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W Kriz

Publications and source records attributed to W Kriz.

At least 19 recordsLinked to original sources
PubMed1992

The glomerular mesangium: capillary support function and its failure under experimental conditions.

We present a structural analysis of the ability of the biomechanical unit consisting of mesangium and glomerular basement membrane to maintain normal capillary architecture in the face of mechanical challenges due to high intraglomerular pressures. Capillary support function may be considered in terms of the stabilization of local form (development of wall tension against capillary dilation) and global form (centripetal fixation of capillary loops to maintain higher order form). The pathologic consequences of the loss of this support are illustrated by way of experimental models of mechanical mesangial failure. Such failure may express itself as mesangial widening, increased transmesangial macromolecule "traffic," ballooning of capillary segments, and unfolding of capillary loops. Mechanisms are described by which these structural changes may lead to segmental glomerular sclerosis.

Animals↗
PubMed1992

Glomerular damage after uninephrectomy in young rats. I. Hypertrophy and distortion of capillary architecture.

Uninephrectomy (UNX) results in a higher incidence of focal glomerular sclerosis (FGS) in young rats than it does in adults. The reason for this higher susceptibility in young animals is not fully understood, but this does suggest that UNX in young rats may represent a particularly promising model in which to study the development of FGS. In the present study 10-day-old rats were subjected to UNX. After 4, 12 and 24 weeks, glomerular hypertrophy, structural lesions and function were analyzed in comparison with sham-operated controls. Up to the twelfth week, remnant kidney growth and glomerular growth proceeded in parallel; thereafter, kidney growth ceased, whereas glomerular growth continued undiminished. Twenty-four weeks after UNX, glomerular tuft volume in experimental animals exceeded that in controls by 80%. Twelve weeks after surgery, total GFR in UNX rats was approximately 80% of that in controls, a value maintained until the end of the observation period. Twenty-four weeks after surgery, heavy proteinuria was present in UNX animals. Structural abnormalities in glomeruli of UNX animals were already encountered 12 weeks after surgery; they were present to a much lesser extent in controls. In UNX animals these proceeded to the FGS stage by the end of the observation period. Three major groups of glomerular lesions were observed: (1) changes in the width and shape of glomerular capillaries. (2) changes in podocyte structure, and (3) tuft adhesions to Bowman's capsule with or without segmental sclerosis. The structural changes are analyzed in this and an accompanying paper [1]. The present paper deals with the widespread formation of irregular, giant capillary loops. They occur predominantly at the tuft periphery with a clear predilection for the vascular pole region. They are not a result of compensatory growth, but rather an expansion of single capillaries due to failure of the mesangium. Local disconnection of the mesangium from its anchoring points at the GBM leads to bulging and "coalescence" of capillary loops, resulting in abnormally-shaped vascular channels. This process is associated with a rearrangement of the corresponding mesangium. In our view, the appearance of dilated capillaries represents a local event pivotal to the development of more severe lesions, such as tuft adhesions and FGS.

Animals↗
PubMed1992

Glomerular damage after uninephrectomy in young rats. II. Mechanical stress on podocytes as a pathway to sclerosis.

