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Biomedical subjects

E Ritz

Publications and source records attributed to E Ritz.

At least 415 records · Page 23Linked to original sources
PubMed1994

[Diagnosis and therapy in systemic vasculitis with renal involvement].

The diagnosis of Wegener's granulomatosis, microscopic polyarteritis and idiopathic rapidly progressive glomerulonephritis as the main cause of renal involvement in systemic necrotizing vasculitis was revolutionized following the introduction of the ANCA test. The different clinical manifestations of these diseases are described. By means of the ANCA test it could be demonstrated that the pulmonary-renal syndrome was mainly caused by these vasculitides and not by Goodpasture's syndrome. Cyclophosphamide and steroids remain the drugs of choice in the treatment. They can be administered in different ways depending upon the clinical manifestation of the diseases. As therapeutic alternatives cyclosporin, trimethoprim/sulfamethoxazole, intravenous immunglobulins and monoclonal antibodies are discussed.

Anti-Glomerular Basement Membrane Disease↗
PubMed1994

Role of infection in the genesis of acute renal failure.

While most experimental models of acute renal failure (ARF) involve ischaemic or toxic damage to the kidney in non-infected animals, a surprisingly large proportion of patients with ARF exhibit signs of septicaemia or systemic reaction to local infections. This clinical observation suggests an important role of infection-related mediator mechanisms in the genesis of ARF. Another important aspect is the occurrence of ARF in the context of infections with nephrotropic viruses (e.g. hantavirus accounting for approximately 5% of non-surgical ARF in Germany) and nephrotropic bacteria (e.g. leptospirosis).

Acute Kidney Injury↗
PubMed1994

Inhibition of growth by calcitriol in a proximal tubular cell line (OK).

Calcitriol has been shown to inhibit (i) cell proliferation of renal carcinoma cell lines and of cultured adult human mesangial cells in vitro, and (ii) renal compensatory growth in vivo. In the present study we examined the effects of calcitriol on DNA synthesis and cell replication in an immortalized cell line showing the phenotypic characteristics of proximal tubular cells (opossum kidney, OK cells). The viability of OK cells was not affected by calcitriol (Trypan-blue exclusion, LDH and K+ release), but the cells did not convert 3H-25(OH)2D3 to 3H-1,25(OH)2D3. In the log growth phase, calcitriol (but not alternative vitamin D metabolites) caused dose-dependent (10(-12) to 10(-6) M) inhibition of radiothymidine incorporation. Inhibition was calcium dependent, i.e. it was more pronounced at the lower nominal calcium concentration in tissue culture media (0.9 versus 1.8 mmol/l) and amplified by coincubation with nifedipine (1 microM). Inhibition of DNA synthesis was paralleled by inhibition of cell replication (growth curve) under basal conditions and after stimulation with EGF (10 ng/ml). In conclusion, calcitriol inhibits proliferation of proximal tubular cells which normally express 1-alpha-hydroxylase activity.

25-Hydroxyvitamin D3 1-alpha-Hydroxylase↗
PubMed1994

Proteinuria and hypertension.

Albuminuria is more prevalent in patients with primary hypertension than in normotensive subjects of the general population. The presence of albuminuria predicts the presence of more severe target organ damage and is related to the risk of cardiovascular events. Preliminary results show albuminuria even in some normotensive individuals with a genetic risk of hypertension and in association with insulin resistance. While albuminuria is generally more frequent in the elderly, it is also found in young patients with mild to moderate primary hypertension. It is uncertain whether in these circumstances albuminuria indicates some "renal component" in the etiology of primary hypertension. Massive albuminuria may occur in subjects with "benign" nephrosclerosis. Whether albuminuria is a predictor of hypertensive renal damage requires further study. Albuminuria is reduced by antihypertensive treatment, but diverse effects on albuminuria are seen with different antihypertensive agents.

Adult↗
PubMed1994

Single-dose oral calcitriol and changes of plasma 1,84iPTH in uremic children.

