Effect Of Bilateral Nephrectomy Research Articles

The Effect of Bilateral Nephrectomy on Renalase and Catecholamines in Hemodialysis Patients.

Background/Aims: Renalase is an enzyme with monoamine oxidase activity that metabolizes catecholamines; therefore, it has a significant influence on arterial blood pressure regulation and the development of cardiovascular diseases. Renalase is mainly produced in the kidneys. Nephrectomy and hemodialysis (HD) may alter the production and metabolism of renalase. The aim of this study was to examine the effect of bilateral nephrectomy on renalase levels in the serum and erythrocytes of hemodialysis patients. Methods: This study included 27 hemodialysis patients post-bilateral nephrectomy, 46 hemodialysis patients without nephrectomy but with chronic kidney disease and anuria and 30 healthy subjects with normal kidney function. Renalase levels in the serum and erythrocytes were measured using an ELISA kit. Results: Serum concentrations of renalase were significantly higher in post-bilateral nephrectomy patients when compared with those of control subjects (101.1 ± 65.5 vs. 19.6 ± 5.0; p < 0.01). Additionally, renalase concentrations, calculated per gram of hemoglobin, were significantly higher in patients after bilateral nephrectomy in comparison with those of healthy subjects (994.9 ± 345.5 vs. 697.6 ± 273.4, p = 0.015). There were no statistically significant differences in plasma concentrations of noradrenaline or adrenaline. In contrast, the concentration of dopamine was significantly lower in post-nephrectomy patients when compared with those of healthy subjects (116.8 ± 147.7 vs. 440.9 ± 343.2, p < 0.01). Conclusions: Increased serum levels of renalase in post-bilateral nephrectomy hemodialysis patients are likely related to production in extra-renal organs as a result of changes in the cardiovascular system and hypertension.

The beneficial effect of bilateral nephrectomy on left ventricular hypertrophy evaluated by cardiovascular magnetic resonance imaging in renal allograft recipients

The beneficial effect of bilateral nephrectomy on left ventricular hypertrophy evaluated by cardiovascular magnetic resonance imaging in renal allograft recipients

BILATERAL NEPHRECTOMY DELAYS GASTRIC EMPTYING OF A LIQUID MEAL IN AWAKE RATS

Aims: This study evaluates the effect of bilateral nephrectomy on the gastric emptying of a liquid meal. Methods: Male rats were submitted under anesthesia to cervical vessels cannulation and bilateral lumbar incision, followed or not by nephrectomy. Next day, they were gavage fed (1.5 mL) with phenol red (0.5 gmL−1) in 5% glucose solution and sacrificed 0, 10, 20, 30 or 45 min later. A blood sample was obtained for biochemical analysis while gastric dye retention was determined by spectrophotometry. Data (mean ± SEM) were compared by ANOVA and Student–Newman–Keuls tests. Results: Gastric emptying values from nephrectomy group at 10, 20, 30 and 45 min were lower (P<0.05) than those of sham-operated animals (22.0 ± 4.0 vs. 38.9 ± 6.1%, 34.1 ± 1.4 vs. 66.9 ± 1.3%, 45.5 ± 6.1 vs. 64.9 ± 5.4% and 59.7 ± 2.4 vs. 81.5 ± 4.0%, respectively). Mean arterial pressure, blood volume, serum osmolarity, urea, creatinine and potassium values were higher (P < 0.05) in nephrectomy group than in sham-operated animals (143.3 ± 2.7 vs. 100.5 ± 4.1 mmHg, 15.7 ± 0.9 vs. 8.9 ± 1.1 mL 100 g−1, 344.0 ± 10.8 vs. 299.4 ± 1.3 mOsm KgH2O−1, 344.0 ± 33.7 vs. 47.0 ± 2.8 mg dL−1, 3.6 ± 0.3 vs. 1.1 ± 0.1 mg dL−1, 6.4 ± 0.7 vs. 3.7 ± 0.2 mEq L−1, respectively). The plasmatic Na+ values did not change (139.3 ± 2.0 in sham-operation vs. 123.0 ± 7.5 mEq L−1 in nephrectomy). Conclusion: Acute loss of kidney function markedly delays the gastric emptying rates, which could be involved in gastrointestinal dysmotility complaints seen after renal failure.

