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Biomedical subjects

E Ritz

Publications and source records attributed to E Ritz.

At least 559 records · Page 31Linked to original sources
PubMed1990

[ACE inhibitors and kidney].

One of the major challenges for today's nephrology is to elucidate the mechanism of action of ACE-inhibitors in damaged kidneys. Clarification of the mechanisms involved will not only increase the understanding of the pathomechanisms involved in progression, but also enrich the therapeutic armamentarium available to the nephrologist.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1990

[Epidemiological studies of the frequency of the abuse of analgesics].

To assess the epidemiology of habitual use of analgesics in South-West Germany (i) urine specimens of employees of a factory, of patients seen by a general practitioner (GP) and of patients attending a renal clinic were examined for paracetamol; (ii) mucosa of the left renal pelvis was examined for the presence of capillary sclerosis as an index of habitual use of phenacetin or paracetamol in 258 consecutive autopsies; (iii) in a regional renal clinic, the frequency of analgesic nephropathy was determined amongst outpatients and amongst patients on hemodialysis. Paracetamol was found in the urine of 4.1% of factory employees, in 3.5% of patients seen by a GP and in 2% of patients seen in the renal clinic. Capillary sclerosis was found in only one of 258 autopsies, in a patient dialysed for analgesic nephropathy. During the past two years, analgesic nephropathy was diagnosed in 3% of all patients seen for nephrological examination. Analgesic nephropathy was the cause of terminal renal failure in 15 of 166 patients (9.4%) on dialysis. The present study documents that habitual use of paracetamol-type analgesics continues in the general population despite the ban of phenacetin.

Acetaminophen↗
PubMed1990

Fluid phase generation of terminal complement complex as a novel index of bioincompatibility.

Blood membrane interactions in hemodialysis have been shown to trigger complement (C) activation. As indicators of C-activation the anaphylatoxins (C3a and C5a) are problematical because of methodological difficulties and their kinetic properties. We developed a sensitive and specific micro-ELISA using a monoclonal antibody against neoantigens on the terminal complement complex (TCC); highly purified human TCC served as standard. Concentrations of TCC were measured in single-path perfusion systems (in vitro) and in the blood lines (arterial inlet; venous outlet) of patients on hemodialysis using steam-sterilized or ETO-sterilized dialyzers with the following membranes: cuprophan (CU), hemophan (HE) and polysulfone F6 (PS), respectively. All dialyzers with identical geometry were run under identical conditions. All membranes tested caused continuously ongoing net generation of TCC. In vitro, contact of serum with CU minidialyzers resulted in fivefold higher net release of TCC compared with HE and PS. In vivo TCC concentration-time profiles differed significantly between membranes in the rank order CU much much greater than HE greater than PS (mean basal concentration 58 x 10(-11) M; peak increase over baseline with CU 40-fold, HE fourfold, PS threefold). In addition, more TCC was generated from the same dialyzers with ETO than steam sterilization. TCC differed from C3a and C5a in the following respects: (i) lower detection limit (4 x 10(-11) vs. less than 5 x 10(-9) M for both C-anaphylatoxins); (ii) higher relative increment (inlet) during CU dialysis (25-fold vs. eightfold and twofold, respectively); (iii) C-anaphylatoxins yielded the same ranking (CU much greater than HE greater than PS), but TCC concentrations were not a linear function of C3a or C5a concentrations, respectively. Kinetic analysis (Bateman function) showed significant differences of invasion constants between membranes, that is, CU 0.088 min-1, HE 0.09, PS 0.168. The net amount of TCC released from the dialyzer was calculated under certain assumptions. It was 75.5 mg/4 hr for CU, 7.3 for HE and 5.0 for PS. The elimination constant was also dependent on the type of membrane. Using flow cytofluorometry and immunohistochemical methods (APAAP), TCC was demonstrated on membranes of granulocytes obtained during dialysis; this is compatible with potential in vivo cell activation. Generation of PGE2 and TNF alpha by adherent monocytes induced by cuprophan was C8 dependent: levels were significantly increased by addition of C8 to C8 deficient human serum concomitantly with generation of TCC.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Diffuse intermyocardiocytic fibrosis in uraemic patients.