Both intravenous and oral 1,25(OH)2 D3 pulse therapy are effective in decreasing iPTH in patients with chronic renal failure. In order to understand why intermittent application of calcitriol is effective, we investigated 10 children with advanced renal failure (4 female, 6 male; median age 6.5 [3-16] years; body surface area 0.58-1.57m2; CCR 7 [5-47] mL/min/1.73m2) with elevated baseline concentrations of 1,84iPTH (median 63.5 [9.4-300] pmol/L). After a standard dose of 2 micrograms calcitriol per os (equal to 1.27-3.45 micrograms/m2), serum 1,25(OH)2D3 concentrations increased. The peak concentration occurred after 6 h (3-12), and 1,25(OH)2D3 serum levels returned to baseline by 48 h. 1,84iPTH concentrations were significantly suppressed by 6-72 h. The median maximal decrease was 51.4% of baseline (22.3%-74%). The decrement was a function of baseline 1,84iPTH, but not of 1,25(OH)2D3 serum peak concentration, area under the curve, body surface area, or change in ionized serum calcium. We conclude: (i) oral 1,25(OH)2D3 has a prolonged (up to 72 h) suppressive effect on 1,84iPTH concentrations in uremic patients, and (ii) the wide interindividual variation in suppression of 1,84iPTH was not explained by the kinetics of 1,25(OH)2D3 concentration, which implies that additional factors influence the 1,84iPTH response to 1,25(OH)2D3.

Administration, Oral↗
PubMed1994

Prevalence of immunecomplex-associated glomerulonephritis in hypertensive subjects.

Glomerulonephritis demonstrable by immunohistochemistry may be present at post mortem in many patients without overt renal diseases. Systematic renal biopsies in severely hypertensive patients have shown a high prevalence of clinically undiagnosed glomerulonephritis. We have examined the kidneys of 423 consecutive subjects who came to post mortem and full-filled criteria for the diagnosis of hypertension. Patients were considered to be hypertensive if this had been clinically documented during life or if the heart weight/body weight ratio was > 0.005 in the absence of known other causes of cardiac hypertrophy. Normotensive controls were selected on the basis of clinically documented normal BP or a heart weight/body weight ratio of < 0.001. Kidneys were examined by immunohistology (PAP technique using human IgA, IgG, IgM antibodies). Excluding cases with liver cirrhosis, only two of the 337 patients with hypertension (= 0.6%) and none of the 49 normotensive patients had mesangial IgA deposits (P = 0.77). This finding argues against the frequent occurrence of latent glomerulonephritis in elderly patients with manifest hypertension.

Adolescent↗
PubMed1994

Atherogenesis and cardiac death: are they related to dialysis procedure and biocompatibility?

Cardiac events are a major cause of death in dialysed patients. This is due, at least in part, to the high prevalence of atherosclerotic coronary heart disease. To a large extent, however, coronary lesions are acquired in the predialytic phase of chronic renal failure. The susceptibility of the heart to ischaemia is modulated by a number of factors, e.g. microvascular abnormalities, increased cardiac pulsatile workload, disturbed cardiac glucose metabolism, imbalanced autonomic innervation. The paradoxical result of there being no relationship of cardiac death in dialysis patients to blood pressure may be explained by confounding factors. Intradialytic hypotension appears to be an independent risk factor. The dialysis patient is exposed to hypertension and dyslipidaemia, two potent risk factors of atherosclerosis. Although no definite information is available, it is conceivable that factors related to dialysis procedures may also influence early or late events in atherogenesis. Such potential factors include oxidative modification of lipids, modulation of insulin resistance or glucose metabolism by non-insulin-dependent pathways, expression of adhesion molecules and activation of potential effector cells in atherogenesis, particularly monocytes and platelets, changes of synthesis and/or response to endothelin and nitroxide (EDRF), and possibly also accelerated formation of advanced plaques by hyperphosphataemia and/or hyperparathyroidism. Such proatherogenic mechanisms must be balanced against factors potentially protecting against atherogenesis; these comprise altered arachidonic acid metabolism (increased prostacyclin and decreased thromboxane synthesis), impaired platelet aggregation, antiatherosclerotic effects of heparin, and diminished concentrations of 1,25(OH)2D3, i.e. of a proatherogenic compound.

