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Biomedical subjects

E Ritz

Publications and source records attributed to E Ritz.

At least 397 records · Page 22Linked to original sources
PubMed1994

Renal involvement in type II diabetes.

The incidence and prevalence of renal failure from type II diabetes have been seriously underestimated in the past. Currently, the incidence of uremia in patients with type II diabetes has increased continuously in Europe and the United States, mainly because of better patient survival (ie, they now live until nephropathy develops) and possibly because of a rising prevalence of type II diabetes in the general population (ie, more patients are at risk of developing nephropathy). Generally, renal hemodynamics and glomerular lesions are similar in type I and type II diabetes, but glomerular histology is more diverse in type II diabetes. Given the high prevalence of diabetes and renal failure from various causes in the elderly, coexistence of the two (even in the absence of glomerulosclerosis) occurs in approximately 20% of uremic type II diabetic patients. The development of nephropathy is controlled by strong genetic determinants, but these have not been further characterized.

Animals↗
PubMed1994

Clinical nephrology in 19th century Germany.

Bright's work led to the recognition that coagulable protein in the urine indicated macroscopic kidney disease. After light microscopy was introduced, Simon, Nasse, Henle and Frerichs identified the major constituents of urinary sediment. By 1896, Senator had deduced that hyalin cylinders arise in the kidney tubules, and only the discovery of the Tamm-Horsfall protein in the next century separated him from the modern concept. Chemical analysis of urine also advanced greatly. Recognition of the pressure-volume relationship by Traube was probably the most brilliant achievement related to renal disease, and became the basis of the later pressure-natriuresis relationship. Traube also linked left ventricular hypertrophy with renal disease, recognizing that it maintained circulatory homeostasis at a higher level of pressure. The concept of nephritis changed considerably with technical progress, and Gluge was the first to see inflamed Malpighian bodies or glomeruli. The primary site of damage was disputed by many, including Henle, Pfeufer, Virchow, Reinhardt and Frerichs, but all these workers had to reconstruct the sequence of events leading to the autopsy findings. The term glomerulonephritis was first coined by Klebs, and the classification of nephritis adopted by Senator in 1896 led directly to the classic monograph of Volhard and Fahr (1914) on Bright's disease.

Germany↗
PubMed1994

The history of urinary microscopy to the end of the 19th century.

In the 17th and 18th centuries, several authors performed urinary microscopy occasionally and were often unable to give their observations a practical diagnostic application. Such men included De Peiresc, Boerhaave, Ledermüller and Galeazzi. In the 1st half of the 19th century, however, urinary microscopy began to be used systematically. Rayer and Vigla identified for the first time elements other than crystals in urine and contributed to the methodology of handling samples for microscopy. Becquerel described dysmorphic erythrocytes, and Simon and Henle observed casts in urine and in histological preparations. In contrast, Bird mentioned casts only in passing, though he described many other elements and published the first complete book on urinary microscopy. The 2nd half of the 19th century was characterized by further advances, and in the book of Beale tubular cells were distinguished from other epithelial cells. Different types of casts were also linked with different renal diseases. By 1875 the classification of casts was complete. The work of the 19th century microscopists culminated in Rieder's book on clinical microscopy, which described each element of urinary sediment through 36 beautiful chromolithographic plates.

England↗
PubMed1994

Pathophysiology and treatment of hypertension and oedema due to renal failure.

Hypertension and oedema resulting from sodium retention are the main indications for diuretic treatment in patients with chronic renal failure. The pharmacokinetics of most loop diuretics and their active metabolites are altered in chronic renal failure, due both to reduced transtubular transport via the proximal tubular anion transporter and to protein binding within the tubule. In chronic renal failure, the reduced number of nephrons leads to adaptive reduction of tubular sodium reabsorption, i.e. high baseline fractional natriuresis and increased absolute distal tubular sodium reabsorption. These processes interfere with the pharmacodynamic actions of diuretics. Therapeutic strategies to overcome the partial resistance to the action of diuretics in patients with chronic renal failure include the use of high doses, continuous administration and the combination of loop and thiazide compounds.

Diuretics↗
PubMed1994

Comparison of intermittent and continuous oral administration of calcitriol in dialysis patients: a randomized prospective trial.

