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To examine the utility of Doppler ultrasound in assessing renal hemodynamics, we investigated the effects of dopamine and dobutamine on renal blood flow using Doppler ultrasound technique and conventional clearance tests in 7 healthy volunteers. After visualization of arterial blood flow in the right renal hilus by two-dimensional color flow mapping, the phasic blood flow velocity in the vessel was obtained by a pulsed Doppler method. Intravenous infusion of dopamine at a low dose increased the velocity and decreased the waveform pulsatility of renal artery blood flow without causing any significant changes in blood pressure, heart rate, or cardiac index. In contrast, dobutamine infusion increased the peak systolic velocity in a dose-dependent manner, but did not increase the mean velocity or decrease the waveform pulsatility. Percent changes of renal blood flow during infusions of both agents correlated well with those of the mean velocity. Furthermore, the degrees of changes of the waveform pulsatility were consistent with those of renal vascular resistance obtained from clearance tests and blood pressure. Our results suggest that mean velocity reflects renal blood flow and the pulsatility of blood flow waveform represents renal vascular resistance. We conclude that the effects of vasoactive agents on renal blood flow and renal vascular resistance can be estimated noninvasively, directly, and repeatedly using Doppler ultrasound.

Renal blood flow (RBF), outer cortioal blood flow (OC-rbf) and inner cortical blood flow were determined by the microsphere method in water-drinking rats and chronic saline-drinking rats at 3, 12 and

In 196 adult patients with chronic renal disease or primary hypertension, the evaluation of glomerular filtration rate (GFR) by means of creatinine clearance, ‘predicted’ creatinine clearance and [

Sulfinpyrazone (800 mg/day for 6 days) significantly reduced the excretion of the main urinary prostaglandin E metabolite by 54% in 6 healthy female volunteers. While sulfinpyrazone did not affect inulin clearance, clearances of creatinine and PAH were significantly diminished by 18.0 and 44.7%, respectively. In the anaesthetized dog sulfinpyrazone decreased PAH clearance and PAH extraction concomitantly without affecting renal blood flow. These results show that clearances of creatinine and PAH do not reliably reflect glomerular filtration and renal perfusion, respectively, during sulfinpyrazone administration. Whereas sodium balance and body weight were not significantly different between the first control period and sulfinpyrazone administration, net sodium excretion significantly increased from 121.6 +/- 5.4 mEq/day during sulfinpyrazone treatment to 139.3 +/- 6.6 mEq/day during the following control period, while body weight significantly decreased indicating modest sodium retention during drug administration. Plasma renin activity, vascular sensitivity to angiotensin II, and urinary excretion of the enzymes N-acetylglucosaminidase and alanineaminopeptidase were not affected by sulfinpyrazone administration. In summary, sulfinpyrazone caused a decrease of total body prostaglandin E formation in healthy female volunteers together with a moderate sodium retention. Despite inhibition of prostaglandin synthesis, glomerular filtration rate, plasma renin activity, or pressor effects of angiotensin II were not altered.

Plasma as well as renal clearance of 51Cr-EDTA, serum creatinine, plasma beta-2-microglobulin and endogenous creatinine clearance were compared and evaluated in patients with diabetic nephr

Thirty-nine hypertensive patients were entered into a randomized, double-blind protocol to assess the effects of enalapril (10-20 mg b.i.d.), or combined enalapril (10-20 mg b.i.d.) and hydrochlorothiazide (25-50 mg b.i.d.) therapy on renal function and hemodynamics. Enalapril, either alone or in combination with hydrochlorothiazide, effectively controlled blood pressure. In patients with an initial inulin clearance less than or equal to 80 ml/min/1.73 m2, inulin and p-aminohippurate clearances were markedly improved toward normal following either drug therapy. The filtration fraction was either unchanged (monotherapy) or increased (combination therapy), suggesting a direct glomerular effect of angiotensin-converting enzyme inhibition. Renal vascular resistance was decreased in all patients. These observations suggest that enalapril, either alone or in combination with a diuretic, has the potential to reverse renal function abnormalities encountered in the hypertensive state.

