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Biomedical subjects

H U Gutsche

Publications and source records attributed to H U Gutsche.

At least 19 recordsLinked to original sources
PubMed1999

[Calciphylaxis of the skin as a sequela of terminal kidney failure. Report and discussion of 3 cases].

Calciphylaxis is a rare syndrome mostly affecting patients with secondary hyperparathyroidism and in some cases with functional protein C or protein S deficiency. Skin lesions begin as superficial painful patches that progress to deep necrotic lesions. The findings are often misdiagnosed as livedo vasculitis and the prognosis is poor. Histopathologically, calcification in the media of small arteries and arterioles with intimal hyperplasia is seen. It is unclear if this morphologic hallmark is pathogenetic. Therapeutically, the calcium-phosphate product should be lowered pharmacologically by an intensified and modified dialysis treatment and parathyroidectomy.

Aged↗
PubMed1996

Lipapheresis: an immunoglobulin-sparing treatment for Refsum's disease.

UNLABELLED: Toxic phytanic acid concentrations in patients with Refsum's disease can be reduced by plasma separation, performed either as plasmapheresis, or as cascade filtration. The latter procedure is as efficient and safe as plasmapheresis, and eliminates the need for albumin replacement. This study investigates the loss of immunoglobulins associated with the procedure. MATERIAL AND METHODS: Immunoglobulin- and phytanic acid serum concentrations before and after cascade filtration (n = 16) were measured in a patient with Refsum's disease and their removal determined. Filters with sieving coefficients for immunoglobulin G of 70% and 30% were compared with each other and with historical data on plasmapheresis. RESULTS: While differences in immunoglobulin M loss are negligible, the loss of immunoglobulin G in cascade filtration is significantly less than that reported for plasmapheresis and depends upon the pore size of the employed filters. The loss is least with larger pore size, but this advantage becomes statistically insignificant if immunoglobulin G loss is related to the lesser decrease in phytanic acid concentration that was achieved simultaneously in this study. CONCLUSION: Unless transplantation of a-hydroxylase containing tissue can be established as treatment for Refsum's disease, cascade filtration appears to be the treatment of choice in order to avoid loss of albumin and to reduce the loss of immunoglobulin G.

Equipment Design↗
PubMed1995

Tubular reabsorption of technetium-99m-DMSA.

UNLABELLED: Intrarenal handling of 99mTc-DMSA is still controversial, particularly in the existence of tubular reabsorption from the tubular fluid. Experiments were performed with micropuncture technique on the rat kidney in an attempt to elucidate this question. METHODS: The concentration profile of 99mTc-DMSA along the nephron was measured in fluid from Bowman's space of surface glomeruli and from the proximal and distal tubules collected by micropuncture. Superficial loops of proximal tubules were micropunctured and microperfused with 99mTc-DMSA or [99mTc] pertechnetate for 10 or 20 min at physiological flow rates; the recovery of activity was measured in the final urine. RESULTS: Bowman's space urine contained only 14% of the 99mTc activity of arterial plasma, indicating low filtration of 99mTc-DMSA, likely due to high plasma protein binding. Tubular fluid-to-plasma activity ratios of 0.31 in the proximal tubules and 1.31 in the distal tubules suggest that 99mTc-DMSA is neither secreted nor reabsorbed along the nephron. Ninety-eight percent of the 99mTc-DMSA activity was recovered in the final ipsilateral urine, while only 0.5% was found in the urine of the contralateral kidney. CONCLUSION: A low fraction of 99mTc-DMSA enters the tubule by glomerular filtration and is not reabsorbed from the tubular fluid. Thus, only peritubular extraction by the tubular cell is responsible for renal uptake of 99mTc-DMSA.

Absorption↗
PubMed1986

Distal pressure-flow relations during in vivo distal microperfusion in the rat.

Distal convoluted tubule reabsorptive fluxes for various substances have been measured using the technique of in vivo microperfusion with quantitative sampling of the perfusate after it traverses a known length of tubule. It is unclear, a priori, whether physiologic pressures can be maintained under these sampling conditions. The present experiments were designed to monitor these pressure changes continuously by means of a microtransducer. We have found that over the range of 10-20 nL/min, during repeat sampling, the rise in pressure is 0.11 mmHg X nL-1 X min-1 (1 mmHg = 133.322 Pa) a value which is similar to 0.15 mmHg X nL-1 X min-1 obtained without sampling. This small rise in pressure over the microperfusion range supports the view that this technique does not introduce unphysiologic pressure effects. The present study also provides for the first time directly measured in vivo distal tubule pressure values over a wide flow range without changing whole kidney urine flow.

Absorption↗
PubMed1986

Effect of cyclosporine on the diluting capacity of the rat kidney.

