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Biomedical subjects

L Ibels

Publications and source records attributed to L Ibels.

7 recordsLinked to original sources
PubMed1995

Comparison of simultaneous renal clearances of true endogenous creatinine and subcutaneously administered iothalamate in man.

125I-iothalamate and true endogenous creatinine clearances, measured over two short collections periods of 1 and 2 h, were compared simultaneously in 70 patients with a variety of renal diseases and a wide range of renal function. Reproducibility of the iothalamate clearance was 18.5% and that of the creatinine clearance 12.2%. The slope of the regression was not significantly different from 1 (95% confidence interval, CI, 0.964-1.155) for the whole group, nor in any subgroup chosen. The intercept at 12.6 ml/min (CI = 5.0-20.2) indicates that there is some creatinine secretion, but this was constant at all levels of GFR. It is concluded that although the clearance of true creatinine obtained during short collection periods consistently overestimates GFR by a constant proportion, it is a reproducible and accurate measure of GFR suitable for use in the clinical setting.

Adult↗
PubMed1989

Dysmorphism of urinary red blood cells--value in diagnosis.

To aid investigation into the clinical problem of hematuria, assessment of abnormalities in the shape of red cells in the urine (dysmorphism) is gaining popularity in nephrology. However, there is uncertainty in the literature regarding both the number of red blood cells (RBC) in normal urine, as well as the quantification of dysmorphism. We have shown that in normal urine (N = 27) the number of RBC is less than 2,000/ml as assessed by scanning electron microscopy of filtered urine specimens from normal volunteers without known renal disease, which compared to less than 1,000/ml by centrifugation and phase contrast microscopy of the same specimen. To determine whether dysmorphism of urinary red blood cells was a significant predictor of glomerular disease we compared the number of dysmorphic cells in the urine of patients with biopsy proven glomerulonephritis (GN), before and immediately after renal biopsy. We also compared the number of dysmorphic cells in patients with glomerulonephritis to those with lower urinary tract bleeding. Renal biopsy caused significant dysmorphic hematuria, indicating that dysmorphism suggests renal rather than glomerular bleeding. Although patients with GN had significantly more dysmorphic urinary RBC when compared to those with lower tract urinary bleeding, the overlap was such that one could only be confident of renal hematuria if they accounted for greater than 75% of the total number of RBC. Non renal hematuria is present if number of dysmorphic cells is less than 17% of total RBC. Thus dysmorphism of urinary RBC is a useful diagnostic tool, but only if strict criteria established for each laboratory are adhered to.

Erythrocyte Count↗
PubMed1984

Fulminant hepatic failure due to allopurinol.

A 58-year-old Chinese woman was admitted to hospital with a presumed hypersensitivity reaction to allopurinol. Her illness was characterised by high fever, eosinophilia, exfoliative dermatitis and jaundice. She developed fulminant hepatic failure and septicemia with a fatal outcome. Clinical details are presented and the possible relationship of allopurinol hypersensitivity to renal impairment is discussed.

Allopurinol↗
PubMedDate not supplied

HLA-DR and -DQ genotyping in anti-GBM disease.

Anti-GBM disease has been associated with the HLA genes of the major histocompatibility complex (MHC) in previous serological studies, with an increased incidence of HLA-DR2 in patients. In this study, 36 patients with anti-GBM disease were genotyped by restriction fragment length polymorphism (RFLP) analysis using cDNA probes for DRB, DQA, and DQB. The frequency of HLA-DRw15(Dw2), a split of DR2, was significantly increased in the patients compared with the controls (63.9 per cent versus 23.3 per cent, chi 2 = 22.4, p(corr) less than 0.0001), and all but one of the patients were positive for either DRw15(Dw2) or DR4 (p less than 0.0001). The frequencies of the remaining DR antigens were not decreased randomly, with a significant decrease in DR7 in the patient group (chi 2 = 8.6, p(corr) less than 0.05). The closely linked gene HLA-DQw6 was found to be significantly increased in frequency in the patients compared with the controls (p(corr) less than 0.0001). No correlations could be made between the genetic data and clinical features of the disease.

Adolescent↗
PubMedDate not supplied

The influence of dialysis treatment modality on the decline of remaining renal function.

A retrospective investigation was undertaken in which the rate of decline of residual renal function (RRF), estimated from creatinine clearance, was compared in 55 continuous ambulatory peritoneal dialysis (CAPD) and 57 hemodialysis (HD) patients for whom a minimum of four (mean of 7.6) well-spaced historic measurements of residual clearance were available. Because of the intrinsic variability that attends such data, specialized nonlinear, growth curve statistical methods were employed. Residual function was found to decline exponentially after the onset of therapy in both cohorts. The rate of decline in the HD group was twice that of the CAPD group (5.8% +/- 0.4% per month for HD vs 2.9% +/- 0.3% per month for CAPD; difference significant at p less than 0.0001). This difference remained highly significant (p less than 0.01) when corrected for other potential risk factors such as age, gender, hypertensive status, and use of angiotensin converting enzyme inhibitors in patients with diabetic or other forms of glomerular nephropathy. Differences between cohorts were not significant for patients with other diagnoses (p greater than 0.1) although the size of some of these subsets was very small. The physiologic mechanism for the more rapid fall-off of RRF on HD remains speculative, but could be related to renal ischemia secondary to intratreatment hypovolemia and/or to nephrotoxic effects of the inflammatory mediators of extracorporeal circulation.

Female↗