PubMed Health⌕ Search

Biomedical subjects

R V Patak

Publications and source records attributed to R V Patak.

At least 19 recordsLinked to original sources
PubMed1992

Acute renal failure in cancer patients.

Compromise of kidney function in patients with serious medical illnesses, including cancer, is a serious and potentially fatal complication. In cancer patients, the types of renal injury that may occur are more varied than in patients with other underlying illnesses, and definition of the etiology of the decline in renal function may have important therapeutic and prognostic implications. This review article discusses the clinical manifestations and the diagnostic workup of insults to the kidney in patients with cancer. Therapy (excluding dialysis) for each type of renal insufficiency is briefly reviewed.

Acute Kidney Injury↗
PubMed1984

Decreased ultrafiltration coefficient of glomeruli isolated from volume-depleted rats.

Decreased glomerular ultrafiltration coefficient (Kf or LpA) has been demonstrated in micropuncture studies of rats subjected to dietary sodium restriction and diuretics. To define the alterations in glomerular filtration characteristics in isolation from systemic hemodynamic influences, we studied filtration of isolated rat glomeruli in vitro. Control rats were maintained on standard laboratory chow and tap water until sacrifice. Experimental rats in groups I, II, and III were maintained on a sodium-deficient diet for 3 to 7 weeks. Further volume depletion was induced in groups II and III as follows: Group II rats were given furosemide, 30 mg/kg, intraperitoneally for 3 consecutive days prior to sacrifice; group III rats were given furosemide, 240 mg/kg, and killed (a) after about 4 hr when diuresis had resulted in 8% to 10% weight loss, (b) after 18 hr during which sodium restriction was continued, or (c) after 18 hr during which they were permitted to drink NaCl solution (0.9 gm/dl). Group IV rats were fed standard laboratory Chow and were subjected to hemorrhage of about 3% body weight and sacrificed after 18 hr of fasting. Plasma protein, serum creatinine and electrolytes, and FENa were measured in each rat prior to sacrifice. Filtration was induced in isolated glomeruli by applying a transcapillary oncotic gradient of about 12 mm Hg. A video recording of individual glomeruli was made during filtration, and glomerular diameter, volume, filtering surface area, Kf, and Lp were estimated from measurements of the video image. Kf was decreased during volume depletion induced by sodium restriction and furosemide or by hemorrhage. Kf averaged 4.0 +/- 0.2 nl/min . mm Hg in control rats (n = 10), 3.4 +/- 0.2 nl/min . mm Hg in group I (n = 8), 3.3 +/- 0.1 nl/min . mm Hg in group II (n = 12), 2.2 +/- 0.1 nl/min . mm Hg in group IIIa (n = 4), 2.6 +/- 0.3 nl/min . mm Hg in group IIIb (n = 4), and 2.3 +/- 0.2 nl/min . mm Hg in group IV (n = 3). Kf returned to control values after volume repletion with orally administered NaCl solution and averaged 4.3 +/- 0.3 nl/min . mm Hg in group IIIc (n = 4). We conclude that Kf falls in a graded and reversible fashion during volume depletion. Modulation of Kf, as well as previously described alterations in renal cortical perfusion, may contribute to decreased GFR in volume depletion.

Animals↗
PubMed1983

Glomerular ultrafiltration coefficient after ischemic renal injury in dogs.

Micropuncture studies of acute renal failure after ischemic renal injury suggest that glomerular ultrafiltration coefficient may remain normal in the period immediately after ischemia and decline significantly during the following 18-24 hours. The present series of in vitro experiments was designed to evaluate glomerular ultrafiltration coefficient and glomerular oncometric and rheological properties in ischemic acute renal failure in dogs. To obtain glomeruli prior to ischemia, a right nephrectomy was performed and glomeruli were isolated for studies of filtration and cell and extracellular spaces. The left renal pedicle then was occluded for 90 minutes; glomeruli isolated from biopsies of this kidney were studied at intervals up to 48 hours after ischemia. Glomeruli were isolated by sieving renal cortical fragments, and filtration was induced by an oncotic gradient. The glomerular ultrafiltration coefficient remained near control levels for the first hour after ischemia, but declined significantly at 24 and 48 hours. Specifically, glomerular ultrafiltration coefficient of glomeruli isolated from normal kidneys was 16.5 +/- 0.9 nl/min per mm Hg (n = 15). Immediately following ischemia, glomerular ultrafiltration coefficient remained essentially unchanged (15.9 +/- 1.1 nl/min per mm Hg, n = 4). At 1 hour, there was a small decrease in glomerular ultrafiltration coefficient (14.4 +/- 1.3 nl/min per mm Hg, n = 4). At 24 hours, glomerular ultrafiltration coefficient was significantly decreased (9.8 +/- 0.5 nl/min per mm Hg, n = 9, P less than 0.01) and remained at that level at 48 hours (9.5 +/- 0.5 nl/min per mm Hg, n = 8, P less than 0.001). In experimental glomeruli, the oncometric response was diminished and erythrocyte movement along glomerular capillaries was impaired. Total water and inulin spaces were measured in glomeruli from control and 48-hour postischemic periods, and glomerular morphology was studied by transmission and scanning electron microscopy at the same time.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Kidney Injury↗
PubMed1983

