Search PubMed⌕ Search

Biomedical subjects

E Ritz

Publications and source records attributed to E Ritz.

At least 487 records · Page 27Linked to original sources
PubMed1992

Long-term therapy with cyclosporin A does not influence serum concentrations of vitamin D metabolites in patients with multiple sclerosis.

Animal studies have shown that cyclosporin A (CyA) stimulates renal 25-hydroxyvitamin D3 [25(OH)D3]-1 alpha-hydroxylase activity; in contrast, studies in renal transplant recipients indirectly suggest that CyA reduces 1 alpha,25-dihydroxyvitamin D3 [1,25(OH)2D3] production. To clarify the effect of CyA on vitamin D metabolite concentrations, we measured parameters of calcium metabolism in 37 CyA-treated patients (median trough whole blood levels 171-222 ng/ml) with multiple sclerosis and initially normal kidney function. The patients participated in a randomized double-blind study to assess the efficacy of CyA in multiple sclerosis. An age- and sex-matched control group (n = 39) received azathioprine (Aza). Measurements were made at the end of a 2-year treatment period. The 1,25(OH)2D3 serum concentrations were not significantly different between the two groups, although they were numerically lower in CyA-treated patients [median (range), 28.4 pg/ml (7.8-85.9) vs 41.0 pg/ml (9.2-105.1) in Aza-treated patients]. The 25(OH)D3 levels were comparable in both groups. There was no correlation between the 25(OH)D3 and 1,25(OH)2D3 concentrations. The renal function in both groups was stable in the last 6 months of the study. At the end of the study period, the endogenous creatinine clearance was significantly lower in the CyA-treated group (85 +/- 17 ml/min versus 99 +/- 22 in the Aza-treated group, P less than 0.05). The carboxyterminal parathyroid hormone (C-PTH) was within the normal range in both groups, although CyA-treated patients had significantly higher concentrations (P less than 0.01). The urinary excretion of mineral ions, cations and protein was similar in both groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Lead intoxication--new insights into an old problem.

The epidemiology, clinical symptomatology, diagnosis and management of acute and chronic lead intoxication are reviewed. While acute lead intoxication has become rare, the elevated environmental lead burden is thought to play a causal role in hypertension. Lead may also be linked with neuropsychological disorders of children and possibly even chronic renal failure. The epidemiological and experimental evidence for this hypothesis is critically discussed.

Adolescent↗
PubMed1992

Dendritic cells in glomerulonephritis.

Renal biopsies (n = 45) from patients with various forms of glomerulonephritis (GN), comprising mesangial IgA-GN (n = 25), focal glomerular sclerosis (n = 13) and acute GN (n = 7), were examined by double staining immunocytochemistry (APAAP, streptavidin-peroxidase) using unconjugated monoclonal antibodies (Ab) against--(i) the CD1b antigen expressed on dendritic cells (DCs), (ii) the invariant chain (Ii), and (iii) biotin-conjugated Ab against HLA-DR. In normal control kidneys (n = 7) without interstitial inflammation, CD1b-positive DCs were not detected. Glomerular endothelial cells and a few cells in mesangial areas showed double staining with the Ab against HLA-DR in Ii. In GN without active interstitial inflammation (n = 9), CD1b-positive DCs were not found. In biopsies with interstitial inflammation (n = 36) CD1b-positive DCs were found interspersed among other inflammatory cells. In seven of the biopsies showing IgA-GN DCs were seen in the vicinity of those glomeruli that exhibited either crescents or glomerular sclerosis with splitting of Bowman's capsule. In proximal tubular epithelial cells de novo expression of HLA-DR/Ii-chain was only seen when DCs were present. We conclude that in different forms of GN: (i) CD1b-positive DCs play an important role in the development of interstitial inflammation, and (ii) their presence may be related to the de novo coexpression of HLA-DR/Ii in tubular epithelial cells, possibly mediated through the production of interferon gamma and other cytokines.

Antigens↗
PubMed1992

Renal hemodynamics in recent-onset type II diabetes.

Glomerular hyperfiltration is thought to play an important role in the genesis of diabetic nephropathy. While hyperfiltration is well documented in early type I diabetes, the evidence for hyperfiltration in type II diabetes is conflicting. We investigated 16 nonproteinuric patients with recently diagnosed type II diabetes. Glomerular filtration rate (GFR) and effective renal plasma flow (ERPF) were measured as inulin clearance (CIN) and p-aminohippuric acid clearance (CPAH) using a constant infusion technique. Lean body mass was measured by densitometry (weighing under water). Renal hemodynamics were also measured in 31 healthy volunteers and six obese nondiabetic individuals. Median GFR in diabetics (133 mL/min/1.73 m2; range, 95 to 165) was significantly (P < 0.01) higher than in obese nondiabetic controls (median, 118; range, 95 to 139). Elevated GFR (ie, > 95th percentile of nonobese healthy controls) was found in 44% of patients. When GFR was factored for lean body mass, it was elevated in 50%. GFR did not correlate with fasting glucose, hemoglobin A1C (HbA1C), insulin-like growth factors, IGF-1 and IGF-2, or somatomedin-binding protein (SMBP). The findings document that hyperfiltration is common in recent-onset type II diabetics.