In a preceding study [1], we showed that within six months after UNX in young rats, glomeruli in the remnant kidney undergo a sequence of serious changes which finally lead to focal segmental glomerulosclerosis (FGS). The formation of abnormally-shaped capillary channels was shown to result from local mesangial failure and is considered to be a nidus for the development of more severe lesions. In the present paper, the development of characteristic lesions in podocyte structure is described and analyzed. Concomitant with overall glomerular growth after UNX, a pronounced hypertrophy of podocytes was observed, while the mean number of podocytes per glomerulus did not change. It appears that podocytes cannot sustain the same degree of growth as the tuft as a whole; podocyte hypertrophy is soon followed by maladaptive changes which eventually lead to cell destruction. The following sequence of pathologic changes can be suggested: cell bodies enlarge in volume and area associated with a dramatic attenuation to cytoplasmic sheets. Primary processes are thinned out and frequently extend to remote capillaries. As a whole, the capillary area served by a single podocyte is dramatically enlarged. Furthermore, the expanding cytoplasmic sheets (derived from podocyte cell bodies) cover an increasingly large proportion of the outer capillary surface, that is, of the filtration area. Consequently, an increasing amount of filtrate is delivered into the subcellbody space. Obstruction of the efflux of this filtrate into the urinary space causes bulging of the overlying cytoplasmic sheets into pseudocysts. Podocytes overlying abnormally-shaped and dilated capillary channels are generally the most seriously affected. Tuft hypertrophy, pseudocyst formation and local capillary expansion cause wide-spread apposition of podocytes to Bowman's capsule. Appositions are a prerequisite for the development of tuft adhesion. Local detachment of a podocyte from the GBM in those areas allows access of parietal cells to the GBM. In early adhesions the connection of the tuft to Bowman's capsule is established by single parietal cells which attach to both the GBM and the basement membrane of Bowman's capsule. An adhesion is considered as a nidus for segmental sclerosis; as the adhesion progresses, the related tuft regions turn into sclerosis. In the present model FGS develops exclusively in areas of tuft adhesion.

Animals↗
PubMed1992

Expression of nitric oxide synthase in kidney macula densa cells.

The distribution of nitric oxide synthase (NOS), the enzyme by which NO is generated from L-arginine, was investigated in rat kidney. The indirect immunofluorescence technique using a polyclonal antibody against type I NOS was applied, followed by the histochemical NADPH diaphorase staining technique on the same sections in order to demonstrate the enzymatic activity of NOS. Macula densa cells were strongly stained by both techniques, demonstrating abundant NOS in the cytoplasm of these cells. In addition, these findings were confirmed by nonradioactive in situ hybridization, thus demonstrating the corresponding messenger RNA in macula densa cells as well. Our findings provide the morphological basis for a possible role of NO as a mediator substance in signal transfer from distal tubular fluid to glomerular arterioles.

Amino Acid Oxidoreductases↗
PubMed1992

Morphometric analysis of kidney hypertrophy in rats after chronic potassium depletion.

Hypertrophic kidney growth in K depletion was analyzed morphometrically in rats fed a K-free diet for 18 days. K excretion decreased rapidly to less than 1% of control, creatinine clearance decreased, and urinary concentrating ability was impaired. Kidney weight in K-depleted rats was 30% higher than in controls. Growth of individual kidney zones was not uniform; hypertrophy of the inner stripe (IS) of the outer medulla was most prominent. Among tubules the most striking enlargement was seen in the outer medullary collecting duct (CD); hypertrophy and hyperplasia of both CD cells and intercalated (IC) cells occurred in the same proportion. In the IS, both luminal and basolateral membrane area per unit tubule length doubled in IC cells and increased 1.2- and 1.7-fold, respectively, in CD cells. Despite overall kidney growth, epithelial volume of thick ascending limb (TAL) per tubule length was unchanged in IS and cortex and only slightly increased in outer stripe. The increased membrane area of CD epithelium in the IS is consistent with previously reported increases in activity of enzymes involved in active reabsorption of K+ and Na+.

Animals↗
PubMed1992

[Adolescents and computers: attitude, personality and motive for interaction].

This empirical study was undertaken to clarify controversial points emanating from previous theoretical and empirical papers dealing with apparently negative consequences on the personality development of young people who have at least a causal working-acquaintance with computers. We tested 174 persons of both sexes (age: 14-18 years) with a "Computer-Attitude-Questionnaire" and the "Mehrdimensionaler Persönlichkeitstest für Jugendliche" (Schmidt, 1981; "Multidimensional-Personality-Test"). A subgroup of 63 persons who have access to and do avail themselves of computers on a regular basis (as leisure-time activity) also answered the "Computer-Motive-Questionnaire". Statistical analyses revealed that the personality test-values of young people with a positive attitude toward computers range within the test-norm. The data for these people describe them as stress resistant, emotionally stable, well-balanced, sociable, achievement-oriented, and less aggressive.