Mechanisms of splenectomy protection in epinephrine-induced renal and cardiac necrosis.

This study was intended to elucidate the mechanism(s) of protection afforded by splenectomy against EPI-induced ATN and myocardial necrosis. Renal function parameters, hematocrit, circulating catecholamines (EPI and NE), serum enzymes (CPK and SGOT), and urinary PGE2 were measured before and during intravenous infusion of EPI (4 micrograms/kg/min for 6 hr) in intact and chronically splenectomized animals. All but serum enzymes were measured in another group of splenectomized animals that were implanted with small fragments of the autologous spleen (autoimplanted animals) 2 weeks prior to EPI infusion. Renal function tests and urinary PGE2 levels were monitored for several hours during the recovery period. The development of ARF in intact animals was accompanied by marked increases in circulating catecholamine levels, hematocrit, and serum enzymes and by a marked decrease in urinary PGE2 levels. These animals had diffuse ATN and hemorrhagic lesions of the heart (myocardial necrosis), and none survived. Chronically splenectomized animals were protected against the adverse effects of EPI infusion. The protected animals showed minimal elevation of circulating catecholamine levels and no changes in urinary PGE2 levels or hematocrit. Serum enzymes and renal and cardiac histopathology remained essentially normal in these animals. Implantation of autologous splenic tissue in splenectomized animals caused reversal of the protective effect of splenectomy. The response of autoimplanted animals to EPI infusion was in all respects similar to that in intact animals with the exception of hematocrit, which did not rise. All autoimplanted animals survived. They showed prompt recovery of renal function associated with significant increase of urinary PGE2 levels during the recovery period. Focal ATN was observed but no hemorrhagic lesion of the heart was found. From these observations we conclude the following: (1) high circulating NE and/or low renal (urinary) PGE2 activity are important in the pathogenesis of EPI-induced ARF, (2) the spleen may release some factor(s) that modulate plasma NE level and/or renal PGE2 activity during EPI infusion, (3) EPI-induced ARF may occur independently of myocardial necrosis, and (4) hematocrit has no major role in EPI-induced ARF.

Acute Kidney Injury↗
PubMed1982

Intestinal absorption and secretion of radioactive vanadium (48VO3-) in rats and effect of Al(OH)3.

Vanadium in the metavanadate form (VO3-) is a powerful inhibitor of Na+, K+-ATPase. Because of the similarity between the oxy anions of vanadium and phosphorus, it was of interest to see whether Al(OH)3 would restrict the intestinal absorption of vanadium, as it does that of phosphorus. VO3- was extensively bound to a suspension of Al(OH)3 at pH 5-8. Sprague-Dawley rats (180-300 g) were fasted overnight and gavaged with 5 mumol Na3 VO4 in 1.0 ml 0.9% NaCl containing 1 microCi 48V. Control animals (n = 12) simultaneously received 1.0 ml diluent and experimental animals (n = 12) received 1 ml Al(OH))3. Diluent and Al(OH)3 were then given daily for 4 d. Urine and feces were collected separately each day. In control animals total 48V recovery (stool and urine) over 4 d was 86.6 +/- 2.4% of the administered dose. Although Al(OH)3 insignificantly increased total 48V recovery (93.6 +/- 3.2%), it markedly increased excretion of 48V in the stool as compared to the urine (control: stool, 69.1 +/- 1.8%; urine, 12.5 +/- 1.3%; Al(OH)3: stool, 85.7 +/- 1.5%; urine, 7.9 +/- 1.8%). Animals were then sacrificed and tissue uptake of tracer measured. The pattern of unexcreted 48V in tissue of both groups was kidney greater than bone greater than liver greater than intestine greater than muscle, but the tissue levels were uniformly higher in controls than in Al(OH)3-treated animals. The ability of Al(OH)3 to remove endogenous VO3- was also examined. 48V was injected ip (n = 20). Half of the animals received diluent and half received 1.0 ml Al(OH)3 by gavage daily for 4 d. There were no differences in the pattern of 48V tissue distribution and excretion. It is concluded that Al(OH)3 may prevent tissue accumulation of VO3- from dietary sources by reducing intestinal VO3- absorption.