Adult↗
PubMed1992

Reduced capillary density in the myocardium of uremic rats--a stereological study.

Using stereological techniques capillaries, interstitium and myocardial fibers were analyzed in perfusion-fixed hearts of subtotally nephrectomized male Sprague-Dawley rats with uremia of 14 months duration (or their sham-operated controls). Uremic rats had higher systolic blood pressure (140 +/- 20.3 mm Hg vs. 119 +/- 6.61 mm Hg) and left ventricular weight/body weight ratio (3.37 +/- 0.09 mg/kg vs. 2.01 +/- 0.12 mg/kg) than controls, and had slight anemia (Hct 35.0 +/- 3.16% vs. 40.4 +/- 3.3%). Length density (Lv) of capillaries, that is, capillary length per unit myocardial volume, was significantly (P < 0.001) decreased in uremia (2485 +/- 264 mm/mm3 vs. 3329 +/- 194 mm/mm3) versus controls. In parallel, surface density and volume density of the capillary lumina were also reduced (7.95 +/- 1.69 cm3/cm3 vs. 11.4 +/- 1.8 cm3/cm3) in the uremic rats. We conclude that in experimental uremia, cardiac hypertrophy is not accompanied by a commensurate increase in capillaries.

Animals↗
PubMed1992

Renal histology in polycystic kidney disease with incipient and advanced renal failure.

Renal specimens were obtained at surgery or postmortem from patients with autosomal dominant polycystic kidney disease (ADPKD). Patients had either serum creatinine (SCr) below 350 mumol/liter (N = 12) or terminal renal failure (N = 50). Specimens were examined by two independent observers using a carefully validated score system. Mean glomerular diameters were similar in ADPKD patients with early renal failure (176 +/- 38 microns) and in victims of traffic accidents (177 +/- 23 microns), while they were significantly greater in diabetics with comparable renal function (205 +/- 16 microns). Glomerular diameters in ADPKD patients with terminal renal failure (191 +/- 45 microns) and with early renal failure were not significantly different. On average, 29% of glomeruli (17 to 62) were globally sclerosed in early renal failure, and 49% (19 to 93) in terminal renal failure. The proportion of glomeruli with segmental sclerosis was less than 4% in both groups. Marked vascular sclerosis, interstitial fibrosis, and tubular atrophy were present in early renal failure, and even more so in terminal renal failure. Interstitial infiltrates were scarce and consisted mainly of CD4 positive lymphocytes and CD68 positive macrophages. Immunestaining with monoclonal renin antibodies showed an increased juxtaglomerular index and expression of renin by arterioles adjacent to cysts, as well as by cyst wall epithelia. The data show more severe vascular and interstitial, but not glomerular, changes in ADPKD with advanced as compared to early renal failure.

Adult↗
PubMed1992

Beneficial effect of nifedipine and moxonidine on glomerulosclerosis in spontaneously hypertensive rats. A micromorphometric study.

The effect of calcium channel blockers on the development of glomerulosclerosis and progression of renal failure in different models of renal injury is still controversial. We compared the effects of blood pressure lowering with high doses of nifedipine (27 mg/kg body weight/day) and with the sympatholytic agent moxonidine (8 mg/kg body weight/day) in 6-month-old male spontaneously hypertensive rats (SHRsp). As controls we studied untreated hypertensive SHRsp and normotensive Wisfar-Kyoto rats (WKY). After 3 months of treatment, left ventricular (LV) weight and systolic blood pressure (tail plethysmography) were lower in both treated groups (144 +/- 21.4 mm Hg and 144 +/- 13.5 mm Hg v 193 +/- 38.6 mm Hg in untreated SHRsp), but remained higher than in WKY (116 +/- 16.0 mm Hg). Stereological analysis of perfusion fixed kidneys showed an unchanged total volume of cortex and medulla, but a higher mean glomerular volume in nifedipine treated SHRsp. The glomerulosclerosis index was similarly reduced by both antihypertensive agents (92.8 +/- 68.1 in untreated SHRsp v 27.2 +/- 12.9 and 18.2 +/- 9.8 in the two treatment groups, respectively). This was accompanied by a similar reduction of total cortical arterial wall volume (from 36.3 +/- 16.5 mm3 to 18.9 +/- 2.53 and 15.3 +/- 2.53 mm3, respectively) and by reduction of tubular atrophy or interstitial fibrosis, respectively. In this model nifedipine lowered blood pressure and inhibited development of glomerulosclerosis to the same extent as a sympatholytic agent. This was accompanied by increased glomerular volume and filtration area in nifedipine treated animals.