Adolescent↗
PubMed1991

Glomerular injury in analbuminemic rats after subtotal nephrectomy.

Progressive proteinuria has been suggested not just to reflect but also to contribute to the development of focal glomerular sclerosis. Development of proteinuria and glomerular lesions was examined up to 18 weeks after 3/4 nephrectomy in Sprague-Dawley (SDR) rats and an analbuminemic SDR variant (NAR). Nephrectomy led to a significantly lesser degree of proteinuria in NAR (42 +/- 14 SD mg/day) than in SDR (140 +/- 54 mg/day), consistent with the fact that 50-60% of urinary protein in SDR after nephrectomy is serum albumin. Nevertheless at 18 weeks NAR showed a significantly higher frequency of moderate and severe glomerular lesions than SDR. We conclude that, in this model, proteinuria itself is not a major cause of progressive glomerular injury.

Animals↗
PubMed1991

Podocytes in glomerulus of rat kidney express a characteristic 44 KD protein.

We describe a new monoclonal antibody (MAb) directed against glomerular visceral epithelial cells (podocytes), generated by immunization with isolated rat kidney glomeruli. In immunoblotting experiments this MAb (IgG1 subclass) reacted with a 44 KD protein. In cryostat sections of normal rat kidney the MAb stained glomerular podocytes; therefore, we called the antigen pp44 (podocyte protein 44 KD). On 0.5-micron cryostat sections the signal could be more precisely ascribed to the podocyte foot processes, whereas the cell bodies appeared virtually unreactive. On ultra-thin frozen sections pp44 was found within the cytoplasm of podocyte foot processes at their origin from their parent processes. The podocyte cell membrane was not labeled. All other parts of the nephron were unreactive. An additional but weaker immunoreaction was found in the arterial endothelium; the endothelia of other vessels (peritubular capillaries, veins) were negative. In human kidney anti-pp44 revealed the same staining pattern as in rat kidney. The expression of pp44 was also studied in newborn rat kidney. The early stages of glomerular development (renal vesicle, S-shaped body) were negative. pp44 first appeared during the capillary loop stage, i.e., when formation of podocyte foot processes commences. In comparing the present results with published data, pp44 is clearly different from other antigens thus far described in podocytes. From the results of this investigation we conclude that pp44 represents a novel cytoplasmic protein of podocytes. Our data suggest a cytoskeletal role for pp44 in preserving the complex architecture of podocytes. This idea is confirmed by the simultaneous appearance of foot processes and anti-pp44 immunoreactivity during glomerular development.

Animals↗
PubMed1991

Branching and confluence pattern of glomerular arterioles in the rat.

In addition to the usual division of the glomerular tuft into lobules, a subdivision into an afferent and an efferent capillary domain is made. Immediately after entering the glomerulus the afferent arteriole splits into superficially located branches which supply the lobules. The capillaries of each lobule first run towards the urinary pole; these parts of each lobule establish the afferent domain. The capillaries of each lobule running back towards the vascular pole establish the efferent domain. The afferent domain represents the major part of the tuft; it has the shape of an incomplete globe with a deep depression on one side within which the efferent domain is situated. The efferent arteriole is established inside the glomerular tuft within the efferent capillary domain. Generally tributaries from each lobule converge to form the intraglomerular segment of the efferent arteriole, which leaves the tuft by passing through the mesangium of the glomerular stalk. At this site the intraglomerular segment of the efferent arteriole is fully surrounded by the mesangium; consequently, it is exposed to the intramesangial pressure.

Animals↗
PubMed1990

Role of mesangial cell contraction in adaptation of the glomerular tuft to changes in extracellular volume.