Aluminum Hydroxide↗
PubMed1982

Studies on the mechanism of sodium excretion during drug-induced vasodilatation in the dog.

The administration of vasodilating agents such as bradykinin and acetylcholine cause an increase in urinary sodium excretion. Yet the mechanisms involved in this natriuretic effect are not clear. Recent studies with another renal vasodilator, secretin have shown this drug also causes a profound increase in renal blood flow but without major changes in sodium excretion. To attempt to delineate the basis of this difference in sodium excretion with these drugs, the renal functional effects of secretin and bradykinin were compared at an equivalent vasodilating dose. Bradykinin increased renal blood flow from 222 to 342 ml/min, urine volume from 0.2 to 1.2 ml/min, and urine sodium excretion from 28 to 115 mueq/min. Urine osmolality fell from 1,230 to 401 mosmol/kg. Secretin caused a comparable increase in renal blood flow (216 to 325 ml/min) while changes in urine flow, sodium excretion, and urine osmolality were significantly less. In further studies papillary plasma flow was estimated using the albumin accumulation technique. Control papillary plasma flow was 29 ml/min per 100 g. Bradykinin increased urinary sodium excretion 108 mueq/min and decreased urinary osmolality from 1,254 to 516 mosmol/kg in association with a rise in papillary plasma flow to 62 ml/min per 100 g. Urine sodium excretion, urinary osmolality, and urine flow rate, as well as papillary plasma flow rate (32 ml/min per 100 g) were unchanged from control when secretin was administered. Studies with acetylcholine were qualitatively similar to those of bradykinin. Renal blood flow increased from 150 to 248 ml/min, urinary sodium excretion increased from 20 to 243 mueq/min, urinary osmolality decreased from 1,237 to 411 mosmol/kg and papillary plasma flow increased from 39 to 52 ml/min per 100 g. It is suggested that the natriuretic effect of some vasodilators is due, at least in part, to alterations in medullary hemodynamics, as evidenced by the increase in papillary plasma flow seen with bradykinin and acetylcholine, but not secretin.

Acetylcholine↗
PubMed1979

Study of factors which modify the development of norepinephrine-induced acute renal failure in the dog.

Previous studies have demonstrated that the fall in inulin clearance which occurs 3 hours after the intrarenal administration of norepinephrine can be markedly attenuated by the prior administration of intrarenal prostaglandin E2 (PGE). Since in the previous studies PGE led to a marked increase in both renal blood flow and solute excretion, we designed the present series of experiments to investigate whether an increase in renal blood flow, solute excretion, or other factors were responsible for the protective effect in the norepinephrine model. Two renal vasodilators, bradykinin and secretin, were evaluated initially. Bradykinin administration prior to norepinephrine administration had a protective effect similar to that previously found with PGE, whereas secretin did not. Both of these vasocilators increased renal blood flow to the same degree, but only bradykinin increased urine flow and solute excretion. The fall in inulin clearance 3 hours after the administration of norepinephrine was also attenuated by two diuretics (mannitol and furosemide) which tended to increase renal blood flow. In contrast, two natriuretic agents, which are also renal vasoconstrictors (chlorothiazide and benzolamide), had no protective effect. Further, chlorothiazide and benzolamide obviated the protective effect of bradykinin. These studies demonstrate that there are several types of pharmacologic agents which can modify the magnitude of renal functional impairment resulting from extreme renal ischemia. Although the mechanism of the protective effects remain unclear, the findings are compatible with the view that the protective effect noted with PGE, bradykinin, mannitol, and furosemide may be related to an increase in osmolar excretion which occurred with administration of each of these agents. This potentially salutory effect (increased osmolar excretion), however, could be overcome by an agent (e.g., chlorothiazide or benzolamide) which also increased renal resistance prior to the administration of norepinephrine.

Acute Kidney Injury↗
PubMed1978

Urinary prostaglandin E excretion: effect of chronic alterations in sodium intake and inhibition of prostaglandin synthesis in the rabbit.

