Redistribution Of Renal Blood Flow Research Articles

Transient Hyperechoic Renal Cortex Caused by Dehydration and Induced Acute Renal Failure in Two Patients with Intra-Abdominal Infection

Increased renal cortical echogenicity can be seen in patients with various underlying renal abnormalities. However, there are no reports of hyperechoic cortex associated with volume depletion until now. Here, we describe two cases of hyperechoic cortex caused by severe dehydration due to liver abscess and acute salmonellosis which lead to nausea, vomiting, and diarrhea. After administering large amounts of fluid supplements, the renal functions dramatically recovered and the echogenicity of the renal cortex returned to normal. Redistribution of renal blood flow and cortical ischemia may play a role in changes in echogenicity that occur in the renal cortex. Additionally, studies on increased renal cortical echogenicity and dehydration are reviewed.

Renal Blood Flow Redistribution During Acute Kidney Injury

We describe a case of acute kidney injury with decreased kidney perfusion in which contrast-enhanced computed tomography of the abdomen was performed for a nonrenal indication. This imaging procedure showed intrarenal blood flow redistribution from the cortex to the medulla that reversed after recovery of kidney function. Renal blood flow redistribution was described first almost a century ago in experimental models of renal ischemia, but clinical imaging studies are scarce. We provide a clear example of this phenomenon using contrast-enhanced computed tomography.

Cardio-renal Interaction

The interactions between the heart and kidney have recently been the focus of intense investigation. Epidemiological studies have shown that even mild reduction of renal function is an important risk factor for worse outcome in patients with heart failure or myocardial infarction. Deterioration of renal function may be a consequence of neuro-hormonal alterations associated with cardiac dysfunction or may be caused by intrinsic renal diseases. In heart failure, the kidney undergoes series of adaptational changes (both functional and structural) that include re-distribution of renal blood flow, altered expression of transporters in distinct nephron segments and altered pressure natriuresis.

Renal renin–angiotensin system contributes to exercise‐induced redistribution of renal blood flow

Renal renin–angiotensin system contributes to exercise‐induced redistribution of renal blood flow

Edema and acute renal failure.

Acute renal failure (ARF) with overhydration and edematous state may follow Acute endocapillary proliferative glomerulonephritis and extracapillary glomerulonephritis, because of reduction of the glomerular capillary area available for filtration. But ARF may also be observed in edematous patients with minimal change nephrotic syndrome; it may require dialysis until recovery and is attributable to some of the following factors: (1) ischemic renal injury, (2) hypovolemia, (3) interstitial edema with tubular collapse, (4) redistribution of renal blood flow (RBF) from cortical to juxtaglomerular nephrons, (5) decrease of capillary filtration coefficient (Kf), (6) use of nonsteroidal antiinflammatory drugs. Congestive heart failure also leads to prerenal azotemia and edema formation secondary to salt retention. Multiple organ dysfunction syndrome (MODS) is frequently associated with ARF; but edema occurs even without ARF in septic patients with severe inflammatory response syndrome (SIRS). ARF may follow severe burns; burned patients are frequently edematous because of a rapid leak of fluid from the vascular bed into the wound; edema in undamaged areas occurs in the 'flow phase', because of a fall of oncotic pressure because of massive loss of plasma proteins into the wound. Edema must be treated with diuretics or by dialysis.

Redistribution of renal blood flow after SWL evaluated by Gd-DTPA-enhanced magnetic resonance imaging.

Extracorporeal shockwave lithotripsy (SWL) is currently accepted as an effective noninvasive treatment for a wide variety of urinary tract calculi. However, the bioeffects of high-energy shockwaves on renal parenchyma have yet to be fully elucidated. The objective of this study was to measure the acute changes in regional renal hemodynamics associated with SWL utilizing dynamic gadolinium-DTPA-enhanced magnetic resonance imaging (MRI). Seven patients who underwent SWL for renal calculi had an MRI study within 4 hours after the treatment. To assess renal hemodynamics, a bolus of Gd DTPA (0.03 mmol/kg) was administered, and dynamic contrast enhanced images was obtained. Regions of interest (ROI) were defined over the cortex and medulla to obtain signal intensity-v-time curves. The contralateral kidney in each patient was used as the control. The initial slope of the contrast-enhanced signal intensity-v-time curve was used as a measure of the perfusion index (PI). In six patients, perfusion imaging showed a consistent trend of decreased cortical flow (29+/-8%) and a concomitant increase in medullary flow (34+/-14%) in the region of the kidney that was targeted with SWL in six patients (86%). This study shows that renal hemodynamics are modified by SWL. We hypothesize that this change represents a shunting of flow from cortex to medulla in an attempt to prevent ischemia of the medulla.

