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Biomedical subjects

H J Reineck

Publications and source records attributed to H J Reineck.

At least 19 recordsLinked to original sources
PubMed1986

Role of volume depletion in the glycerol model of acute renal failure.

Previous studies have demonstrated significant volume depletion early in the course of glycerol-induced acute renal failure. In addition, it has been shown that acute volume expansion within 6 h of glycerol administration reverses the fall in inulin clearance but volume expansion 12-24 h after glycerol fails to restore that parameter to normal. The current studies were performed to determine whether chronic volume expansion would prevent the fall in inulin clearance normally observed 18-20 h after the insult. Inulin clearance was therefore compared 18-20 h after glycerol in hydropenic rats and in rats undergoing chronic volume expansion by the constant infusion of Ringer solution at a rate of 5 ml/h initiated at the time of the glycerol injection. Inulin clearance was well maintained in the latter group, averaging 1.77 compared with 0.22 ml/min in the hydropenic group. Renal histology revealed no difference in the degree of tubular necrosis between groups but did show a marked decrease in cast formation in the animals undergoing chronic volume expansion. To determine the possible significance of these casts, micropuncture studies were carried out to measure proximal tubular pressures. Under hydropenic conditions these pressures were not different control animals and rats receiving glycerol when studied 18-20 h after glycerol. Following acute volume expansion, however, glycerol-treated rats demonstrated significantly higher pressures than control rats. On the other hand, proximal tubular pressures were comparable in glycerol-treated and control animals receiving the chronic volume expansion.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Kidney Injury↗
PubMed1985

Urea reabsorption along the papillary collecting duct in potassium-deficient rats.

These experiments were designed to evaluate the hypothesis that K+ deficiency may be associated with decreased delivery of urea to the renal papillary collecting duct and/or decreased reabsorption of urea from the papillary collecting duct. Either of these factors would result in diminished capacity for urea recycling and might explain the mechanism of the urinary concentrating defect that is observed in K+ depletion. Munich-Wistar rats were fed 25 ml of water and 12 g of normal (CON) or K+-deficient (KD) diet each day for 21 days. Papillary collecting duct samples were obtained by micropuncture through the intact ureter. Fractional delivery of H2O to the base and tip of the papillary collecting duct was increased in KD as compared to CON rats (1.50 +/- 0.30% in KD vs 0.72 +/- 0.09% in CON at the base, P less than 0.01; and 0.55 +/- 0.08% in KD vs 0.30 +/- 0.05% in CON at the tip, P less than 0.01). However, fractional delivery of urea to the base and tip of the papillary collecting duct was not different between KD and CON rats (26.9 +/- 5.6% in KD vs 21.4 +/- 3.3% in CON at the base, P greater than 0.05; and 12.4 +/- 1.5% in KD vs 10.4 +/- 1.4% in CON at the tip, P greater than 0.05). Furthermore, reabsorption of water or urea between the base and tip of the papillary collecting duct was not decreased in KD as compared to CON rats (water reabsorption was 57.8 +/- 4.4% in KD and 55.9 +/- 5.11% in CON and urea reabsorption was 45.0 +/- 6.5% in KD and 45.9 +/- 5.4% in CON, P greater than 0.05). These results demonstrate that water reabsorption, but not urea reabsorption, is impaired in renal tubules proximal to the accessible papillary collecting duct in hydropenic rats.

Absorption↗
PubMed1985

The role of complement in the pathogenesis of postischemic acute renal failure.

One hour occlusion of total renal blood flow results in oliguric acute renal failure as defined by an abrupt and severe diminution in glomerular filtration rate. In rats, after 1-2 h of such ischemia, the acute renal failure which follows is characterized by decreased renal blood flow and by intratubular obstruction with necrotic cellular debris. The present study has examined the possible role of the complement system in the development of this model of acute renal failure. Immunoreactive C3 was extensively localized within necrotic tubular epithelial cells and the walls of small muscular arteries in reperfused kidneys after 1 h of total renal ischemia. Depletion of complement by the administration of cobra venom factor 18 h prior to the induction of ischemia abrogated C3 localization and significantly attenuated the subsequent fall in renal blood flow following reperfusion but did not alter the oliguria or marked fall in glomerular filtration.