Different chronic states of mesangial cell contraction were induced by variation of extracellular volume in Munich-Wistar rats for 6 days to study the influence of mesangial cells on the geometry of the glomerular tuft. Stereological analysis of superficial glomeruli in volume-expanded rats (VE, treated with enalapril) and volume-reduced rats (VR, treated with indomethacin) revealed a glomerular tuft volume 28.7% smaller, and a capillary luminal volume 32% smaller in VR than in VE rats. The filtration area [defined as glomerular basement membrane (GBM) area facing fenestrated endothelium] was greatly reduced in VR rats (97 +/- 16 X 10(3) micron 2 vs 137 +/- 13 x 10(3) micron 2). The surface density (Sv) of the GBM was higher by approximately 10% in VR rats primarily due to the considerable increase in Sv of the perimesangial GBM subdivision (0.189 +/- 0.01 micron 2/micron 3 vs 0.153 +/- 0.01 micron 2/micron 3), indicating a higher degree of mesangial cell contraction in these animals. Our results suggest (1) that mesangial cell contraction plays a major role in the adaptation of the glomerular tuft to variations in extracellular volume; (2) that the relevance of mesangial cell contraction for the regulation of glomerular haemodynamics appears to be small; and (3) that the reduction in filtration area, although prominent, cannot fully account for the considerable decreases in the ultrafiltration coefficient observed by others in acute and chronic studies.

Adaptation, Physiological↗
PubMed1990

Mesangial cell-glomerular basement membrane connections counteract glomerular capillary and mesangium expansion.

Glomerular capillaries are perfused at a high hydraulic pressure. Since the capillary mesangium interface presents no morphologically apparent pressure barrier, it is suggested that the hydraulic pressure in the mesangium may also be high. This paper analyzes the structures in the glomerular tuft that are capable of counteracting the distending forces exerted on the tuft by the high hydraulic pressure in its center. The skeletal element of the glomerular tuft is the glomerular basement membrane (GBM). The combination of the GBM with the contractile apparatus of mesangial cells represents the main system stabilizing the glomerular tuft. The mesangial cell-GBM connections counteracting the expansion of glomerular capillaries appear less susceptible to injury than those counteracting mesangial expansion.

Animals↗
PubMed1990

Structure of the glomerular mesangium: a biomechanical interpretation.

This paper summarizes our current knowledge of the structural details and probable functional significance of the system of contractile filaments in the glomerular mesangium. The description is based mainly on studies of superficial glomeruli of the rat kidney. The contractile apparatus of mesangial cells consists of microfilament bundles located predominantly within mesangial cell processes. The thickest microfilament bundles occur in the juxtacapillary mesangial cell processes, which directly abut the glomerular capillaries. The effector structure of mesangial cell contractility is the GBM. Mesangial cell processes are connected to the GBM either directly or through the interposition of extracellular microfibrils. In general, the contractile system of the mesangium interconnects opposing parts of the GBM. This arrangement is particularly obvious in the juxtacapillary processes, which underlie a mechanical connection between the GBM at the two opposing mesangial angles of a single capillary. The geometry and structural composition of the contractile apparatus of the mesangium indeed suggest a static rather than a dynamic function. In conjunction with the GBM, the mesangial contractile apparatus seems capable of supporting sufficient wall tension to counteract the distending forces acting across the capillary walls; the apparatus also seems capable of directly balancing the distending forces on the perimesangial walls. Assuming that mesangial cells are capable of isotonic contractions, the effect of such a contraction on capillary diameter and, consequently, on filtration area would be small.

Actin Cytoskeleton↗
PubMed1990

Ultrastructural organization of contractile proteins in rat glomerular mesangial cells.