Pathophysiologic mechanisms in analgesic-induced papillary necrosis

The nonnarcotic analgesics have been implicated as a significant cause of chronic renal failure worldwide. Epidemiologic studies of habitual abuse and necropsy studies show a strong relationship between the two. Animal studies designed to elucidate underlying mechanisms have been hampered because the lesion occurs infrequently and only after very high doses are given for prolonged periods; however, the Fischer 344 and Wistar rats appear to be more sensitive, and substantial new information should be forthcoming. In this review, some of the evidence for the possible mechanisms of papillary necrosis are presented: prostaglandin inhibition, reduction or redistribution of renal blood flow, direct cellular injury, free radical formation, and immunologic injury. At present, most data support prostaglandin inhibition and reduction or redistribution of renal blood flow, but direct cellular injury also appears to be very important.

Nitric Oxide Mediates Redistribution of Intrarenal Blood Flow during Bacteremia

The normal or hyperdynamic circulatory response during the early phases of the systemic septic response is associated with renal microvascular constriction and can result in renal dysfunction. Intrarenal redistribution of blood flow from the outer cortex to the medulla appears to account for decreased glomerular filtration in spite of normal or elevated renal blood flow, but the mechanisms of this response are not well described. Nitric oxide is recognized as an important regulator of regional blood flow during both normal and pathologic conditions including sepsis, and we hypothesized that alterations in nitric oxide contribute to redistribution of renal blood flow during sepsis. The current study used laser Doppler fluximetry and clearance of p-aminohippuric acid (effective renal plasma flow, ERPF) to study intrarenal distribution of blood flow during basal conditions and during normodynamic Escherichia coli bacteremia, with and without inhibition of nitric oxide. Inhibition of nitric oxide in normal animals resulted in a decrease in ERPF (-19%) with a decrease in cortical flux (-39%) without alteration of medullary flux. Bacteremia resulted in a decrease in cortical flow (-17%), an increase in medullary flow (36%), and a modest reduction (-9%) in ERPF. Inhibition of nitric oxide synthase during bacteremia worsened cortical flow (-43%), reversed the increase in medullary flux (-42%), and further impaired ERPF (-28%). These data suggest that nitric oxide regulates renovascular tone during normal conditions and bacteremia, and indicate that it is a prime mediator of intrarenal redistribution of blood flow during sepsis.

Effect of volume expansion on papillary blood flow and sodium excretion

The present study examined whether changes in plasma oncotic pressure or hematocrit play a role in the redistribution of renal blood flow and the natriuretic response to extracellular fluid volume (ECFV) expansion with saline. Intravenous infusion of saline produced a 46% increase in the flow of red blood cells (RBCs) in the papilla of Inactin-anesthetized euvolemic Munich-Wistar rats (n = 6). This was primarily due to an increase in the number of functional capillaries perfused with moving RBCs, as indicated both by laser-Doppler flowmetry and videomicroscopy. The velocity of RBCs in ascending or descending vasa recta was not significantly altered by the infusion of saline. Plasma volume expansion with a 6% solution of albumin (n = 6) did not increase papillary RBC flow, whereas volume expansion with whole blood produced a 17% increase in the flow of RBCs in the papilla. Sodium excretion after ECFV expansion with saline (n = 6) was greater than that seen after plasma volume expansion with a 6% solution of albumin (n = 5). The results indicate that the rise in papillary RBC flow after ECFV expansion with saline is due to an increase in the number of perfused vasa recta capillaries. The failure of plasma volume expansion to alter papillary RBC flow suggests that changes in plasma oncotic pressure and/or renal interstitial pressure may signal the rise in papillary RBC flow after intravenous infusion of saline. The present study also indicates that laser-Doppler flowmetry is a useful technique to monitor changes in the flow, velocity, and concentration of moving RBCs in tissue.

