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E Ritz

Publications and source records attributed to E Ritz.

At least 469 records · Page 26Linked to original sources
PubMed1993

Nephroprotective effect of ACE inhibitors.

In most cases of renal disease, progression of renal failure occurs via nonspecific mechanisms that can be dissociated from the primary cause of renal damage. Progression of disease is accompanied by glomerulosclerosis and tubulointerstitial fibrosis. Loss of autoregulation and afferent renal vasodilation renders the glomerular microcirculation particularly susceptible to systemic hypertension. Glomerular growth is an ancillary factor permitting the development of glomerulosclerosis. Experimental and clinical studies indicate that angiotensin converting enzyme (ACE) inhibitors may prevent progressive renal deterioration. Furthermore, it appears that this effect can be dissociated, at least in part, from the haemodynamic effects of ACE inhibitors. Some evidence indicates that the renal-protective effects of ACE inhibitors results from their effects on glomerular growth and glomerular permselectivity. The role of reduced generation of angiotensin II or accumulation of kinins in the renal effects of ACE inhibitors is under investigation. Prospective clinical trials have demonstrated that ACE inhibitors reduce proteinuria and interfere with progression of renal disease to a greater degree than can be explained by their blood pressure lowering effects alone.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1993

Differential effects of ACE inhibitors and vasodilators on renal function curve in patients with primary hypertension.

OBJECTIVE: In experimental studies differential effects of antihypertensive agents on the renal function curve have been observed: in SHR captopril lowered the slope of the renal function curve, i.e. blood pressure (BP) became salt sensitive, whereas hydralazine shifted the curve without changing its slope. To evaluate whether ACE inhibitors and vasodilators have different effects on salt sensitivity of BP in humans, we compared the effect of the ACE inhibitor cilazapril and the vasodilator dihydralazine on the renal function curve in a randomized prospective single blind cross-over study. DESIGN: Nine patients (1 f, 8 m, mean age 41 +/- 4 y) with mild to moderate primary hypertension were put on low (20 mmol/d) and on high salt diet (200 mmol/d). Drugs were given in random low salt+cilazapril, high salt+cilazapril; low salt+dihydralazine, high salt+dihydralazine; or in reverse order. RESULTS: All antihypertensive interventions lowered BP, but the averaged posttreatment MAP was significantly (p < 0.02) lower with cilazapril on low salt intake (83.6 +/- 2.8 mmHg) than with all of the following: cilazapril on high salt intake (86.4 +/- 2.9 mmHg), dihydralazine on low (91.6 +/- 3.2 mmHg) and high salt (90.1 +/- 3.3 mmHg) intake. Probably as a result of sympathetic activation, average daily heart rate was higher after dihydralazine on low (72.9 +/- 2.9 b/min) and high salt intake (72.4 +/- 2.8 b/min) than after cilazapril on either salt intake (68.7 +/- 3.1 and 62.7 +/- 3.2 b/min). CONCLUSIONS: The results document that BP reduction after acute ACE inhibition is a function of salt intake, i.e. with ACE inhibitor therapy, BP is "salt sensitive". In contrast, vasodilators of the dihydralazine type have similar antihypertensive effects on low and high salt intake. To the extent that the findings of this short-term study can be extrapolated to long-term effects they suggest that intrarenal mechanisms, i.e. resetting of the pressure-natriuresis relationship, are involved in the long-term antihypertensive action of ACE inhibitors.

Adult↗
PubMed1993

Structural causes of cardiac dysfunction in uremia.

While coronary heart disease is undoubtedly a major cause of cardiac morbidity and mortality in uremia, important noncoronary problems contribute to the common presence of cardiac problems. Based on clinical and experimental studies, we could show: (i) Left ventricular hypertrophy (LVH) can be dissociated, at least in part, from elevation of blood pressure. (ii) In uremia, PTH-dependent intermyocardiocytic fibrosis occurs; it may account, at least in part, for disturbed LV compliance and contribute to the arrhythmogenic potential. (iii) Blood pressure-independent abnormalities of intracardiac arterioles and reduced myocardial capillary supply are observed.

Animals↗
PubMed1993

Serum lipid changes on low salt diet. Effects of alpha 1-adrenergic blockade.