Animals↗
PubMed1992

Beta-2-microglobulin-derived amyloidosis: onset, distribution and clinical features in 13 hemodialysed patients.

Postmortem examinations were carried out in 13 patients (6 males, 7 females, age 58 +/- 9 years) who had been on regular hemodialysis treatment for 10-90 months using disposable regenerated cellulose membrane dialyzers. The prevalence of beta 2-microglobulin (beta 2m)-derived AB-amyloid deposits in different sites was determined. At autopsy, specimens were obtained from different joints, paravertebral tissue, intervertebral discs and from visceral organs. During life, routine laboratory parameters and radiographic studies had been carried out at 6-month intervals. Serum levels of beta 2m were elevated in all patients (57.5 +/- 13.4 mg/l). Synovial AB-amyloid deposits were shown in different joints of 4 patients, aged between 59 and 73 years, and dialysed for 10-90 months, respectively. All had been unremarkable by X-ray and asymptomatic. No amyloid could be detected in the intervertebral discs of 2 further patients suffering from destructive spondylarthropathy. In 11 of the 13 patients, extracellular beta 2m deposits were observed by immunohistochemistry in different tissues. The results document that (a) AB-amyloidosis may occur in elderly patients even when dialysed for less than 5 years; (b) most cases are completely asymptomatic; the appearance of symptoms must be dependent on additional factors, e.g., site of AB-amyloid deposition and intensity of inflammatory reaction, and (c) AB-amyloid is not the exclusive cause of destructive spondylarthropathy, as 2 typical cases were observed who were devoid of amyloid.

Amyloidosis↗
PubMed1992

25-Hydroxyvitamin D3 metabolism in vitro by mononuclear cells from hemodialysis patients.

Hemodialysis patients have a capacity for extrarenal production of 1 alpha,25-dihydroxyvitamin D3 [1,25(OH)2D3]; however, the source of the hormone is unknown in these patients. Since 1,25(OH)2D3 synthesis by cultured hematopoietic cells has been demonstrated previously, we assessed hormone production by mononuclear cells from peripheral blood obtained from normal subjects (n = 6), uremic patients not yet requiring dialysis (n = 4) and hemodialysis patients (n = 14). 1,25(OH)2D3 production was analyzed by sequential straight phase and reverse phase HPLC. In the hemodialysis group, the mean specific production of a metabolite co-eluting with 1,25(OH)2D3 (in fmol/100,000 cells/h) both by monocyte-enriched adherent cells (Mo) and lymphocyte-enriched non-adherent cells (Ly) was increased as compared to non-dialyzed subjects (119 vs. 22 for Mo, not significant, 65 vs. 14 for Ly, p < 0.05). Taken together, Mo and Ly from hemodialysis patients synthesized significantly more 1,25(OH)2D3 (p < 0.02) than non-dialyzed subjects (184 vs. 36, means). No differences were found between cells from normal subjects and patients with preterminal renal failure. Exposure of cultured normal Mo (n = 6) to cuprophane (CU), polyacrylonitrile (AN69) or polycarbonate-polyether (PC) membrane devices resulted in increased 1,25(OH)2D3 production as compared to control incubations without membrane. The rank order of increase was PC > AN69 > CU, whereby only PC (p < 0.05) was significantly different from control. Our results suggest that blood mononuclear cells contribute to extrarenal 1,25(OH)2D3 synthesis in hemodialysis patients, and that this synthetic activity may be related to the hemodialysis procedures.

Calcifediol↗
PubMed1992

The effect of uninephrectomy on progression of renal failure in autosomal dominant polycystic kidney disease.

The evolution of renal failure was compared in 47 patients (21 male, 26 female) with autosomal dominant polycystic kidney disease (ADPKD) in Germany, France, Spain, and Portugal who had undergone uninephrectomy (UNX) (median age at uninephrectomy, 41 yr; range, 22 to 54) and 47 non-UNX matched controls. UNX was usually performed because of uncontrolled urinary tract infection (N = 30), stones (N = 8), trauma (N = 2), or hemorrhage (N = 7). Median serum creatinine at UNX was 2.1 mg/dL (0.9 to 4.3). Twenty-eight of the 47 uninephrectomized patients progressed to end-stage renal failure. When the age at renal death was evaluated by survival analysis, only minor and nonsignificant acceleration was seen in the uninephrectomized patients (median, 50 yr; p25 = 43.6 yr; p75 = 58.3 yr, where p is the percentile) compared with non-UNX patients matched for age, sex, and serum creatinine at the time of UNX in the propositus (51.2 yr; p25 = 48.6 yr; p75 = 56.1 yr). In addition, the median interval for serum creatinine to rise from 4 to 8 mg/dL was similar in UNX (21.3 months) versus nonuninephrectomized ADPKD patients (21.9 months). Renal survival differed in the two genders. In females, no significant difference of age at renal death was found between UNX (median age, 51.6 yr) and non-UNX ADPKD patients (53.7 yr). In male UNX patients, age at renal death was slightly (but not significantly) less than in non-UNX patients (median age, 47.3 versus 52.7 yr). All male patients reaching end-stage renal failure before age 44 were severely hypertensive.