Arteriosclerosis↗
PubMed1994

Treatment with high doses of loop diuretics in chronic renal failure.

In the late 60s, A. Heidland and his collaborators were amongst the first to characterize the renal action of frusemide in preterminal renal failure by giving quantitative information on dose requirements, fractional Na and K excretion, effects on renal haemodynamics, and by recognizing reversible inner ear dysfunction as the major dose-limiting side-effects. These early studies have been largely reconfirmed. They have been extended by more clearly characterizing (a) altered pharmacokinetics of frusemide, e.g. the importance of altered transepithelial transport in the proximal tubule and intratubular protein binding, and (b) the mechanisms underlying altered pharmacodynamics, particularly high baseline fractional Na rejection and increased absolute distal Na reabsorption. Apart from increasing the dose of frusemide, continuous administration by infusion and combination of frusemide with thiazide diuretics have emerged as rational therapeutic strategies in chronic renal failure.

Animals↗
PubMed1994

Haemodialysis-associated beta 2M amyloidosis: current controversies.

Beta 2M amyloidosis is a major complication of long-term haemodialysis. Beta 2M, the precursor molecule of amyloid fibrils, accumulates in renal failure because of diminished renal excretion. Whether, in addition, a minor increase of synthesis occurs in dialysed patients is still controversial. Beta 2M amyloidosis differs from most other forms of amyloid by its preferential osteoarticular location. This points to some peculiar role of the microenvironment in the synovial space, which is currently poorly defined. A finding which remains so far unexplained is the more delayed appearance of beta 2M amyloidosis in patients dialysed with polyacrylonitrile membranes. In principle, however, beta 2M amyloidosis is seen with all dialysis modalities and possibly even before maintenance dialysis. Differences between treatment modalities relate either to removal of beta 2M or some aspect of bioincompatibility, e.g. proteolytic processing. Finally, the exact chemical nature of amyloid fibrils, i.e. whether they constitute native beta 2M molecules or processed molecules, is currently controversial.

Amyloid↗
PubMed1994

Bioincompatibility--perspectives in 1993.

Bioincompatibility reactions related to the non-physiology of the procedure have plagued dialysis from its early days. Although the problem is certainly multifactorial, the present overview selectively focuses on some aspects of activation of late complement (C) components, the importance of which may have been underappreciated in the past. Dialysis patients are poised for intense C activation because of cumulation of the low molecular weight factor D, an intrinsically active serine esterase which is not inhibited by any known endogenous inhibitor and catalyzes an early step in the alternative pathway. C activation reflects the net balance between activation and inhibition, the latter particularly via factor H binding. Dialyzer membrane characteristics that are related to factor H binding and regulation of initial activation steps include not only membrane surface chemistry but also its microdomain structure. Kinetic studies of the generation of the terminal complement complex (TCC) suggest ongoing generation throughout the duration of a dialysis session (in contrast to the transient release of C-derived anaphylatoxins). Potential consequences of TCC generation include amplification of the non-C-dependent cell activation signals through L-fucose-dependent steps. Efforts to reduce TCC generation by membrane engineering, for example, end group derivatization and optimization of microdomain structure, open perspectives for the development of more biocompatible membranes.

Biocompatible Materials↗
PubMed1994

Postinfectious glomerulonephritis--is there a link to alcoholism?

From January 1984 to May 1993, we observed 30 cases of postinfectious glomerulonephritis (GN)--endocapillary, exudative GN with humps (23 males, 7 females; median age 49 years; range 17-77). They represented 4.5% of all renal biopsies. Crescents were present in 9/26 who had renal biopsies (35%) and there was a mesangioproliferative pattern in 14 (54%). Seventeen of the 30 patients (57%) were alcoholics by history and biochemistry. Cirrhosis was present in 8/17 (47%), but alcoholic hepatitis in none. Nine of the 17 alcoholic (53%) but none of the non-alcoholic patients developed chronic renal failure. Adverse renal prognosis was significantly correlated to alcoholism. We conclude that (i) alcoholism is common in patients with postinfectious GN, and, (ii) alcoholism adversely affects renal prognosis in patients with postinfectious GN.

Adolescent↗