Effect of bilateral nephrectomy on active renin, angiotensinogen, and renin glycoforms in plasma and myocardium.

In an attempt to clarify the relationship of the circulating and myocardial renin-angiotensin systems, active renin concentration, its constituent major glycoforms (active renin glycoforms I through V), and angiotensinogen were measured in plasma and left ventricular homogenates from sodium-depleted rats under control conditions or 2 minutes, 3 hours, 6 hours, and 48 hours after bilateral nephrectomy (BNX). Control myocardial renin concentration was 1.4+/-0.1 ng angiotensin I (Ang I) per gram myocardium per hour and plasma renin concentration was 6.7+/-1.1 ng Ang I per milliliter plasma per hour. Control myocardial angiotensinogen was 0.042+/-0.004 micromol/kg myocardium and plasma angiotensinogen was 1.5 micromol/L plasma. Two minutes after BNX and corresponding stimulation of renin secretion by anesthesia and surgery, plasma renin concentration was increased disproportionately compared with myocardial renin. Three, 6, and 48 hours after BNX, renin decay occurred significantly faster from the plasma than from the myocardium. Forty-eight hours after BNX, myocardial renin concentrations had fallen to 15% of control values, while myocardial angiotensinogen concentrations had increased 12-fold and plasma angiotensinogen concentrations had increased by only 3.5-fold. Myocardial renin glycoform proportions were identical in myocardial homogenates and plasma in control animals. At 6 hours BNX, the proportions of plasma active renin glycoforms I+II fell, while those in the myocardium significantly increased. We conclude that in control rats, active renin and active renin glycoforms are distributed as if in diffusion equilibrium between plasma and the myocardial interstitial space. After BNX, myocardial renin concentration falls dramatically, suggesting that most cardiac renin is derived from plasma renin of renal origin. After BNX, renin glycoforms I+II are preferentially cleared from the plasma but preferentially retained by the myocardium. Control myocardial angiotensinogen concentrations are too low to result from simple diffusion equilibrium between plasma and the myocardial interstitium.

Is there an internal cardiac renin-angiotensin system?

The beneficial effects of angiotensin converting enzyme (ACE) inhibitors in heart failure appear to be independent, at least in part, of their effect on blood pressure. The existence of a local cardiac renin angiotensin system is often suggested as an explanation. It has been known for some time that a substantial proportion of arterially delivered angiotensin I is converted to angiotensin II by ACE of the coronary vascular endothelium. The levels of angiotensin II in cardiac tissue are several times the levels of angiotensin II in circulating blood. Recent evidence suggests that most of the angiotensin II in the heart is not derived from angiotensin I in the circulation, and that most of the angiotensin I in cardiac tissue is generated in the tissue itself. On the other hand, renin mRNA levels are very low or undetectable in the normal heart. In addition, studies on the effects of bilateral nephrectomy on the cardiac tissue levels of renin, angiotensin I, and angiotensin II in pigs have indicated that cardiac renin originates from the kidney and that cardiac generation of angiotensin I and angiotensin II depends on renin from the kidney. Intracardiac synthesis of renin may occur under pathological conditions and during fetal development. The fact that angiotensins are generated by the heart raises the possibility of local mechanisms to regulate the concentrations of these peptides at certain tissue sites. For example, preliminary evidence suggests that binding of renin to cardiac membranes is a mechanism by which renin is taken up by the heart. A specific renin binding protein has been identified in cardiac tissue. Cardiac ACE levels may also influence local angiotensin II formation and are, in part, determined by the so called insertion/deletion ACE gene polymorphism. More detailed knowledge on the site of angiotensin generation and on its regulation will improve our understanding of the role of the renin-angiotensin system in cardiac function, hypertrophy, and postinfarction remodelling.

Adrenal and circulating renin-angiotensin system in stroke-prone hypertensive rats.