Adult↗
PubMed1992

Albuminuria of hypertensive patients.

Renal dysfunction as a consequence of malignant hypertension has been recognized for decades in patients with essential hypertension. It has been shown only recently, however, that albuminuria (including underlying albuminuria not detectable by conventional tests, i.e. microalbuminuria) has emerged as a frequent sequela of essential hypertension. Furthermore, renal dysfunction of the elderly as a result of ischemic nephropathy, in the absence of malignant hypertension, has turned out to be an important long-term outcome in the patient with essential hypertension. The presence of albuminuria is a strong predictor of cardiovascular events. Albuminuria is associated with more severe hypertension and with evidence of more advanced target organ damage (e.g. LVH). It is more prevalent in the elderly. It is unknown whether the predictive value of albuminuria reflects its association with more severe hypertension and end-organ damage, or whether albuminuria serves as an indicator of capillary leakiness which causes detectable abnormalities in the renal microcirculation but reflects more generalized endothelial barrier dysfunction predisposing to accelerated atherogenesis.

Adult↗
PubMed1992

ACE inhibition and renal protection.

In patients with renal disease, altered renal function causes elevation of blood pressure, but hypertension in its turn accelerates progression of renal failure. Lowering of blood pressure into the normotensive range is beneficial for slowing progression. Increasing incidence suggests that in this respect ACE inhibitors have unique benefits (renoprotective action).

Albuminuria↗
PubMed1992

Frusemide therapy and intact parathyroid hormone plasma concentrations in chronic renal insufficiency.

It has been suggested that frusemide affects plasma parathyroid hormone (PTH) concentrations. To further investigate this issue we analysed plasma intact PTH in 77 patients with chronic renal failure (CCr 8.0-89.8 ml/min per 1.73 m2) as a function of frusemide therapy. The rate of increase of plasma PTH observed with progression of renal failure was faster in patients who received frusemide as compared to patients who did not receive the drug. The slope of the regression line of PTH on CCr was steeper (P less than 0.02) for patients with frusemide (n = 40, slope -0.34) than without frusemide (n = 37, slope -0.20). This effect was specific for frusemide therapy since therapy with other antihypertensive drugs (including thiazides and beta-blockers) was not correlated with PTH plasma concentrations. Frusemide therapy was also associated with a significantly greater urinary calcium excretion in uraemic patients but did not influence other parameters of calcium metabolism. To clarify mechanisms involved in the effect of frusemide on plasma PTH values, seven normal subjects were studied for 24 h before and for 24 h after oral administration of 80 mg frusemide. The main findings were: (1) Median PTH values were higher than on a control day (P less than 0.05) 3 h after frusemide (3.9 pmol/l vs 1.8) and 6 h after frusemide (4.0 vs 2.6); (2) ionised plasma calcium did not change significantly, whereas mean calcium/creatinine ratio increased from 0.20 to 0.46 after frusemide treatment through an increase in absolute calcium excretion; (3) plasma 1 alpha,25-dihydroxyvitamin D3, catecholamines, and magnesium concentrations did not change significantly after frusemide.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

The response of GFR to amino acids differs between autosomal dominant polycystic kidney disease (ADPKD) and glomerular disease.

We compared the glomerular filtration rate (GFR) response to amino acids in patients with glomerular disease and polycystic kidney disease. The GFR response to infusion of amino acids (75 g/12 h), of dopamine (2 micrograms/kg per min), or their combination was evaluated in nine healthy probands and in patients with two types of renal diseases at various degrees of renal function: 15 patients with ADPKD and 11 patients with glomerular disease (IgA glomerulonephritis or diabetic nephropathy). Steady-state inulin infusion technique was used. In healthy subjects amino acids increased median C(in) in response to amino acids was not found in glomerular disease. In contrast in most ADPKD patients median C(in) increased after amino acids (+6.0 ml/min; range -4 to +68), (P less than 0.05). The response to amino acids was not modified by dopamine. The results demonstrate that amino acid-induced acute changes of glomerular filtration differ in polycystic kidney disease compared with glomerular disease. These observations may have implications with respect to mechanisms of progression.

Adult↗