Acute Kidney Injury↗
PubMed1983

In vitro perfusion of the isolated dog glomerulus.

Recent technological advances allowing direct in vivo measurements of the determinants of glomerular ultrafiltration have greatly expanded our understanding of that process. In addition, these in vivo studies have clarified the dynamics of glomerular ultrafiltration in a number of physiologic and pathophysiologic conditions. Despite this progress, important issues remain unresolved and beyond the scrutiny of in vivo techniques. We have therefore devised a technique for in vitro glomerular perfusion of the isolated dog glomerulus. In eight glomeruli perfused at physiologic rates, the glomerular filtration rate averaged 39 nl/min and the filtration fraction was 0.19. Filtration pressure disequilibrium was observed in all studies and thus allowed calculation of a unique value for the ultrafiltration coefficient. That parameter averaged 2.34 nl/(min X mmHg). Morphologic studies employing transmission electron microscopy indicate that isolated perfused glomeruli remain ultrastructurally intact. The method for glomerular isolation and in vitro perfusion is presented in detail, the results obtained are compared with published in vivo results, and the advantages offered by the technique are discussed.

Animals↗
PubMed1982

Calcium metabolism in young rats during early dietary phosphate deprivation.

A series of in vivo experiments were designed to study the early effects of phosphate depletion on calcium metabolism in young adult (8-10 week old) rats with intact thyroid--parathyroid glands. Hypercalciuria occurred within 24 h of dietary phosphate deprivation. It was the consequence of mobilization of calcium stores from the exchangeable calcium pool of the diaphysis of bone. Increased net intestinal absorption of calcium also occurred early. This was at least in part due to decreased net intestinal secretion of calcium into the gut lumen. Thus the early onset of hypercalciuria and hypercalcemia associated with Pi deprivation in normal growing young rats is the combined result of increased net intestinal calcium absorption and increased calcium mobilization from bone.

Age Factors↗
PubMed1982

Methodologic considerations in the study of glomerular ultrafiltration.

Over the past decade numerous studies have detailed the dynamics of glomerular ultrafiltration. Observations in a unique strain of Munich-Wistar rats, which afford the direct measurement of intraglomerular capillary hydrostatic pressure, have determined that under normal physiologic conditions these animals are in a state of filtration equilibrium. Both mathematical models based on this observation and experimental evidence indicate that under these circumstances the primary determinant of glomerular filtration rate (GFR) is the rate of glomerular plasma flow. In addition, this state of filtration equilibrium provides a condition in which changes in the product of glomerular surface area and glomerular capillary hydraulic conductivity (ultrafiltration coefficient) have no influence on glomerular filtration rate. Similarly, changes in glomerular hydrostatic pressure have a relatively small influence on GFR. These conclusions represent a marked alteration of the previously held concepts of the determinants of GFR. Unfortunately, studies in other strains of rats and in other animal species, particularly the dog, have led to the conclusion that filtration disequilibrium is the normal physiologic condition. The validity of this conclusion, however, is made uncertain by methodologic necessities that may lead to erroneous physiologic measurements of the determinants of GFR. In the present Editorial Review we examine the data reflecting on the applicability of filtration equilibrium to mammalian species. In addition, we summarize two new in vitro techniques for the further study of the dynamics of glomerular ultrafiltration.

Animals↗
PubMed1982

Effect of medullary tonicity on urinary sodium excretion in the rat.