The plasma and adrenal renin-angiotensin system in stroke-prone spontaneously hypertensive rats (SHRSP) and Wistar-Kyoto (WKY) rats were examined in animals at 5, 11, 18, and 25 weeks of age. Plasma active renin was significantly increased in 18- and 25-week-old SHRSP with impaired renal function, whereas there was no difference in the plasma prorenin level or renal renin content between the two strains at all ages examined. Thus, the rate of activation of prorenin seems to be enhanced in the kidney of SHRSP with malignant hypertension. Adrenal renin contents were severalfold higher in SHRSP than WKY rats at all ages. However, adrenal angiotensin peptides were not increased in SHRSP aged 5 and 11 weeks. In 18-week-old SHRSP, adrenal angiotensin II (Ang II) and III (Ang III) levels were fourfold and 1.8-fold higher, respectively, than in WKY rats, accompanied by 1.5-fold higher plasma aldosterone. Increased adrenal angiotensin and plasma aldosterone were also found in 25-week-old SHRSP. Zonal distribution studies indicated that the elevated Ang II and III in SHRSP were derived mainly from the capsular tissue (the zona glomerulosa). To examine the contribution of circulating angiotensin to the adrenal angiotensin content, effects of bilateral nephrectomy on adrenal angiotensin and renin were examined in 18-week-old rats. At 24 hours after nephrectomy, plasma angiotensin, prorenin, and active renin were decreased to almost negligible concentrations. Conversely, in both adrenal capsular and decapsular tissues of SHRSP and WKY rats, neither angiotensin nor renin was significantly decreased after nephrectomy. These results suggest that the increase in adrenal capsular Ang II contents in SHRSP may be partly due to an enhanced local production of Ang II.

Effect of Angiotensinogen Concentration on Renin Activity Following Nephrectomy and Adrenalectomy: Implications in the Activation of Plasma Prorenin

We have studied the effects of bilateral nephrectomy and adrenalectomy on angiotensinogen concentration, plasma renin activity, and total plasma renin activity obtained after trypsin activation in rats and compared with controls. Our results show that the plasma angiotensinogen concentration of nephrectomized (NX) rats is 5-fold higher than that of adrenalectomized (AX) rats. On the other hand, plasma angiotensinogen concentration of AX rats was about 2.5-fold lower than that of control rats. While NX rat plasma possess no renin activity, its mixing (1:1, v/v) with AX plasma results in 2-fold increase in renin activity over that observed for AX plasma alone. These results suggest that the apparent increase in renin activity upon mixing these two plasmas is at least partly due to an overall increase in angiotensinogen concentration in the mixture. To show that it is not due to activation of NX plasma prorenin by a convertase from AX plasma, prorenin-free NX rat plasma was prepared by using an anti-renin immunoaffinity column. When this prorenin-free NX plasma was mixed (1:1, v/v) with AX, again a 2-fold increase in renin activity was observed which is attributed to the overall increase in plasma angiotensinogen in the mixture. It is concluded that rat plasma prorenin is probably not activated within the circulation by a prorenin convertase from the rat kidney.

Effect of bilateral nephrectomy on the recovery of blood pressure after acute hemorrhage in rats: role of renin-angiotensin system.

The effect of bilateral nephrectomy, and administration of an inhibitor of angiotensin converting enzyme, on the recovery of arterial blood pressure after hemorrhage (loss of 1% of b.wt), was studied in male Sprague-Dawley rats. Neither manoeuver significantly affected the recovery of blood pressure within the first 10 min after hemorrhage. Thereafter, the recovery of the blood pressure was markedly suppressed. The study suggests that the initial recovery of blood pressure is unrelated to the kidneys, but the later one requires their presence and depends on the activity of the renin-angiotensin system.

Effects of bilateral nephrectomy on endocrine cells of rat stomach [proceedings

These changes seem to accord with activation of the ECL and A-like cells and deactivation of the parietal cells. The results suggest that the G cells are probably also deactivated, conceivably by auto-feedback resulting from the hypergastrinaemia.

Effects of Bilateral Nephrectomy on Endocrine Cells of Rat Stomach

It has previously been shown that in the rat nephrectomy is followed by hypergastrinemia, elevated histidine decarboxylase activity, and lowered histamine content in the gastric mucosa; paradoxically this is accompanied by low gastric acid secretion and lack of response to pentagastrin. The present report deals with the morphological changes in the histamine-containing cells, gastrin (G) cells, and the parietal cells after nephrectomy. The number of gastric enterochromaffin, enterochromaffin-like and G cells was assessed by fluorescence histochemistry. In addition, the concentration of 5-HT in the pyloric mucosa and of histamine in the oxyntic mucosa was determined. Under the fluorescence microscope the enterochromaffin-like cells appeared reduced in number (p < 0.001) corresponding with significant lowering of gastric mucosal histamine content (p < 0.01) after nephrectomy. The number of enterochromaffin cells and gastrin cells was not affected, neither was the 5-HT content. The histamine-containing enter...