In normal subjects a relation was found between the log plasma aldosterone concentration (PAC) and the ratio of renal potassium excretion (Uĸ) and sodium delivery to the sodium-potassium exchange site (UNa+ĸ). This relationship was independent of plasma renin activity (PRA). On these grounds, the Uĸ/UNa+ĸ ratio disturbance was considered to be a function of the PAC, and this relation was considered to reflect an altered sensitivity of the distal tubule to aldosterone. In several pathological conditions involving the kidney, the relation between the PAC and Uĸ/UNa+ĸ remained normal while the glomerular filtration rate was within normal limits. Under these conditions, however, the serum potassium concentration had some influence on this relation, in that a low potassium concentration was accompanied by an elevated (though still normal) PAC relative to the Uĸ/UNa+ĸ ratio. The relation was completely abolished when the effect of endogenous aldosterone was impaired by chronic spironolactone administration in patients with essential hypertension. Analysis to these relations in chronic renal disease made it possible to classify them according to the pathophysiological disturbance in question. We conclude that determination of the Uĸ/UNa+ĸ ratio and its relation to the PAC, PRA, and serum potassium level is very useful for the analysis of disorders of potassium metabolism.

Clearance techniques were used to evaluate renal tubular sodium and water excretion in 4 patients with antibiotic-induced acute renal failure (ARF). Creatinine clearances and maximal urine flow rates

p -Aminohippurate (PAH) clearance studies were carried out on 15 patients suffering from renal disorders of different origin. In 6 patients the two kidneys were tested separately. It

To probe renal hemodynamic measurements in relation to simultaneous systemic hemodynamic measurements in normal, adult, conscious dogs on a magnesium-deficient diet, 6 experimental animals were given 4 weeks of a magnesium-deficient diet compared to 9 animals whose dietary magnesium was normal. Systemic hemodynamics were estimated using a thermodilution catheter, and renal hemodynamics were estimated by standard renal clearance techniques. Electrolytes and hormones were also surveyed in these same animals at the time of hemodynamic measurements. Heart rate was significantly higher in magnesium-deficient dogs, but there were no other systemic hemodynamic differences between the two groups of dogs. Renal blood flow, effective renal plasma flow, and urinary osmolalilty were significantly higher in the magnesium-deficient animals. Whole-blood ionized calcium and potassium, serum magnesium, and fractional excretion of magnesium were lower in the magnesium-deficient dogs. We conclude that the renal circulation is more sensitive than the systemic circulation to disturbances in magnesium balance. Disturbances of other electrolytes accompanying magnesium deficiency were also confirmed.

Plasma prostaglandins PGE2 and PGF2α, cardiac hemodynamics, total effective vascular compliance, plasma (PV), interstitial (IFV) and extracellular fluid volumes, and renal indices were determined in 13 men with either borderline or sustained essential hypertension. PGE2 measured in the central venous blood was increased in borderline and in sustained hypertensives (p 2α remained within normal ranges. Pulmonary degradation of both prostaglandins was decreased. In the overall population, the PGE2/PGF2α ratio was: (i) negatively correlated with central venous pressure (r=-0.68; p 2 and PGF2α play an important role on the compliance of the venous system and on the control of renal blood flow, contributing to the autoregulatory mechanisms of the hypertensive vascular disease.

In 32 patients with chronic renal disease due to glomerulonephritis, pyelonephritis, advanced nephrosclerosis or renal allograft rejection, xenon washout from the diseased kidney was analyzed by the m

The function of the kidney in adult subjects with Cooley’s disease has been hitherto inadequately investigated. In 10 patients suffering from thalassemia major, glomerular filtration rate, renal plasma flow, renal blood flow have been studied, together with urine concentration capacity. The authors emphasize certain pathological changes, such as the increase in renal plasma flow and the failure of the urine concentration ability. On the basis of renal biopsies, two pathogenetic theories are discussed: the functional impairment of the countercurrent system and fibrosis of the medullary tissue.