At post-mortem we examined heart tissue of (i) 31 patients with uraemia not on dialysis, (ii) 42 patients on haemodialysis for less than 6 months, (iii) 60 patients on haemodialysis for more than 6 months, (iv) 16 patients after renal transplantation, and (v) 11 patients on CAPD. Patients with stenosing coronary lesions were excluded. Diffuse non-coronary intermyocardiocytic fibrosis, assessed by a score system in trichrome-stained sections, was found in 91% of chronically uraemic patients, but not in non-hypertensive, non-diabetic controls. The lesion was present even in non-dialysed uraemic patients; in dialysed patients its severity was related to the duration of dialysis; it was demonstrable even years after renal transplantation. On electron-microscopy, collagen fibres were seen, while beta 2-M amyloid was consistently absent. Logistic regression analysis showed that uraemia was a determinant of intermyocardiocytic fibrosis independent of hypertension, diabetes mellitus, anaemia, heart weight, and presence or absence of dialysis procedure.

Anemia, Aplastic↗
PubMed1990

Improved sexual function during recombinant human erythropoietin therapy.

In seven male haemodialysis patients, living with a constant sexual partner, sexual life (self-administered questionnaire) and sex hormones were evaluated before and 3 or 10 months after commencement of recombinant human erythropoietin (rHuEpo) therapy respectively. Haematocrit increased from 22.2 +/- 2.1% to 30.6 +/- 1% with a maintenance dose of 140 +/- 55 U/kg per week. Two patients were hypertensive before and after rHuEpo therapy; antihypertensive medication was kept constant during the study. Self-reported sexual function improved in four of seven patients, including libido and erection. This was paralleled by improved indices of wellbeing (physical fitness, mental alertness). In contrast, serum values of sexual hormones (testosterone or oestradiol) and of basal and stimulated (LHRH/TRH), prolactin and LH, and FSH were not significantly changed during rHuEpo therapy.

Adult↗
PubMed1990

Particles from dialysis tubing stimulate interleukin-1 secretion by macrophages.

Loading of tissue macrophages with dialysis-tubing-derived particles may occur during chronic haemodialysis. Previous studies have demonstrated that these particle-laden macrophages release significant quantities of prostaglandins. In these experiments, the effects of dialysis-tubing-particle loading on the release of the central inflammatory mediator, interleukin 1 (IL 1), was examined. Rats received daily injections of silicone or polyvinylchloride (PVC) particles, and were compared to animals given saline alone. The silicone and PVC groups received a total of 3 x 10(9) particles over a 4-week period. Non-stimulated peritoneal macrophages from control animals released a median of 4.1 (range 1.2-10.3) U IL 1 per 10(6) cells. In contrast, macrophages from silicone- and PVC-loaded animals spontaneously released high levels of IL 1 (median 21.8; range 10-36.7) and 94 (range 36-336) U per 10(6) cells respectively). Following in vitro stimulation with bacterial lipopolysaccharide (LPS), peritoneal macrophages from silicone- and PVC-treated animals released large amounts of IL 1 (median 538 (range 359-2017) U and median 653 (range 326-1134) U per 10(6) cells, respectively) as compared to LPS-stimulated macrophages from control animals (median 332 (range 130-306) U per 10(6) cells]. Zymosan or LPS stimulation of splenic cells from silicone- and PVC-loaded animals also secreted increased quantities of IL 1 as compared to controls. The chronic loading of tissue macrophages in dialysis patients with tubing-derived particles may result in augmented release of IL 1, with subsequent activation of inflammatory processes.

Animals↗
PubMed1990

Doppler echocardiographic findings in dialysis patients.