In previous reports from this laboratory we have suggested that a reduction in medullary tonicity decreases the thin ascending loop of Henle sodium reabsorption and is in part responsible for the magnitude for the natriuresis accompanying 10% body weight Ringer loading. According to this postulate, one would expect that the medullary washout associated with water diuresis would also result in a natriuresis, but this does not occur. It is possible, however, that increased delivery from the proximal tubule is necessary to demonstrate an effect of medullary tonicity on urinary sodium excretion. Micropuncture studies were designed to test that possibility by increasing distal delivery by 2% Ringer loading in animals with and without reduced medullary tonicity. In an initial series of experiments the alpha-adrenergic agonist clonidine was used to induce a water diuresis. When given alone, this agent caused a marked decrease in urine osmolality and an increase in urine flow rate but had no effect on proximal reabsorption in either superficial or juxtamedullary nephrons, and did not alter urinary sodium excretion. Volume expansion with 2% body weight Ringer solution resulted in a significant fall in proximal reabsorption and a trivial increment in sodium excretion. When this same degree of volume expansion was conferred on animals undergoing a water diuresis, a marked increase in absolute and fractional sodium excretion occurred. In a second group of studies medullary tonicity was reduced in the left kidney only by removal of the left ureter 1 h before micropuncture. When these animals were infused with 2% body weight Ringer solution, proximal reabsorption was decreased in juxtamedullary nephrons, and a marked increase in sodium excretion was observed only from the left kidney. Finally, the effect of water diuresis on fractional sodium delivery to the early and late distal tubule of superficial nephrons during 2% Ringer loading was evaluated. Delivery to both of these sites was comparable after 2% Ringer loading alone and during 2% Ringer loading plus water diuresis. From these data, we conclude that medullary tonicity does influence renal sodium handling but that this effect is manifest in the final urine only under conditions in which proximal reabsorption is decreased. The data also suggest that this effect is limited to juxtamedullary nephrons and is probably localized to the thin ascending limb of the loop of Henle.

Absorption↗
PubMed1981

Renal lesions in acute rheumatic fever.

In the past 4 years, four patients with acute rheumatic fever and abnormalities of renal function, urinary sediment, or both have undergone percutaneous renal biopsy at this institution. Distinctly different renal lesions were found and included focal glomerulonephritis, classic acute exudative poststreptococcal glomerulonephritis, mesangioproliferative glomerulonephritis, and severe interstitial nephritis. In each case, the clinical abnormalities were transient. In this report we describe the clinical and pathologic findings in each of these patients to stress the variability of renal lesions that may accompany acute rheumatic fever.

Acute Disease↗
PubMed1980

Sequential studies on the pathophysiology of glycerol-induced acute renal failure.

The role of volume depletion and renal ischemia in the development of renal functional impairment in glycerol-induced ARF is not clear. This study was designed to evaluate the role of volume depletion in this model by determining the hemodynamic and functional alterations which occur between 3 and 18 hr after glycerol administration and the reversibility of these changes in response to Ringer loading. Three hours after glycerol, Cln and RBF, measured by flowmeter, were reduced 70% and 52%, respectively, in comparison with control values. FeNa was 0.04%. Ringer loading increased Clkn to 103% and RBF to 93% of control values. Qualitatively similar results were found 6 hr after glycerol. At 18 hr, Cln and RBF were 47% of control values. After Ringer loading, RBF rose to 100% of control. The response of Cln, however, was a function of the baseline FeNa. Cln incrased substantijally in rats with low FeNa but changed only slightly in animals in which this parameter was increased. These studies indicate that the early reduction in the Cln is dependent upon the fall in RBF. At 12 and 18 hr, however, the fall in Cln is not blood flow-dependent, and a second mechanism must be operative. FeNa seems to be a reliable index of the functional status of a given animal.

Acute Kidney Injury↗
PubMed1979

Effect of fasting on tubular phosphorus reabsorption.

In the thyroparathyroidectomized (TPTX) rat, fasting increased urinary phosphorus excretion by decreasing the tubular reabsorption of P1 (TRP) and resulted in hypophosphatemia. The administration of either sucrose or NaHCO3 prevented the metabolic acidosis associated with fasting and decreased the phosphaturia, indicating that the phosphaturia in fasting is in part due to metabolic acidosis. In rats on partial reduction of P1 intake selectively, the phosphaturic response to parathyroid hormone (PTH) was completely suppressed. On the other hand, the fasting rat partially retained the phosphaturic response to PTH, although dietary P1 intake was totally absent. These findings suggest that the renal P1 wasting in fasting may take place by dual mechanisms: a) the PTH-independent decrease in TRP, and b) an inability to totally suppress the response to PTH. Cyclic AMP generation in response to PTH, determined both in vivo and in vitro, was not measurably altered in fasting. However, the phosphaturic response to cyclic AMP was decreased in fasting, suggesting that the mechanism of partial resistance to PTH is probably not at but after cyclic AMP generation.