In patients with renovascular hypertension, a significant decrease in glomerular filtration rate (GFR) and in renal plasma flow (RPF) in the stenotic kidney was accompanied by a significant homolatera

Recovery of renal function to a self-sustaining level was observed in 4 patients with accelerated malignant hypertension who required chronic hemodialysis therapy. Excellent blood pressure control was achieved in all the patients on captopril therapy. Hemodialysis could be discontinued after 2-9 months of captopril therapy; on recovery of renal function levels of creatinine clearance became stable ranging from 28 to 56 ml/min within 5-15 months of captopril treatment, and remained at this level during 21-64 months of observation. The management of hypertension and the inhibition of the renin-angiotensin system afforded by chronic angiotensin-converting enzyme inhibition is very promising as a means of reversing the process of malignant nephrosclerosis.

Rats subjected to chronic occlusion of the bile duct developed marked retention of sodium, expanded plasma volumes, increased renal vascular resistance, and a fall in renal blood flow and glomerular filtration rate. The cardiac output was low and almost all the animals were shown to have systemic endotoxemia. The purpose of this study was to investigate renal and cardiovascular function in unanesthetized rats with chronic obstructive jaundice. The results suggest the importance of a reduced cardiac output amongst the factors leading to the renal retention of sodium.

To evaluate the clinical usefulness in terms of estimation for glomerular filtration rate (GFR), we determined the levels of α1-microglobulin (α1m) in the serum and urine of pati

There is evidence to suggest that the sympatheticnervous system plays a role in the regulation of renal sodium excretion. In the present experiments, the pattern of renal sodium and water excretion fo

Nine unmodified canine renal allografts were examined immediately before and after transplantation and on removal 4–7 days later. The renal blood flow, extraction of PAH and radio vitamin B12

A method is presented for determining effective renal plasma flow in man utilizing a single injection of Hippuran 131I and two plasma samples. The radioactivity remaining in the plasma at 2

Standard inulin and PAH clearances utilizing blood and urine collections were determined in 50 individuals with chronic kidney disease. Each of these patients, as well as 14 anephric patients, also ha

The effects of renal function on human renal fluoride (F-) excretion and serum F- concentrations were studied in subjects with normal renal function, in patients with variable degrees of renal insufficiency and in patients undergoing regular hemodialysis treatment. The mechanisms of human renal F- excretion include glomerular filtration and tubular reabsorption. Patients suffering from chronic renal disease tend to continue to excrete normal dietary loads of F- until the creatinine clearance decreases below 25 ml/min. In chronic renal failure elevation of the serum fluoride concentration is delayed and less than might be expected from impairment of the glomerular filtration rate, because tubular reabsorption diminishes presumably due to expansion of the extracellular fluid compartiment.

The present study was designed to refute or confirm the postulate that the use of high dose frusemide in chronic renal failure will increase the glomerular filtration rate (GFR). 7 patients in stable chronic renal failure were admitted to hospital for 20 days. For 10 days fluid balance was maintained and no diuretics given. During the next 10 days, a gram of frusemide was given orally, with fluid and electrolyte replacement based on the 24-hour urine collections which were made throughout the 20-day period. Daily estimations of sodium, potassium, urea, creatinine and osmolality were made on plasma and urine. The excretion of water (p less than 0.01), sodium (p less than 0.01) and potassium (p less than 0.05) increased significantly during the treatment period. There was no significant change in blood pressure, weight, creatinine clearance (C/CR), clearance of urea (C/Urea), total urea and creatinine excretion, serum sodium, potassium or osmolality. The results demonstrate that a gram of frusemide, administered to patients in stable chronic renal failure, does not have any effect on intrinsic renal function. However, there was a significant increase in urine volume, as well as sodium and potassium excretion.