Intermittent bolus administration of calcitriol--i.e., 1,25-dihydroxycholecalciferol or 1,25-(OH)2D3--is highly efficacious in dialysis patients. In experimental studies, intermittent administration of calcitriol is superior to continuous administration in suppressing preproparathyroid hormone (PTH) mRNA and circulating PTH concentrations. In a randomized, prospective, open multicenter trial 45 dialysis patients with elevated 1,84-iPTH (> or = 20 pmol/l, normal 1-6 pmol/l) levels were randomly allocated to daily administration of 0.75 microgram calcitriol (continuous) or twice weekly administration (intermittent); the two protocols provided an identical total weekly doses of 5.25 micrograms calcitriol. Patients were dialyzed with a dialysate Ca concentration of 1.75 mmol/l and had oral CaCO3 or Ca acetate. 1,84-iPTH (immunoradiometric assay) and serum Ca and Pi levels were measured weekly. At the beginning of the study, the median 1,84-iPTH value was 37 pmol/l (range 20-115) in the intermittent versus 36 pmol/l (range 21-72) in the continuous calcitriol group. After 2 weeks, the median 1,84-iPTH level was 18.5 pmol/l (range 1.4-106) versus 18 pmol/l (range 1.2-48). After 12 weeks, 11 of 21 of the patients in the intermittent and 18 of 24 patients in the continuous group had reached the treatment goal, i.e., 1,84-iPTH < or = 10 pmol/l without hypercalcemia or hyperphosphatemia. There were seven episodes of hypercalcemia (> 2.7 mmol/l) in the intermittent versus two in the continuous group; the mean peak Ca level was 2.8 mmol/l (range 2.76-3.0) versus 2.9 mmol/l (range 2.74-3.06). There were 21 versus 17 episodes, respectively, of hyperphosphatemia (> 2.2 mmol/l).

Administration, Oral↗
PubMed1994

Metabolic clearance of recombinant human growth hormone in health and chronic renal failure.

Despite the increasing therapeutic use of recombinant human growth hormone (rhGH), its metabolic clearance has not been investigated in detail. To evaluate the kinetics of rhGH as a possible function of GH plasma concentration and glomerular filtration rate (GFR), we investigated the steady state metabolic clearance rate (MCR), disappearance half-life, and apparent volume of distribution of rhGH at low and high physiological as well as supraphysiological plasma GH levels during pharmacological suppression of endogenous GH secretion in human subjects with normal and reduced renal function. GH in plasma and urine was determined by an immunoradiometric assay, and GFR by inulin clearance. In all subjects MCR decreased and plasma half-life increased with increasing plasma GH concentrations (P < 0.001). MCR of rhGH was approximately half in patients with chronic renal failure at each GH level and plasma half-life was increased by 25-50%. Allowing for the linear dependence of MCR on GFR and assuming single-compartment distribution, the estimated renal fraction of total MCR was 25-53 and 4-15% in controls and patients, respectively. Saturation of extrarenal disposal of GH was suggested by an inverse hyperbolic relationship between extrarenal MCR and plasma GH concentrations in all subjects. Fractional GH excretion was up to 1,000-fold higher in patients than in controls. We conclude that MCR of hGH is a function of plasma GH concentrations and GFR. Extrarenal elimination is saturable in the upper physiological range of GH concentrations, whereas renal MCR is independent of plasma GH levels. The kidney handles GH like a microprotein involving glomerular filtration, tubular reabsorption, and urinary excretion.

Adolescent↗
PubMed1994

Synergistic effects of parathyroid hormone and 1,25-dihydroxyvitamin D3 on proliferation and vitamin D receptor expression of rat growth cartilage cells.