An increase of some serum lipid fractions has been documented in normotensive healthy volunteers and patients with essential hypertension during acute drastic restriction of salt intake. To clarify the potential role of vasopressor systems, particularly the sympathetic system, in the lipid changes induced by salt restriction, we compared fasting serum lipids, glucose, insulin, and C-peptide levels in 16 normotensive healthy volunteers during 7 days of high (200 mmol/day) and 7 days of low (20 mmol/day) salt intake. The individuals were examined on either placebo or on the alpha 1-adrenergic blocker doxazosin (2 mg/day). The study was carried out using a single blind parallel group random order design with two arms of treatment. In the volunteers on placebo, total cholesterol (corrected for hemoconcentration) was significantly higher (P < .01) during low salt intake. The same was true for LDL-cholesterol, whereas HDL-cholesterol and triglycerides did not change with salt intake. The lipid changes, and, in parallel, the changes of hemoconcentration indicators, were more pronounced after 2 days than after 7 days of low salt intake. The rise of total and LDL-cholesterol on low salt was blunted after alpha 1-adrenergic blockade with doxazosin. Fasting glycemia was similar on low salt and high salt, respectively, but in placebo treated volunteers, C-peptide levels were significantly (P < .01) higher on low, rather than high, salt intake. alpha 1-Adrenergic blockade with doxazosin attenuated the rise of C-peptide levels on low salt. The results confirm previous findings that levels of total cholesterol and LDL-cholesterol change inversely with salt intake in normotensive healthy volunteers.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Antagonists↗
PubMed1993

[Dyslipoproteinemia: its importance in nephrology].

Dyslipidemia is a common feature of renal failure. It is primarily caused by delayed catabolism of lipoprotein particles. This is due to decreased activity of the key enzymes of delipidation of lipoprotein particles (LPL, HTGL) and of HDL remodeling (LCAT). In epidemiological studies no correlation has been found in dialysis patients between total lipids and atherosclerotic endpoints and a modest relation, at best, between more sophisticated apolipoprotein indices and vascular disease. Such lack of correlations are presumably explained by malnutrition as a confounding factor. Fascinating new observations in animal studies document that in various models of renal damage, development of glomerulosclerosis is accelerated by hyperlipoproteinemia, either endogenous hyperlipoproteinemia or hyperlipoproteinemia induced by feeding of fat. Conversely, correction of hyperlipoproteinemia mitigates development of glomerulosclerosis. Currently there is no firm evidence that the same is true in humans.

Animals↗
PubMed1993

ANCA in haemodialysis patients.

The prevalence of positive ANCA as well as the prevalence of PR-3 and MPO antibodies were examined in a cross-sectional sample of 1277 haemodialysis patients from 16 German haemodialysis centres. We found 32 patients positive for c-ANCA (median titre 1:40; range 1:20-1:320) and 65 for p-ANCA (1:80; 1:20-1:1280). Twenty-two percent of the c-ANCA-positive and 31% of the p-ANCA-positive patients had PR-3 and MPO antibodies by ELISA respectively. Clinical evidence of vasculitis was found in 11 of 32 c-ANCA-positive and 19 of 65 p-ANCA-positive patients. Of the 11 c-ANCA-positive, four had a known diagnosis of Wegener's granulomatosis (WG); WG was recognized after the test in a further five patients and two had renal limited RPGN. Of the 19 p-ANCA-positive patients, three had a clinical diagnosis of microscopic polyarteritis (MP), MP was newly diagnosed in a further 12, WG in one and renal limited RPGN in three. The patients had not received cyclophosphamide (the diagnosis had been non-specified 'systemic disease'). Thus false-positive ANCA, as defined by absence of vasculitis, was found in 5% of dialysis patients versus 0% in patients with preterminal renal failure (n = 152) or blood donors (n = 150). Patients with vasculitis tended to have higher c-ANCA and p-ANCA titres respectively, but there was a considerable overlap. Titres were not higher in patients symptomatic at the time of examination (6 of 11 c-ANCA and 10 of 19 p-ANCA), but PR-3 and MPO ELISA were positive in all but two.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Contrasting renal haemodynamic effects of protein in normal subjects and glomerulonephritic patients with impaired renal function.