Effect of parathormone on reactivity of the renal blood flow to vasopressin in normotensive and spontaneously hypertensive rats

It has been shown that after parathyroid hormone (PTG) administration vasopressin increases the falling rate of the renal cortical blood flow and decreases the falling rate of the renal medullary blood flow in normotensive rats. In spontaneously hypertensive rats (SHR) the PTG decreases the falling rate of the cortical and medullary blood flow after vasopressin administration. PTG-induced hypercalcemia in SHR followed by vasopressin administration leads to the renal blood flow redistribution reaction due to which the medullary blood flow dominates over the cortical one.

Role of prostaglandins in mediating the renal effects of atrial natriuretic factor.

The natriuretic response to the intrarenal administration of atrial natriuretic factor (ANF) is accompanied by an increase in the synthesis of prostaglandins and by a redistribution of renal blood flow from the superficial to the deep cortex. This study was undertaken to define whether prostaglandins mediate the ANF-induced redistribution of renal blood flow and if prostaglandins and renal blood flow redistribution contribute to the natriuretic actions of ANF. In anesthetized dogs, the intrarenal administration of indomethacin (10 micrograms/kg/min) or the intravenous administration of meclofenamate (5 mg/kg) completely prevented the sixfold and twofold increments in urinary prostaglandin E2 and 6-keto-prostaglandin F1 alpha excretion, respectively; it also abolished the redistribution of renal blood flow to the deep cortex. However, ANF induced a similar natriuresis before (from 53 +/- 17 to 281 +/- 48 microEq/min) and after (from 45 +/- 13 to 273 +/- 60 microEq/min) the administration of prostaglandin synthesis inhibitors. It is concluded that the ANF-induced redistribution of renal blood flow to the deep cortex is prostaglandin-mediated but that neither redistribution nor increased prostaglandin synthesis is an important mediator of ANF's natriuretic action.

Multiple effects of calcium entry blockers on renal function in hypertension.

Characterization of the renal effects of calcium entry blockers has not been easy because the inhibition of Ca2+ cellular influx alters several regulatory functions. The ability of calcium blockers to dilate renal vasculature and to increase glomerular filtration rate is largely determined by the preexisting vascular tone. However, the increments in sodium excretion could occur without alterations in renal hemodynamics. Calcium blockers could increase sodium excretion by inducing a redistribution of renal blood flow toward juxtamedullary nephrons, by inhibiting tubuloglomerular feedback responses, or by a direct action on the tubular transport of sodium. These effects are poorly understood at present. In vitro studies show that the blockade of calcium entry enhances renin secretion and decreases prostaglandin synthesis. This dissociation has not been found during long-term administration, which has been proved to be effective for the treatment of essential hypertension with normal maintenance of renal function. In this respect, there are reports indicating that calcium blockers are particularly effective in a subgroup of patients with essential hypertension who exhibit subtle but detectable alterations in calcium metabolism. Further studies are needed to determine whether this significant response to calcium blockers is due to correction of an early defect of calcium cellular kinetics that initiated the increase in blood pressure.

Alterations in Renal Perfusion and Renal Energy Charge in Murine Peritonitis

Whether acute renal failure following overwhelming bacterial septicemia is a initially a consequence primarily of a cytotoxic insult or a perfusion insufficiency remains unclear. To assess the effects of intra-abdominal sepsis on the distribution of renal blood flow and renal cell bioenergy status, the glomerular filtration rate (GFR), effective renal plasma flow (ERPF), and energy-charge ratios were measured in rats following cecal ligation/puncture (CLP) or sham laparotomies. The CLP animals demonstrated a decrease in ERPF of 42% and 58% from sham groups at ten and 20 hours, respectively. The GFR showed similar but more severe impairments of 53% and 71% at ten and 20 hours, respectively, following insult despite moderate increases in cardiac output. The disproportionate decrease in GFR over ERPF supports the hypothesis of a corticomedullary redistribution of renal blood flow in sepsis. Renal energy charge, unchanged at ten hours, decreased significantly at 20 hours. Diminished renal perfusion and the redistribution of renal blood flow precedes and may contribute to the renal cell bioenergy derangements in septic acute renal failure.