We investigated possible interaction of 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3] and PTH on: 1) proliferation (monolayer culture) and colony formation (agarose stabilized suspension cultures); 2) expression of 1,25-(OH)2D3 receptor (VDR); and 3) cAMP response to PTH, using primary cultures of chondrocytes from rat tibia proximal epiphysis. 1 alpha,25-(OH)2D3 stereospecifically stimulated DNA synthesis, cell counts, and colony formation at low concentration (10(-12) M). Within 6 h bovine PTH (bPTH)(1-34), human PTH (hPTH)(28-48) (10(-10) M), (Bu)2cAMP (1-2 mM), and 12-O-tetradecanoyl-13-acetate (10(-8) M) increased [3H]thymidine incorporation in the absence and presence of 1,25-(OH)2D3. Both PTH fragments also stimulated chondrocyte growth and colony formation in a Ca-dependent fashion. Prolonged exposure to bPTH(1-34) or hPTH(28-48) did not affect baseline DNA synthesis but increased the stimulatory effect of 1,25-(OH)2D3. This increase was inhibited in the presence of H7 (inhibition of PKC) or the monoclonal hPTH(1-38) antibody A1-70. In subconfluent chondrocyte cultures VDR was up-regulated by bPTH(1-34) and hPTH(28-48) (10(-10) M) or activators of protein kinase C (PKC), but not by (Bu)2cAMP. It was blocked by cycloheximide and actinomycin D and persisted in the presence of Ca-channel blockers. Inhibition of PKC by H7 also blocked the effect of bPTH(1-34) on VDR. The cAMP response to bPTH(1-34) was not affected by 1,25-(OH)2D3. We conclude that: 1) DNA synthesis, cell proliferation, and colony formation in chondrocyte monolayer or suspension cultures is increased by aminoterminal and midregional PTH fragments and by cAMP analogs in a Ca- dependent fashion; 2) bPTH(1-34) and hPTH(28-48) up-regulate VDR by cAMP-independent, PKC-dependent steps requiring transcriptional and translational processes; both PTH fragments also amplify the effect of 1,25-(OH)2D3 on DNA synthesis; and 3) no difference is found between the bPTH(1-34) and hPTH(28-48) fragments with respect to chondrocyte proliferation and VDR up-regulation, although the two differ with respect to stimulation of cAMP production.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1994

A role of parathyroid hormone for the activation of cardiac fibroblasts in uremia.

Intermyocardiocytic fibrosis, i.e., nonreparative interstitial fibrosis with collagen fiber deposition, is commonly found in uremic patients and animals. The volume density of interstitial tissue in the left papillary muscle of uremic animals was found to be increased (from 1.9 +/- 0.7 to 4.2 +/- 1.1%; P < 0.001). The nuclei of interstitial cells, but not of endothelial cells, were enlarged, pointing to an activating signal that specifically acts on interstitial cells. Because of the known action of parathyroid hormone (PTH) on the heart, a potential role of PTH in the genesis of fibrosis was explored by comparing subtotally nephrectomized (NX) parathyroidectomized (PTX) rats receiving by osmotic minipump either saline or rat 1,34 PTH (100 ng/kg per hour dissolved in NaCl). Animals were on a standard 0.95% Ca diet. After PTX, they were switched to a high-calcium (3%) diet. At the end of the 14-day experiments, NX-PTX-PTH animals and NX-PTX-solvent animals were comparable with respect to mean body weight (335 versus 338 g), serum creatinine (1.2 versus 1.2 mg/dL), and serum-Ca (2.66 versus 2.63 mmol/L). The volume densities of cardiac interstitium were 4.71 +/- 0.87 versus 1.49 +/- 0.49, and those of capillaries were 8.07 +/- 1.54 versus 7.94 +/- 2.62, respectively (P < 0.001 by analysis of variance). Thus, PTX abolished and PTH restored intermyocardiocytic changes of experimental uremia. These observations argue for a permissive role of PTH for fibroblast activation and the genesis of the cardiac fibrosis of uremia.

Animals↗
PubMed1994

Changes in the kinetics and biopotency of luteinizing hormone in hemodialyzed men during treatment with recombinant human erythropoietin.