Micropuncture experiments were carried out on rat kidneys in order to analyze the diluting ability of the thick ascending limb of Henle's loop (TAL) after acute and chronic administration of cyclosporine. Male albino Wistar rats weighing 190 to 250 g were either given cyclosporine (CSA) orally for 10 days or received single i.v. infusions of the drug before the micropuncture experiments. Drug free vehicle was administered to animals of two respective control groups. The electrolyte concentration of fluid from individual TALs was measured by continuous conductivity monitoring of early distal tubular fluid during pulse perfusion procedures. The transport dependent decrease of the electrolyte concentrations within the diluting segment showed a semi-logarithmic time course in all groups of rats. Lowest conductivity values were reached within 60 seconds of flow equilibrium in controls as well as in CSA treated rats. Chronic CSA feeding (15 mg/24 h/kg b.w., dissolved in 0.3 ml olive oil) as well as a single i.v. infusion of 5 mg/kg b.w. resulted in a significantly higher electrolyte concentration of TAL fluid. Infusion of the solvent alone was without significant effect on the diluting segment. We conclude that the impairment of the diluting ability of the TAL and hence the delivery of tubular fluid with increased NaCl concentrations to the macula densa should lead to a stimulation of the tubulo-glomerular feedback mechanism. Feedback activation per se could be the cause of the consistent GFR decrease and thus contribute to the basic nephrotoxicity of CSA.

Animals↗
PubMed1984

Effect of diuretics on the tubuloglomerular feedback response.

To study the influence of diuretics on the tubuloglomerular feedback mechanism, early proximal stop-flow pressure (SFP) was measured during loop exposure to different drug concentrations. SFP was recorded continuously during arrested flow and at a perfusion rate of 50 nL/min. The perfusate consisted of isotonic saline, to which varying amounts of furosemide. bumetanide, piretanide, or hydrochlorothiazide were added to obtain final concentrations between 10(-6) and 10(-4)M. The loop diuretics furosemide, bumetanide, and piretanide showed inhibition: an inverse log-linear relation between the luminal concentration and the respective feedback response. No differences between the dose-response curves of furosemide, bumetanide, or piretanide could be demonstrated. The effective concentration range was between 10(-6) and 10(-4)M, the mean effective dose (ED50) was close to 10(-5)M for each of them. In contrast, hydrochlorothiazide did not alter the feedback response. The effect of loop diuretics was rapidly and repeatedly reversible.

Animals↗
PubMed1984

Impaired diluting capacity of the thick ascending limb during loop bicarbonate and nitrate perfusion in vivo.

Previous whole animal studies have indicated that when nitrate or bicarbonate is substituted for chloride, renal concentrating defects can be demonstrated. It has been proposed that function of the "distal nephron" or thick ascending limb may be impaired when chloride is replaced by other anions. To examine this proposal, microstop-flow experiments were performed in rats in which loops were perfused with solutions containing 110 mM NaCl, NaHCO3, or NaNO3. Solute reabsorption by the thick ascending limb was assessed by measuring the minimum conductivity of fluid emerging from the loop following intervals of stop-flow. Thick ascending limb solute transport was impaired in loops perfused with HCO3 or NO3 evidenced by the marked increase in solute remaining in the loop after 60 s of stop-flow. The calculated corresponding sodium concentrations were in the range of 17-24 mM Na for the NaCl perfusion, 57-88 mM Na for the NaHCO3 perfusion, and 57-69 mM Na for the NaNO3 perfusion. Clearly, the minimum concentration achieved with NaCl was approximately one-third of that reached with the nitrate or bicarbonate solutions. These results indicate that when chloride-poor solutions reach the thick ascending limb, an important impairment of diluting capacity is demonstrable in vivo in the rat. The present studies, therefore, provide an important link between recent information regarding the mechanism of NaCl transport in the thick ascending limb and older whole animal studies suggesting an important role for distal chloride delivery in urine concentration.

Animals↗
PubMed1984

In vivo evidence of impaired solute transport by the thick ascending limb in potassium-depleted rats.

The objective of this investigation was to determine if thick ascending limb (TAL) solute removal is impaired in potassium-depleted rats, in vivo. We estimated TAL NaCl concentration by measuring in situ conductivity of tubular fluid presented to the early distal site after stop-flow periods of 10-60 s, during which a proximal equilibrium solution remained in contact with the reabsorbing epithelium. This allowed us to calculate the rate constant of the decrease in tubular fluid NaCl concentration and to determine equilibrium values for control, potassium-depleted, and potassium-repleted rats. After 60 s of stop-flow, NaCl concentration of TAL fluid decreased to 18.3 +/- 2.73 mM in control rats, while potassium-depleted rats had values almost twice as high (36.5 +/- 2.97 mM, P less than 0.01). The amount of NaCl remaining after 60 s of stop-flow in K-depleted rats was highly correlated with the plasma K concentration. Calculated rates of NaCl efflux from the TAL appeared to be normal in K-depleted rats while the concentration of NaCl achieved at equilibrium was nearly twice that measured in control rats. Acute systemic administration of KCl by gavage or infusion in K-depleted rats was associated with a decrease in TAL NaCl concentration to normal values. Addition of K to the perfusate, however, did not repair the defect. Our results can best be explained by assigning a special role to the peritubular K concentration. We suggest that the defect in TAL solute removal in K-depletion can be rapidly reversed, because decreases in peritubular K concentration limit Na efflux across the peritubular membrane by decreasing the activity of the Na-K-ATPase pump. We recognize that factors such as regional renal blood flow, local angiotensin II levels, and products of the cyclo-oxygenase enzyme system may play a role.