Redistribution of renal blood flow in patients with liver cirrhosis: The role of renal PGE 2

Cirrhotic patients frequently show a decrease in renal blood flow and redistribution of the flow from the outer cortex to the juxtamedullary cortex. The cause of the maintenance of juxtamedullary perfusion is not presently known. Prostaglandin E2 (PGE2) has its vasodilating effect on medullary and juxtamedullary vessels where it is synthesized. Therefore, its increased production, frequently shown in cirrhotics, could be responsible for the relative preservation of juxtamedullary blood flow. To verify this hypothesis we examined 13 cirrhotic patients. In these patients we determined mean renal blood flow (MRBF), blood flow in the 1st compartment (ICBF) and in the 2nd compartment (IICBF) with the 133-Xenon washout technique and PGE2 plasma levels in the renal veins (PGE2V). MRBF and ICBF were significantly reduced as compared to control subjects (P less than 0.01); IICBF resulted unaltered. Significant correlation was found between IICBF and PGE2V (P less than 0.01). Our data confirm the decrease in renal blood flow and the redistribution of intrarenal blood flow in cirrhotic patients. The maintenance of IICBF is likely to be a consequence of PGE2 renal production.

Effects of a synthetic human atrial natriuretic polypeptide on regional blood flow in rats

The effects of α-hANP on systemic hemodynamics and regional blood flow were examined in conscious WKY and SHR. An intravenous infusion of α-hANP (3 μg/kg per min) resulted in a rapid and marked fall of blood pressure and of total peripheral resistance but with no change in cardiac output in both strains. α-hANP decreased vascular resistance in most organs and there was a redistribution of renal blood flow. Thus, the acute hypotensive effect of α-hANP is probably related to a vasodilator action.

Effect of neonatal sympathectomy by 6-hydroxydopamine on renal hemodynamic parameters in adult rats

Newborn rats were sympathectomized with 6-hydroxydopamine (6-OHDA) (10 mg/100 g b.w., once daily on the first 4 postnatal days). Hemodynamic parameters were determined at the 55th d of life. In comparison to non-sympathectomized control rats the blood pressure and total peripheral resistance of 6-OHDA treated animals were significantly diminished whereas the cardiac output was enhanced. In sympathectomized rats the resistance values of the whole kidney as well as of the cortex and outer medulla were lower than in control animals. No redistribution of renal blood flow was detectable. The results show a long lasting effect of neonatal denervation by 6-OHDA at least up to the 55th d of life.

Effects of infrarenal aortic cross-clamping on renal hemodynamics in humans.

While the systemic cardiovascular consequences of infrarenal aortic cross-clamping during aortic abdominal surgery are well documented, its repercussions on renal hemodynamics in humans have not been reported. In 12 patients, scheduled for elective aortic surgery, renal clearances, using 51Cr EDTA and 125I hippuran, were measured before, during, and after infrarenal aortic cross-clamping. A continuous infusion of mannitol 20% at a rate of 100 ml/h was administered throughout the study. Arterial and renal venous blood sampling, obtained at the midpoint of each period, permitted calculation of the extraction fraction of 125I hippuran and accurate determination of renal blood flow and its cortical-extracortical distribution. Although cardiac output and systemic vascular resistance did not change significantly between the three study periods, infrarenal aortic cross-clamping decreased 125I hippuran clearance by 29 +/- 15% (P less than 0.05) and renal blood flow by 38 +/- 14% (P less than 0.001). Simultaneously, an increase of 75 +/- 31% in renal vascular resistance (P less than 0.05) was observed and the extraction fraction of 125I hippuran increased from 0.67 +/- 0.05 to 0.74 +/- 0.05 (P less than 0.01). All of these changes, which indicate global diminution of renal perfusion with a redistribution of renal blood flow toward the cortical compartment, persisted for at least 1 h after release of the aortic clamp. Early signs of renal tubular damage, such as the appearance of lysozyme and ligandine in the urine, however, were never observed. The authors conclude that infrarenal aortic cross-clamping produces profound and sustained alterations in renal hemodynamics and may be harmful in patients with impaired renal function or when surgical occlusion of the aorta is prolonged.