To investigate the effect of recombinant human erythropoietin (rh-EPO) on the hypothalamo-pituitary-gonadal axis in end-stage renal failure, plasma luteinizing hormone (LH) concentration release was assessed by frequent blood sampling (every 10 min), both during an 8-h baseline period and after stimulation with an iv bolus of gonadotropin-releasing hormone (GnRH). Seven adult hemodialyzed men were studied before and after partial correction of anemia by rh-EPO treatment. LH was determined by an in vitro Leydig cell bioassay (bio-LH) and a highly sensitive immunoradiometric assay. Pulsatile bio-LH secretion and clearance characteristics were assessed by multiple-parameter deconvolution analysis. Although the rh-EPO treatment did not lead to a change in average concentrations of plasma bio-LH, the mass of hormone released per secretory burst more than doubled, and the estimated bio-LH production rate increased from 8.8 +/- 2.3 to 15.6 +/- 5.2 IU/L per hour (P = 0.05). The lack of change in mean plasma bio-LH is explained by a simultaneous decrease in plasma half-life from 106 +/- 27 to 67 +/- 19 min (P < 0.02). The decrease in the plasma half-life of bio-LH was closely associated with the rise in hematocrit, suggesting an effect of the increased red blood cell mass on LH distribution space and elimination kinetics. As a consequence of the changes in hormone kinetics, the incremental amplitudes of the plasma concentration pulses of bio-LH increased from 112 to 121% of nadir levels (P < 0.05), resulting in a more distinctly pulsatile pattern of hormone signals.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Role of proteinase/antiproteinase inhibitor disequilibrium in the bioincompatibility induced by artificial surfaces.

As one aspect of bioincompatibility, the importance of activation of proteolytic systems as a result of an imbalance between protease and antiprotease activity has been increasingly recognized. This principle is illustrated by selected studies in our laboratory. These concern (i) generation of kinins on membranes with negative surface charge, (ii) activation of the complement system as a function of binding to the membrane of the regulatory protein H, (iii) generation of thrombin-antithrombin complexes (TAT), and (iv) generation of plasmin/antiplasmin complexes with an interesting discrepancy between in vivo and in vitro.

Animals↗
PubMed1994

Progression of renal failure in the Han: SPRD polycystic kidney rat.

The Han: SPRD Pkd rat mutant is an autosomal dominant rat model with incomplete penetration of polycystic renal transformation. Progressive renal failure occurs in heterozygous male animals. The mechanisms of progression have not been elucidated. To identify some pathogenetic factors involved we subjected male SPRD Pkd rats (and their non-affected littermates as controls) to uninephrectomy (UNX), castration or enalapril treatment. To assess progression S-urea at age 150 days was chosen as endpoint. (i) In uninephrectomized male Han: SPRD Pkd (n = 12 animals per group) S-urea at age 150 days was consistently above 300 mg/dl, while it was 245 mg/dl (191-290) in control Han: SPRD Pkd. (ii) In castrated male Han: SPRD median S urea at 150 days was 100 mg/dl (69-211) compared to sham-operated male Han: SPRD controls (245; 191-290). Castration did not, however, prevent accelerated progression after uninephrectomy. (iii) Enalapril (50 mg/l) in the drinking fluid did not significantly lower median systolic blood pressure (by plethysmography) in animals on 0.2% sodium diet (at 185 days 160 mmHg; 140-170 versus 170; 140-195 in non-enalapril controls), although circulating ACE was significantly inhibited (17 U; 11-33 versus 89; 52-108 in controls). S-urea at age 185 days was not significantly different in the 2 groups. In conclusion, the Han: SPRD Pkd model differs from human ADPKD to some extent. Uninephrectomy accelerates renal failure in the rat, but not in humans. On the other hand, in contrast to human ADPKD the renin system is suppressed in the rat model and ACE inhibition does not affect the course of renal failure.

Animals↗
PubMed1994

Excess cardiovascular mortality in the uremic patient--what does it teach for other risk factors in the non-renal patient?

A high rate of cardiovascular death in renal patients, particularly patients with endstage renal failure, has not been well appreciated in the past. It is obvious that cardiovascular lesions are more severe than can be explained by the classical risk factors of elevated blood pressure and dyslipidemia. In renal failure, a number of pathomechanisms are operative which may be paradigms of more general relevance, e.g. activation of the renin and sympathetic system, inhibition of the vasoconstrictor NO system, left ventricular hypertrophy in excess of what is expected for high blood pressure. A paradox inverse relation between lipid concentrations and cardiovascular death, i.e. a protective effect of hyperlipidemia, in dialysed patients, presumably results from the confounding effect of malnutrition, high lipid levels being a substitute marker of adequate nutrition.

Animals↗