Animals↗
PubMed1983

Dose-related effects of furosemide, bumetanide, and piretanide on the thick ascending limb function in the rat.

To assess the action of piretanide, bumetanide, and furosemide on the thick ascending limb of Henle's loop, perfusion experiments were performed on rat kidneys, using a recently developed conductivity microprobe for the analysis of distal tubular fluid. Surface nephrons were perfused downstream from a solid paraffin block through Henle's loop with isotonic saline solution containing either 10(-6), 3 X 10(-6), or 10(-5) mol/L piretanide, bumetanide, or furosemide, respectively. For control values, diuretic-free saline was used. Conductivity measurements of early distal tubular fluid were performed in situ with a conductivity microprobe and were recorded continuously during variations of loop perfusion rate. A recently described micro-stop-flow technique was used to measure the conductivity of fluid emerging from the ascending limb, thereby evaluating the amount of sodium chloride reabsorbed. A significant electrolyte transport inhibition occurred within the concentration range between 10(-6) and 10(-4) M. Bumetanide and piretanide were slightly more effective than furosemide. Luminal diuretic concentrations of 10(-6) M or below were without influence on electrolyte reabsorption. Concentrations of 10(-4) M resulted in complete inhibition of the diluting segment electrolyte transfer.

Absorption↗
PubMed1981

[On the etiology of water excretion inhibition in Addison's disease].

Micropuncture experiments, performed on adrenalectomized rats disclosed an impairment of the hypertonic sodium chloride transport of the thick ascending limb of Henle's loop (the diluting segment). This transport inhibition was documented by a delayed time course of NaCl-concentration decrease within the diluting segment. Assuming a pump leak model of the hypertonic NaCl-transport, we calculated a 50% inhibition of the NaCl-transport velocity compared with controls. Dexamethasone treatment for 3 days led to a normalization of the impaired transport velocity. Both, the reduced GFR as well as the impaired free water clearance are functionally linked to the diminished transport capacity of the diluting segment by the tubuloglomerular feedback mechanism and the ADH mechanism respectively. A new hypothesis on the pathogenesis of the water excretion inhibition in adrenal insufficiency is discussed.

Addison Disease↗
PubMed1980

Influence of aldosterone on epithelial leakiness of rat proximal tubules. Microconductivity Measurements*.

Oil blocked superficial segments of late proximal tubules were perfused with salt free isosmolal mannitol solution. Time course of total net ion influx into the lumen after sudden stop of perfusion was monitored by continuous measurement of the conductivity of tubular fluid inside the lumen. Double barreled microelectrodes with high coupling resistance (Rc = 350-450 kOhm) were used as microconductivity probes. The observed time course was interpreted in terms of a two compartment system. Time constants for equilibration were 5.9 plus or minus 2.8 (SD) s in control rats, 14.4 plus or minus 8.0 s in adrenalectomized rats and 5.5 plus or minus 2.3 s in adrenalectomized rats substituted with 100 microgram . kg-1 . d-1 aldosterone for 3 days. The observed effect of aldosterone on the equilibration time constant indicates that this hormone increases the leakiness of proximal tabular epithelium for passive ion influx into the lumen.

Aldosterone↗
PubMed1979

The early phase of experimental acute renal failure. IV. The diluting ability of the short loops of Henle.

Experiments were conducted to establish whether diminished solute reabsorption in the loop of Henle during acute renal failure could explain the loss of urinary concentration and participate in generating a tubuloglomerular feedback-mediated reduction in filtration rate. The electrolyte content of the fluid in the ascending limb of the loop of Henle was determined in situ by monitoring its electrical conductivity after propulsion into the distal tubule with a sudden burst perfusion. The value of the minimum electrolyte concentration decreased exponentially with increasing equilibration time, reaching a steady-state value equivalent to 27 +/- 9 mM NaCl in normal kidneys, 34 +/- 15 mM in mercuric chloride kidneys and 53 +/- 22 mM following ischaemia. A mathematical model was derived to describe the process of sodium chloride dilution from which it was possible to calculate both the permeability and transport velocity of the cortical thick ascending limb. In the normal kidney, the transport velocity was calculated to be 4.65 +/- 0.92 . 10(-5) cm/s, a value not significantly different from that of the mercuric chloride of ischaemic kidneys, and the estimated permeability was 1.13 +/- 0.52 . 10(-5) cm/s, not different from that of the mercuric chloride kidneys but significantly lower than that calculated for the ischaemic kidneys. It is concluded that for the more severely damaged ischaemic model, the loss of urinary concentrating ability was accompanied by a reduction in diluting ability of the ascending limb of the short loop of Henle, which appears to be due, at least in part, to an elevation of the passive permeability to sodium chloride in this segment.

Acute Kidney Injury↗