Adenylyl Cyclases↗
PubMed1978

Studies on the mechanism of reduced urinary osmolality after exposure of renal papilla.

Studies were performed in Munich-Wistar rats to determine whether changes in papillary plasma flow might be responsible for the concentrating defect which occurs after exposure of the extrarenal papilla. Papillary plasma flow was measured by (125)I-albumin accumulation. Initial studies in hydropenic animals revealed that papillary plasma flow was 40% higher in the kidney with the exposured papilla, 41 vs. 29 ml/min per 100 g of papilla (P < 0.001). This increase in papillary plasma flow was detectable 15 or 45 min after removing the ureter. Because it was unclear whether the rise in papillary plasma flow was a cause or the result of the fall in urine osmolality, similar studies were performed in animals undergoing a water diuresis. In this setting, papillary plasma flow still increased on the exposed side compared to the control side, 81 vs. 60 ml/min per 100 g, despite similarly low urine osmolalities of 155 and 174 mosmol/kg, respectively. This finding is compatible with the possibility that papillary exposure per se causes an increase in papillary plasma flow and that this hemodynamic alteration may lead to a reduction in urinary osmolality secondary to washout of the medullary interstitium. A final group of hydropenic rats was given either indomethacin or meclofenamate before removing the ureter. In these studies, there was no difference in either the papillary plasma flow or the urine osmolality between control and exposed kidneys. It is therefore suggested that opening the ureter induces an increase in papillary plasma flow by some mechanism which may involve an alteration in prostaglandin synthesis.

Animals↗
PubMed1978

Further studies on segmental sodium transport in the rat kidney during expansion of the extracellular fluid volume.

The present studies were designed to further investigate the possibility of heterogeneity of nephron function during Ringer loading in the rat, and to determine the specific nephron segment responsible for this finding. As in previous studies from this laboratory with smaller rats (50-125 g), net addition of sodium between late distal tubule and papillary base (6.9 vs. 10.4% of the filtered load, respectively, P <0.005) was found in more mature rats (170-230 g). In contrast, there was net reabsorption of sodium between these two segments in nonvolume-expanded animals, 1.70 vs. 0.45% of the filtered sodium load, P <0.005. Because nephron heterogeneity of sodium transport during extracellular volume expansion is the most likely explanation for these findings, further studies were performed to determine the specific juxtamedullary nephron segment responsible for the net addition pattern between late distal tubule and papillary base in Ringer-loaded animals. First, a comparison was made of sodium delivery to the late proximal tubule of superficial nephrons vs. the delivery rate to the bend of Henle's loop of juxtamedullary nephrons in both hydropenia and Ringer loading. Fractional sodium delivery was quite comparable between the superficial and juxtamedullary nephrons in both hydropenia and Ringer loading although the absolute level was much greater in both groups of nephrons in the Ringer studies. Chlorothiazide (15 mg/kg loading and 15 mg/kg per h) given during Ringer loading markedly increased late distal sodium delivery, 19% of the filtered load, but did not prevent net addition of sodium at the papillary base. In contrast, furosemide (5 mg/kg loading and 5/mg/kg per h) given during Ringer loading completely reversed the segmental pattern, 35.5 and 28.8% at late distal tubule and papillary base, respectively, P <0.005. These studies demonstrate that the net addition of sodium between late distal tubule and papillary base during Ringer loading is not limited to immature rats and that the segmental pattern does not occur in non-volume-expanded animals. Further, the reversal of the net addition pattern with furosemide, but not chlorothiazide, and the comparable proximal nephron delivery rates in Ringer loading suggest that the loop of Henle of juxtamedullary nephrons reabsorbs less sodium than the same portion of superficial nephrons in this setting. A model is proposed to explain this finding.

Animals↗