Computed Tomography in Renal Ischemia

Postcontrast computed tomography in 2 patients with renal ischemia demonstrated the presence of patchy wedge-shaped high density areas in the renal parenchyma. These abnormalities were transient and gradually reverted to normal after correction of the ischemic incident. We propose that these findings were secondary to vasoconstriction and postulate that similar changes may be expected in other conditions where renal blood flow redistribution or vasoconstriction, or both, occur.

171 HEMODYNAMIC BASIS FOR RENAL FAILURE IN REYE SYNDROME

The relationship of intravascular volume depletion (IVVD) to hemodynamics and renal failure in Reye syndrome (RS) was studied in three comatose children managed with mannitol osmotherapy (dosage total 7 ± 0.7 gm/kg) without barbiturate loading. Common hemodynamic parameters proved insensitive indicators of IVVD, remaining elevated (CVP 8 ±2 torr, PWP 10 ± 2 torr, MAP 109 ± 30 torr, CI 3.2 ± 0.9 1/min/m2) despite microcardia, reduced stroke index (25 ± 8 ml/beat/m2), and intense peripheral vasoconstriction (SVR 33 ± 7 units). Nonoliguric renal failure (hourly output 2.7 ± 1.2 ml/kg) developed in 2 of 3 cases (peak BUN 50 ± 2 mg/dl and peak creatinine 3.3 ± 0.5 mg/dl). Peak serum osmolality was 337 ± 6 mOsm/1. Systemic vasoconstriction responded to volume expansion on 6 occasions (5% albumin 11 ± 6 ml/kg) with a 38% decrease (P=0.005) in SVR (20.5 ± 2 units) and a 41% increase (P=0.047) in stroke index (35 ± 12 ml/beat/m2). Filling pressures rose slightly (CVP 10 ± 2 torr, PWP 11 ± 3 torr), MAP fell slightly (92 ± 11 torr), and CI rose (P=0.010) by 28% (4.1 ± 0.7 1/min/m2). Fluid challenge effects were transient but diagnostic. Renal failure resolved with liberalized fluid intake. The data suggest that a vasoconstrictive response to IVVD may cause a redistribution of renal blood flow and play a role in the development of renal failure in RS.

The role of renal metabolism of PGE 2 in determining its activity as a renal vasodilator in the dog

Since the mammalian renal cortex avidly metabolizes prostaglandin E 2 (PGE 2), we examined the importance of renal metabolism of PGE 2 in determining its renal vascular activity in the dog. We used 13, 14 dihydro PGE 2 (DHPGE 2) as a model compound to study this because DHPGE 2 retains similar activity to the parent prostaglandin, PGE 2, but is a poorer substrate than PGE 2 for both the metabolism and the cellular uptake of the prostaglandins. Using dog renal cortical slices, we found that under similar experimental conditions, PGE 2 was metabolized several-fold faster than DHPGE 2. Both prostaglandins were metabolized to the 15 keto 13, 14 dihydro PGE 2, which was positively identified using GC-MS. In vivo, we infused increasing concentrations of DHPGE 2 into the renal artery of dogs and measured renal hemodynamic changes using radioactive microspheres. DHPGE 2 was a potent renal vasodilator beginning at an infusion rate of 10 −9g/kg/min. When compared to PGE 2, DHPGE 2 was about 10 times more potent in affecting renal vasodilation. The intrarenal redistribution of blood flow towards the inner cortex seen with DHPGE 2 was identical to that seen with PGE 2. We conclude that renal catabolism of PGE 2 is very important in limiting the in vivo biological activity of PGE 2, but regional differences in metabolism of PGE 2 within the cortex are an unlikely determinant of the pattern of redistribution of renal blood flow.