritides like IgA nephropathy and those secondary to systemic vasculitides and in control subjects (healthy subjects, and patients with a variety of non-renal disorders including inflammatory diseases).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMed1991

Racial differences in the incidence and progression of renal diseases.

There is an excess incidence of ESRD treatment among non-White North Americans that is not completely explained by the racial prevalences of the underlying diseases, including hypertension, which can potentially cause renal disease. The racial difference is particularly striking for presumed nephrosclerosis from hypertension and for nephropathy from Type II diabetes, but is not yet substantiated for ESRD attributed to polycystic kidney disease or Type I diabetes. The existing data are insufficient to support the notion that poorer blood pressure control alone is responsible for the racial differences in incident ESRD. Black race (and possibly Mexican or Native American heritage) may be a specific risk factor for ESRD, independent of hypertension and its treatment.

Black People↗

PubMed1994

Renal TGF-beta regulation in spontaneously diabetic NOD mice with correlations in mesangial cells.

Diabetic nephropathy is characterized by excessive glomerular matrix accumulation, basement membrane thickening and sclerosis. Although it is clear that systemic metabolic disturbances precipitate such renal changes, the signals and pathways involved in this process are not fully elucidated. Recent evidence suggests that growth factors/cytokines are intimately involved in the pathogenesis of diabetic nephropathy. Because of its prosclerotic properties, transforming growth factor-beta (TGF-beta) is a prime candidate mediator of diabetic nephrosclerosis. We examined perfused kidney tissues isolated from spontaneously diabetic, non-obese diabetic mice (NOD) for TGF-beta content. By using murine isotype specific TGF-beta probes, we demonstrate that within 5 to 10 days of hyperglycuria renal TGF-beta 2 mRNA and protein content increases. By immunohistochemical analysis, de novo TGF-beta immunoreactivity was detected within both glomeruli and the interstitium. In order to determine the signals involved in promoting kidney TGF-beta content in vivo, TGF-beta regulation was examined in renal mesangial cells in vitro. Murine mesangial cells stimulated with glycosylated protein secrete bioactive TGF-beta and demonstrate a disproportionate increase in the steady state levels of TGF-beta 2 mRNA. These data suggest that a major early renal response in NOD mice to hyperglycemia or to glycosylated proteins is characterized by increases in TGF-beta.

Animals↗