We used Doppler echocardiographic techniques firstly to examine left ventricular (LV) filling patterns in dialysis patients, secondly to analyse whether Doppler echocardiographic left ventricular filling pattern is different in patients with recurrent intradialytic hypotension, and thirdly to study the relation between blood pressure decrease during volume subtraction and left ventricular filling pattern. Indices of left ventricular filling patterns of 47 dialysis patients were consistently different when compared to normotensive healthy controls. To further assess the relation of left ventricular filling pattern to blood pressure stability on dialysis, we first compared 24 patients with stable intradialytic blood pressure (BP) and 23 patients with one or more episodes or intradialytic hypotension per month. Patients with recurrent intradialytic hypotension had lower predialysis blood pressure (MAP 89 +/- 13 vs 96 +/- 14 mmHg), more severe concentric hypertrophy (left ventricular mass/volume ratio 2.7 +/- 1.4 vs 2.0 +/- 0.7), and impaired left ventricular filling (Doppler) as indicated by the ratio of early diastolic vs late (atrial) filling (0.66 +/- 0.2 vs 0.95 +/- 0.22). Subsequently we assessed by Doppler technique the effect of a predetermined rate of volume subtraction (during one dialysis session) in patients with or without recurrent intradialytic hypotension. Diastolic filling indices deteriorated consistently prior to the reduction in blood pressure (early diastolic filling 26.8 +/- 15.2 vs 45.4 +/- 10.9% of diastolic filling). It is suggested that impaired left ventricular filling, presumably reflecting disturbed left ventricular compliance, is common in dialysis patients. Findings by noninvasive Doppler techniques suggest a role of abnormal left ventricular distensibility in recurrent dialysis hypotension.

Adult↗
PubMed1990

Cardiac changes in uraemia and their possible relationship to cardiovascular instability on dialysis.

In the past, cardiac changes in renal failure have commonly been ascribed to hypertension and poorly specified toxic effects ('uraemic cardiomyopathy'). Our recent experimental and clinical studies suggest (a) that cardiac hypertrophy can be dissociated from hypertension and that blood pressures may have only a permissive role, (b) that experimental uraemia is associated with specific activation of pericytes and intermyocardiocytic fibrosis. Cardiac hypertrophy not correlated with elevated blood pressure, and intermyocardiocytic fibrosis not observed in similarly hypertensive non-uraemic patients, have recently been documented in dialysis patients. The implications of these findings may be (a) electrical instability and predisposition to a sudden cardiac death and (b) diastolic cardiac malfunction with impaired LV filling and predisposition to dialysis hypotension. Some evidence for the latter possibility is provided.

Cardiomegaly↗
PubMed1990

Increased genetic risk of hypertension in glomerulonephritis?

The present study was carried out to test the hypothesis that the familial risk of hypertension is elevated in individuals with glomerulonephritis. Sixty-three parents of 39 consecutive patients below the age of 50 years who were admitted with biopsy-confirmed primary glomerulonephritis (excluding familial glomerulonephritis) were examined. Of these parents, 57% had blood pressure greater than or equal to 160/95 mmHg and/or were taking antihypertensive medication (81% of hypertensives). In 138 parents of 87 controls (age- and sex-matched patients admitted to a surgical ward for trauma), hypertension was found in 32.6% (of whom 73% were on antihypertensive medication). Age, sex ratio and body mass index were comparable in both groups of parents. A similar proportion of parents of patients with glomerulonephritis (27%) and parents of controls (25%) had already died. There was no evidence of excess cardiovascular or renal mortality in either group of parents. Urinary abnormalities were found in a similar proportion of the parents of patients with glomerulonephritis (5%) and controls (8%). Although the effects of a shared environment are not formally excluded, the data are consistent with a possible increased genetic risk of hypertension in patients with primary chronic glomerulonephritis.

Age Factors↗
PubMed1990

Detrimental and beneficial effects of converting enzyme inhibitors on the kidney.