A simplified method of renal scintigraphy carried out with 1311-Hippuran and 99mTc-DTPA diethylenetriaminopentacetate is described in man. Results were expressed as tubular clearance (with Hippuran) and glomerular clearance (with DTPA) per kidney, and compared to PAH and inulin clearances measured in the same patients. There was a close positive correlation between clearances calculated by means of renal scintigraphy and those measured by standard procedure for studying renal function. This study showed that a simple calculation allowed to express scintigraphical findings in terms of clearance.

The renal disease of inorganic fluoride was studied in 5/6-nephrectomized and kidney-intact rats in order to evaluate the influence of the extracellular fluid volume status on net tubular fluoride reabsorption. Loss of renal functional mass impaired the ability of the hydropenic uremic rat to excrete fluoride, although tubular reabsorption of fluoride was depressed. Fractional fluoride excretion was closely correlated to urinary flow rate in hydropenic rats; no influence of urinary pH from 5.80 to 6.18 could be demonstrated. Acute, moderate expansion of the extracellular fluid volume by isotonic saline was followed by a significant rise in fractional fluoride excretion in uremic as well as in control rats, indicating that extracellular fluid volume is an important physiological determinant of passive tubular fluoride reabsorption.

The influence of the renin-angiotensin system on renal autoregulation and intrarenal distribution of blood flow was studied in 10 dogs. Using a femoral-renal bypass, total renal blood flow and perfusi

Results from many laboratories, including our own, support the following view of the status of renal blood flow (RBF) in acute renal failure (ARF). During the initiation phase of virtually all forms of experimental ARF, RBF appears to be substantially decreased. The mechanisms for the decrease in RBF vary depending on the model employed. However, we have shown that changes in cardiac output are involved in both HgCl2 and glycerol models of ARF. The degree to which the decreased RBF contributes to the impaired glomerular filtration rate (GFR) characterizing the initial phase of ARF also depends on the particular model that is studied. In terms of the maintenance phase of ARF, out studies show that total RBF is essentially normal in both glycerol and HgCl2 models of ARF. A general consensus exists that RBF is not related to the decreased GFR in the maintenance phase of ARF, regardless of the model of ARF employed. Results from this laboratory suggest, however, that a hemodynamic mechanism may still contribute to the decreased filtration in ARF despite the dissociation between total RBF and GFR. This mechanism may involve an increase in preglomerular resistance, either alone or in association with a decrease in postglomerular resistance. An extensive amount of research has been performed on the renal circulation in ARF over the past two decades. It appears that this research has basically confirmed Ole Munck's impression of the role of renal blood flow in the pathophysiology of ARF.

The high blood flow rate/gram of kidney tissue supplies mainly the renal cortex. The net effect of the interaction of the renin-angiotensin system, the kallikrein-kinin system and prostaglandins is to autoregulate renal blood flow within a narrow range. Drugs and neurogenic factors also influence renal hemodynamics. The renal circulation responds to changes in extracellular fluid volume, and in cardiac output. Renal ischemia occurs readily as these parameters decrease and prompt correction of circulatory dynamics can restore renal blood flow and prevent tubular necrosis. With hypovolemia or heart failure, angiotensin II is a mediator of efferent arteriolar constriction promoting a proportionately greater fall in renal plasma flow than in glomerular filtration rate, thereby augmenting sodium reabsorption. With renal failure, glomerulotubular balance is affected conversely promoting sodium loss. Appreciating these distinctions allows recognition of inappropriate sodium retention or loss. With such data, prognosis can be estimated more accurately and attempts to restore circulatory dynamics can be guided.

We have investigated the influence of renal mobility on both renal blood flow and glomerular filtration, in order to evaluate its role as a potential intermediate cause of hypertension. In 25 untreated patients we compared between recumbent and upright position the relative change in the following five parameters: effective renal plasma flow (ERPF), glomerular filtration rate (GFR), renal mobility, peripheral plasma renin activity (PRA) and blood pressure. We found a positive correlation between the degree of renal mobility and an observed decrease in ERPF. On the other hand, no relation was found between the former and an observed decrease in GFR. The PRA appeared to rise following the decrease of the ERPF. These observations suggest that renal mobility adds to the orthostatic reduction in renal blood flow.