On the basis of acute experiments in animals, a role for prostaglandin E (PGE) in the regulation of urinary sodium excretion has been suggested. Limited information is available, however, concerning the possible role of PGE in chronic adjustments to sodium intake. These studies were designed to determine whether chronic changes in sodium balance would modify renal PGE excretion and whether partial inhibition of prostaglandin synthesis would alter the ability of the kidney to adjust to an alteration in sodium intake. Thus, we measured sodium and PGE excretion in rabbits on chronic high and low salt diets before and after inhibition of prostaglandin synthesis with indomethacin or meclofenamate. Although the alterations in salt intake resulted in large changes in sodium excretion there was no significant change in urinary PGE excretion. After administration of either indomethacin or meclofenamate for several days there was a significant fall in PGE excretion, but no significant change in sodium excretion. These results suggest that in the rabbit 1) chronic changes in sodium excretion can occur without modifying PGE excretion (and presumably renal PGE synthesis) and 2) inhibition of PGE synthesis does not impair the kidney's ability to adjust to a chronic high or low sodium intake.

Animals↗
PubMed1978

Organic acid secretory pathway and urinary excretion of prostaglandin E in the dog.

Urinary prostaglandin E (PGE) has been utilized as an index of renal PGE production. Recent studies, however, have suggested that the organic acid secretory pathway is a major determinant of endogenous UPGEV (urinary excretion of PGE). The following experiments were designed to quantitatively test this latter view. In clearance studies the administration of para-aminohippurate (PAH) or probenecid (25 mg/kg) failed to alter endogenous UPGEV although PAH clearance fell with probenecid. Comparison of the excretion patterns of exogenously administered [3H]PGE and [14C]inulin after intra-arterial injection into the dog renal artery (Chinard technique) demonstrated both glomerular filtration and secretion of [3H]PGE. Blockade of the organic acid pathway by probenecid (25 mg/kg) abolished [3H]PGE secretion. Indomethacin (1 mg/kg) did not alter the secretion pattern of [3H]PGE, but decreased endogenous UPGEV by over 80%. Because this low dose of indomethacin did not decrease [3H]PGE secretion, it probably decreased endogenous UPGEV by inhibiting synthesis. Thus, these tracer studies do indeed confirm the suggestion that PGE may be excreted by the organic acid pathway. However, the failure of total endogenous UPGEV to fall after blockade of the organic acid pathway would suggest that the component of UPGEV due to this mechanism is quantitatively insignificant.

Animals↗
PubMed1978

Acute renal failure: clinical aspects and pathophysiology.

Acute renal failure may be caused by multiple conditions including those which are due to some direct hemodynamic or nephrotoxic insult. In considering the pathophysiology of these entities, it seems appropriate to differentiate between the initiating and the maintenance phase of the disorder. In the former, renal ischemia and/or a direct effect of a given nephrotoxic agent seems to be the basis for the underlying renal damage. In the maintenance phase, renal functional impairment is maintained by a number of factors which include persistent renal vasoconstriction, tubular obstruction, a leakage of filtrate across damaged tubular epithelium, and a reduction in glomerular capillary permeability. The therapy and possible preventive aspects of these entities are discussed.

Acute Kidney Injury↗
PubMed1976

Renal prostaglandins and the regulation of blood pressure and sodium and water homeostasis.

In addition to its well known prohypertensive role in various states of experimental and human hypertension, the kidney has also been shown to exert an antihypertensive "endocrine" function. According to this hypothesis, certain forms of experimental and human hypertension might not solely be the result of an excess in the activity of such renal pressor systems as the renin-angiotensin system and the sympathetic nervous system, but might also result from an absolute or relative deficiency of intra-renal vasodilator antihypertensive factors which might allow pressor systems to act unopposed to produce peripheral arteriolar vasoconstriction and sustained hypertension. At least four factors have been characterized in the kidney of various animal species and man which might be responsible for such an antihypertensive function. These are (1) the renomedullary prostaglandins (PGs), (2) the renomedullary antihypertensive neutral lipid, (3) antirenin phospholipid and (4) the renal kinins. This review is restricted to an examination of the possibility that the vasodepressor renomedullary prostaglandins (PGA and/or PGE) may, at least in part, mediate the so-called antihypertensive function of the kidney and participate in the regulation of renal blood flow and natriuresis by physiologic antagonism of various renal vasoconstrictor stimuli such as the renal renin-angiotensin and the sympathetic nervous systems.

Animals↗