The effects of a protein load on renal haemodynamics in patients with renal failure are controversial. We measured insulin clearance (Cin) and PAH clearance (CPAH) by constant infusion technique in six healthy subjects and 13 patients with biopsy-confirmed glomerulonephritis and chronic renal failure. The subjects were pre-equilibrated on their usual diet and studied before and 2 h after 1 g protein/kg as cooked red meat. In healthy subjects this caused a significant increase of Cin (from 136 +/- 7.2 (SD) to 148 +/- 7.9 ml/min/1.73 m2) and of CPAH (from 547 +/- 142 to 639 +/- 89). In contrast Cin decreased from 72.7 +/- 7.7 to 60.3 +/- 8.4 in patients with chronic renal failure, whereas CPAH showed no significant change (from 275 +/- 67.8 to 278 +/- 72.7). A similar decrease of Cin was also seen with acute infusion of amino acids (AA). The change in Cin was not related to changes of PRA or concentrations of plasma amino acids. While absolute and fractional Na excretion increased in controls, they decreased in patients in parallel with the decrease of Cin. The decrease of Cin after infusion of AA was amplified by pre-equilibration on low-sodium diet (20 mmol Na/day). The effect of meat ingestion on Cin was not obliterated, however, by pretreatment with captopril (25 mg b.i.d. for 7 days). In conclusion, in patients with chronic renal failure, a paradoxical decrease in Cin is seen both after oral protein and after amino-acid infusion.

Adult↗
PubMed1993

[Dialysis-associated amyloidosis. Part 1: Biochemistry, clinical aspects, roentgen morphology].

Dialysis-related amyloidosis is characterized clinically by the carpal tunnel syndrome, pain and swelling of joints. These alterations are due to amyloid deposits in the carpal tunnel, in the synovia, ligaments and bones. It has been shown that beta 2m is the major component of this amyloidosis. Serum and urine concentration of beta 2m are markedly elevated in chronic renal failure due to failure of filtration and lack of metabolism by the renal tubular epithelium. beta 2m-derived amyloid is identified by immunohistochemistry using antibodies derived against beta 2m. Radiology shows cyst-like periarticular bone defects, destructive arthropathy and spondylarthropathy.

Amyloidosis↗
PubMed1993

[Dialysis-associated amyloidosis. Part 2: Incidence and site of osseous amyloidosis. Dialysis characteristics and clinical findings].

In a conventional radiographic skeletal survey of 90 hemodialyzed patients, 28% (25 patients) showed renal osteopathy; 27 patients (30%) had periarticular bone cysts and 3 patients (3%) presented radiological evidence of destructive spondylarthropathy. The bone cysts were most commonly identified in the carpal bones and around the hips and shoulders; destructive spondylarthropathy was seen in the cervical and lumbar spine. Whereas characteristic radiographic changes of renal osteodystrophy could already be identified in the 1st year of dialysis, periarticular bone cysts occurred at the earliest after 2 years, most frequently after 5 years of dialysis. Destructive spondylarthropathy was seen after more than 10 years of dialysis. A positive correlation between these bone lesions and secondary hyperparathyreoidism, dialysis membranes or renal diseases was not found.

Adult↗
PubMed1993

Immunogenetic findings in glomerulonephritis.

In the 19th century, several authors recognized that some renal diseases tend to run in families. Alport pointed to the constellation of nephritic urinary sediment, hearing loss and progression into renal failure. Today this is recognized to result from abnormal basement membrane (BM) collagen synthesis. Recently it has been recognized, however, that other forms of glomerulonephritis may also run in families. In about 10% of patients with glomerulonephritis one or more sibling also suffers from glomerulonephritis. Genetically determined derangements of immune regulation may play a role in the genesis of primary chronic glomerulonephritis. Potentially associated immunogenetic abnormalities include inherited defects of the complement system, increased prevalence of certain HLA-types, altered frequencies of polymorphisms in immunoglobulins and TCR genes and others. This overview summarizes immunogenetic studies performed in patients with glomerulonephritis with special emphasis on patients with mesangial IgA GN.

Complement System Proteins↗
PubMed1993

[Hypercalcemia].

Explore the source record for details and available documents.

Adult↗
PubMed1993

Kinetics of serum 1,84 iPTH after high dose of calcitriol in uremic patients.