It has been recognized recently that even minor elevations in blood pressure contribute to progression of renal failure and that antihypertensive treatment retards progression. Despite suggestive experimental data, no unequivocal clinical evidence is available to date to document that converting enzyme inhibitors (CEIs) are superior to alternative antihypertensive agents with respect to halting progression. CEIs undoubtedly reduce albuminuria, independent of their effect on systemic blood pressure, and this is related to alteration of glomerular permselectivity. Recent experimental data suggest that growth processes in damaged kidneys are an important aspect of progression. It is a fascinating perspective, but yet unproven, that CEIs interfere with these processes.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1990

Blood pressure in minimal change and other types of nephrotic syndrome.

Blood pressure was evaluated in adult patients (n = 9) and children (n = 57) with nephrotic syndrome and minimal change glomerulonephritis (GN). Prior to steroid treatment in the edematous phase, hypertension was found in 78% of adults (BP greater than or equal to 140/90 mm Hg or antihypertensive treatment other than diuretics) and 95% of children (BP greater than 95 percentile of age). After complete remission, the prevalence of hypertension decreased to 33% in adults and 19% in children. In 21 children with early focal segmental glomerulosclerosis, the prevalence of hypertension (BP greater than 95th percentile) was 91% and 24% after complete remission. In 20 adult patients with membranous GN, the prevalence of hypertension in the edematous phase was 89% and 30% after complete or partial remission. It is concluded that, irrespective of age, hypertension is a common feature of the nephrotic syndrome unrelated to steroid therapy or renal failure.

Adult↗
PubMed1990

Growth hormone induced rise in glomerular filtration rate is not obliterated by angiotensin-converting enzyme inhibitors.

In 8 healthy normotensive probands with normal glomerular filtration rate, the effect of recombinant human growth hormone (rhGH) on inulin clearance (Cin) was examined in an open study with intraindividual crossover with or without enalapril pretreatment (20 mg/day). rhGH was administered by subcutaneous injection (4.5 U twice daly) for 3 days. On the following day Cin was measured with an enzymatic steady state infusion technique. Systemic hemodynamics and potential metabolic effects of rhGH, i.e., inulin-like growth factors I and II, somatomedin-binding protein, glucagon, C peptide, amino acid pattern, etc., were monitored. On controlled dietary intake of protein, the median Cin rose 72 h after start of rhGh administration from 114 (range 91-158) to 135 (108-167) ml/min/1.73 m2 without enalapril pretreatment (p less than 0.01) and from 111 (88-153) to 131 (100-173 ml/min/1.73 m2 with enalapril pretreatment (p less than 0.02). The results confirm that (1) rhGH increases Cin to a similar extent as extractive GH and (2) further demonstrate that this action is not obliterated by blocking the circulating converting enzyme.

Adult↗
PubMed1990

Use of angiotensin-converting enzyme inhibitors for the preservation of kidney function. A retrospective study.

To investigate the effects of angiotensin-converting enzyme (ACE) inhibitors on renal outcome in patients with renal insufficiency, a 2-part study was conducted. Part A consisted of a retrospective 1-year analysis of 80 hypertensive outpatients with serum creatinine levels of 1.5-6 mg/dl, 39 of whom received ACE inhibitors and other antihypertensive agents and 41 of whom received only other antihypertensive agents. Median serum creatinine levels in the ACE group rose acutely from 2.33 to 2.7 mg/dl after 1 month of therapy and remained stable thereafter. Serum creatinine levels more than doubled in 2 patients. In controls, median serum creatinine levels rose gradually over 12 months from 2.39 to 3.45 mg/dl, and serum creatinine more than doubled in 9 patients. Part B consisted of a prospective follow-up of patients for a second year; 34 patients in the treatment group and 32 controls were then analyzed; median serum creatinine level was 3.0 vs. 4.4 mg/dl after 2 years; 2 of 34 vs. 6 of 32 patients were on dialysis; serum creatinine level had more than doubled in 4 of 34 vs. 8 of 32. These results suggest that ACE inhibitors are more effective than other antihypertensive agents in reducing the progression of renal failure.

Adult↗