The effects of mannitol on the hemodynamics and excretory function of the kidney in control rats and in rats with acute renal failure (ARF), induced by glycerol, were studied using clearance, micropuncture and flowmeter techniques. In control animals, 20% mannitol significantly increased renal blood flow (RBF), urinary volume and sodium excretion and decreased urinary sodium concentration and fractional tubular sodium reabsorption. Glomerular filtration rate (GFR) and effective filtration pressure remained unchanged. 50% glycerol (10 ml/kg bw) was injected intramuscularly in other groups of rats to induce ARF. Functional impairment of the glycerol-treated animals consisted in a significant decrease in urinary sodium concentration, RBF, GFR and effective filtration pressure of superficial nephrons. Urea concentration in arterial plasma and urine volume increased significantly. Infusion of 20% mannitol into these animals led to a significant further decrease in GFR and net filtration pressure, but not in RBF. Urine volume increased to the same degree as in controls.

Renal blood flow (RBF) and its distribution were measured in acute renal failure induced by glycerol injection to water-drinking rats and to rats chronically loaded with NaCl solution. Mean RBF and intracortical blood flow distribution of both water-drinking and saline-loaded rats at 24 h after glycerol injection were not different from those of control rats. Although chronic saline loading blunted the impairment of renal function caused by glycerol as evidenced by serum creatinine values, no differences in renal hemodynamics were noted. This suggests that changes in glomerular arteriolar resistance or glomerular permeability might be of greater importance in the reduction of glomerular filtration rate than are alterations of blood flow.

Cardiac output (CO), renal blood flow (RBF) and hepatic blood flow (HBF) were measured by the microsphere method before (control) and at 4 and 10 h after the induction of acute renal failure by intramuscular injection of glycerol in water-drinking, long-term saline-drinking and long-term captopril (converting enzyme inhibitor)-drinking rats. At 4 h after glycerol injection, CO, RBF and HBF significantly decreased in all three groups. At 10 h after glycerol injection, CO, RBF and HBF recovered to 88% of the respective control levels in only the saline-drinking rats, whereas CO, RBF and HBF further decreased to 53, 38 and 58% of the control levels, respectively in the captopril-drinking rats. At this time, not only acute renal failure but also hepatic disorder developed in the water-drinking and captopril-drinking rats as indicated by elevations of serum creatinine, urea nitrogen, alanine aminotransferase and other blood chemistry levels. The development of acute renal failure was not suppressed by captopril, but by long-term saline load. Thus, we conclude that the decrease in CO is an important variable of the early decrease in renal and hepatic perfusion in glycerol-induced acute renal failure, and that the early recovery of HBF as well as RBF may play an important role in preventing the development of acute renal failure.

The purpose of this study was to confirm, using longitudinal observations in a normal population, that the rate of decline in renal function (creatinine clearance) is inversely correlated with blood pressure. The negative regression coefficients plotting individual rates of decline over time (Bcr) against mean blood pressures (MBP) were highly significant (p less than 0.001) for all subjects and subjects in category 3 (normals). Although the Bcr also decreases significantly with age and MBP increases with age suggesting this might be an age effect, a multiple regression analysis shows that both MBP and age as independent variables exert statistically significant effects on Bcr, the dependent variable.

The effect of ischemia on renal blood flow (RBF) in the rat has been an unsettled question. This study used a totally extractable indicator, radioactive microspheres, with a reference arterial sample, to study RBF quantitatively 10 and 60 min after 1 h of unilateral renal artery clamping in anesthetized, heparinized rats. The results indicate that after release of the arterial clamp, the kidney is enlarged and exhibits an increase in renal vascular resistance. RBF to the contralateral non-ischemic kidney is not different from that of a time-control series.