Glomerular mesangial cells of the rat kidney contain actin, nonmuscle myosin, tropomyosin, and the muscular Z-line protein, alpha-actinin. This was shown for actin, myosin, and alpha-actinin by immunoblotting as well as by immunoelectron microscopy. Tropomyosin was localized in mesangial cells by immunofluorescence. In cultured mesangial cells, actin, myosin, and alpha-actinin constitute a considerable amount of the total cellular protein contents. In mesangial cells in situ actin, myosin and alpha-actinin were found to be colocalized within conspicuous microfilament bundles that traverse the cell body or major processes in various directions and project into either the tonguelike pericapillary processes, which run toward mesangial angles, or into the microvilluslike lateral extensions that abut on the perimesangial portion of the glomerular basement membrane (GBM). Thereby, the GBM of opposing mesangial angles as well as of opposing portions of the perimesangial GBM are regularly interconnected by filament bundles within mesangial cells that contain actin, myosin, and alpha-actinin. The authors suggest that the major function of actin-, myosin-, and alpha-actinin-containing filament bundles in mesangial cells is to create an isometric tension (or minute isotonic contractions) to counteract the distending forces of the rather high intracapillary hydraulic pressure and its resulting pressure gradients across the capillary wall and across the perimesangial GBM.

Animals↗
PubMed1989

Vascular congestion in ischemic renal failure: the role of cell swelling.

Experiments were performed on rats to examine the cause of the vascular congestion that accompanies renal ischemia, and the potential role of cell swelling in its generation. Renal function and gross morphology were examined after reflow, whereas tissue morphometry was performed both before and after reflow in kidneys. Small doses of mannitol applied into the renal artery just before ischemia greatly reduced the incidence of vascular congestion and the depression of renal function. During ischemia the outwardly directed swelling of the proximal tubule depleted the interstitial and vascular space of the cortex and outer medullary outer stripe and the inwardly directed swelling of the thick ascending limb occluded the lumen. Mannitol reduced cell swelling, lessened the depletion of the interstitial and vascular space and eliminated the occlusion of the thick ascending limb. It is proposed that the loss of interstitial and vascular fluid during ischemia is the cause of the vascular congestion, which, in turn, is responsible for the poor perfusion and impaired renal function seen after ischemia.

Acute Kidney Injury↗
PubMed1988

Ultrastructure of the kidney of a South American caecilian, Typhlonectes compressicaudus (Amphibia, Gymnophiona). I. Renal corpuscle, neck segment, proximal tubule and intermediate segment.

The ultrastructure of the renal corpuscle, the neck segment, the proximal tubule and the intermediate segment of the kidney of a South American caecilian, Typhlonectes compressicaudus (Amphibia, Gymnophiona) was examined by means of transmission electron microscopy (TEM), scanning electron microscopy (SEM) and freeze-fracture technique. The glomerular filter apparatus consists of the podocyte epithelium, a distinct basement membrane, a subendothelial space and the capillary endothelium. Emanating from the podocyte cell body, several long primary processes encircle neighboring capillaries. The short slender foot processes originating from the primary processes interdigitate with those from other primary processes, thereby forming the meandering filtration slit. Thick bundles of microfilaments are found in the primary processes, but absent in the foot processes. The basement membrane consists of a lamina rara externa and a rather thin lamina densa (50 nm thickness). The wide subendothelial space contains abundant microfibrils, a few collagen fibrils and many thin processes of mesangial cells. The endothelium is flat and fenestrated (compared to mammals displaying relatively few fenestrations); some of the fenestrations are bridged by a diaphragm. The glomerular mesangium is made up of the mesangial cells and a prominent mesangial matrix containing microfibrils and collagen fibrils. The cells of the neck and intermediate segments display numerous cilia with their microtubules arranged in the typical 9 + 2 pattern. The basal bodies of the cilia are attached to thick filaments with a clear crossbanding pattern of 65 nm periodicity. The proximal tubule is composed of cells typical for this segment (PT cells) and light cells lacking a brush border (bald-headed cells). The PT cells measure 10-25 micron in height and 15-30 micron in width and do not interdigitate at their lateral borders with each other. Their basolateral cell membrane is amplified by many folds projecting into lateral intercellular spaces and into basal recesses. The brush border is scarce and composed of loosely arranged short microvilli.

Amphibians↗