The temporal relation between oral administration of calcitriol and the nadir of PTH concentration is important for selecting optimal schedules of administration of calcitriol in the treatment of secondary hyperparathyroidism. To further assess this issue we examined 9 patients with preterminal renal failure (3 females, 6 males; median age 58.0 years, range 47-64, median S-Crea 4.8 mg/dl, range 3.7-6.8) with elevated baseline concentrations of 1,84 iPTH (median 46.0 pmol/l, range 18-100). After ingestion of a single oral dose of 2.0 micrograms calcitriol a transient rise in 1,25(OH)2D3 levels was seen with a peak at 6 h (from 20 pg/ml; 14-52 to 43 pg/ml; 35-102). 1,84 iPTH levels did not significantly change in the first 24 h, but were decreased significantly (p 0.01) 48 h after a single oral dose of calcitriol, the time to reach nadir varying from 24 to 96 hours. The percent decrease wa highest in patients with the highest baseline concentrations of 1,84 iPTH. Median 1,84 iPTH levels continued to remain below baseline at 48 h (25.0 pmol/l), 72 h (24.0 pmol/l) and 96 h (24.0 pmol/l) after oral calcitriol. A modest increase of S-Ca was noted which was not statistically significant. We conclude that 1. a single dose of oral calcitriol causes a delayed but long-lasting decrease of 1,84 iPTH, 2. decreased 1,84 iPTH levels persist despite return of calcitriol concentrations to baseline levels and 3. 1,84 iPTH may remain below baseline for more than 96 h.

Calcitriol↗
PubMed1992

Subacute effects of thiazide administration on renal hemodynamics and calcium metabolism.

To elucidate the renal effects of thiazides as a function of sodium intake, 8 healthy volunteers without renal disease were studied at baseline and 1 day as well as 4 days after the administration of 100 mg hydrochlorothiazide/day. The subjects were compared on two different dietary sodium intakes (120 mmol/day and 220 mmol/day). Measurements comprised inulin clearance (Cin) and paraaminohippurate clearance (Cpah) by infusion clearance technique, total and ionised calcium, immunoreactive parathyroid hormone (1.84 iPTH), 1.25 (OH)2 vitamin D3, and indices of hemoconcentration. Acute administration of hydrochlorothiazide (HCTZ) caused no change in Cin (before 111 +/- 3 ml/min 1.73 m2; 24 h after, 107 +/- 2 ml/min 1.73 m2) or Cpah (before, 579 +/- 9 ml/min 1.73 m2; after, 584 +/- 12 ml/min 1.73 m2), while a significant (P less than 0.01) decrease was noted on the 4th day after 100 mg HCTZ/day and normal sodium intake. No significant change of creatinine clearance (Ccr) was seen with either manouever. Renal hemodynamic changes after HCTZ administration were marginal when hemoconcentration was prevented by a high salt intake. Acute administration (1 h) of HCTZ caused suppression of 1.84 iPTH (before, 2.3 +/- 0.5 pmol/l; after, 1.9 +/- 0.2 pmol/l; P less than 0.01), but after 4 days a lower ionised calcium (baseline, 1.25 +/- 0.01 mmol/l; day 5, 1.20 +/- 0.02 mmol/l; P less than 0.01) was noticed in parallel with hemoconcentration, metabolic alkalosis, and reduced 1.25 (OH)2 vitamin D3 concentrations.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Disturbed calcium metabolism in subjects with elevated diastolic blood pressure.

Essential hypertension has been associated with disturbed calcium metabolism, but the available data are controversial. We measured parameters of calcium metabolism in groups of untreated male subjects (n = 78) with elevated diastolic blood pressure (101 +/- 6 mmHg, mean +/- SD) and age-matched male subjects (n = 79) with low diastolic blood pressure (62 +/- 4 mmHg). The participants of the study were drawn from a random population sample. Subjects with high diastolic blood pressure had significantly higher carboxy-terminal parathyroid hormone (PTH) plasma concentrations than controls with low diastolic blood pressure (median 114 vs. 43 pmol/l, P less than 0.01). The 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D concentrations were comparable in both groups. Individuals with high diastolic blood pressure had significantly lower total serum calcium (2.41 +/- 0.10 vs. 2.47 +/- 0.10 mmol/l, mean +/- SD; P less than 0.01). PTH concentrations were correlated with diastolic pressure (r = -0.39, P less than 0.001). The data are compatible with increased parathyroid activity despite unchanged concentrations of vitamin D metabolites in human hypertension.

Adult↗