Changes in histologic and biochemical indexes of bone turnover after bilateral nephrectomy in patients on hemodialysis. Evidence for a possible role of endogenous calcitonin.

We studied the effects of bilateral nephrectomy on bone metabolism in 27 patients on maintenance hemodialysis. After nephrectomy plasma alkaline phosphatase fell rapidly in 10 patients whose preoperative plasma levels had been higher than normal. This fall was associated with a transient decrease in osteoblast counts of iliac-bone biopsies. A fall in plasma phosphate and a rise in plasma immunoreactive calcitonin also occurred, but calcium and immunoreactive parathyroid hormone levels did not change. Alkaline phosphatase levels remained unchanged in a control group of 17 patients on dialysis who had undergone an operation other than nephrectomy. In 26 nonsurgical patients on dialysis, immunoreactive calcitonin was inversely related to osteoblast counts. Rises in immunoreactive calcitonin may be partly responsible for the transient decreases in bone turnover after bilateral nephrectomy. Low levels of endogenous calcitonin may allow an increase in bone turnover in chronic renal failure.

Sodium restriction and inhibition of the renin-angiotensin system in renovascular hypertension in the rat.

1. In the early phase of hypertension produced by renal artery constriction with the opposite kidney intact, infusion of the angiotensin antagonist Sar1-Ala8-angiotensin II or bilateral nephrectomy lowered blood pressure. However, the extent of the fall was variable and some animals remained hypertensive after each procedure. 2. To assess whether sodium retention was the additional factor which maintained blood pressure when the renin-angiotensin system was suppressed, rats were maintained on a low-salt diet before and during the development of hypertension. The blood pressure-lowering effect of bilateral nephrectomy or antagonist infusion was not enhanced. 3. Infusion of antagonist or converting-enzyme inhibitor 6 h after bilateral nephrectomy had only a minor blood pressure-lowering action, indicating that, at this late stage after nephrectomy, the renin-angiotensin system makes only a very small contribution to blood pressure maintenance.

Anemia in Hemodialysis Patients

The association between anemia and chronic renal failure has been recognized since the early 19th century. With the introduction of regular dialysis treatment, an understanding of all aspects of this uremic complication has become of great importance, including an appreciation of the hazards of multiple blood transfusions. This analysis of hemoglobin levels and transfusion requirements in 84 dialysis patients focuses specific attention on hemolytic mechanisms, blood loss, and the effect of bilateral nephrectomy on erythropoiesis. Because no replacement for renal erythropoietin is available, particular attention must be paid to less important, but partially correctable factors that contribute to anemia. Blood transfusion requirements can then be reduced to a minimum, together with the risks of hypersplenism, hepatitis, and sensitization of the patient to alloantigens.

Anemia in hemodialysis patients

The association between anemia and chronic renal failure has been recognized since the early 19th century. With the introduction of regular dialysis treatment, an understanding of all aspects of this uremic complication has become of great importance, including an appreciation of the hazards of multiple blood transfusions. This analysis of hemoglobin levels and transfusion requirements in 84 dialysis patients focuses specific attention on hemolytic mechanisms, blood loss, and the effect of bilateral nephrectomy on erythropoiesis. Because no replacement for renal erythropoietin is available, particular attention must be paid to less important, but partially correctable factors that contribute to anemia. Blood transfusion requirements can then be reduced to a minimum, together with the risks of hypersplenism, hepatitis, and sensitization of the patient to alloantigens.

Hypertension in End‐stage Renal Disease

Blood pressure (BP), plasma renin concentration (PRC), plasma renin substrate concentration (PRSC) and exchangeable sodium (ES) have been studied in 27 patients undergoing regular hemodialysis because of end-stage renal disease. PRC was significantly higher in the hypertensive than in the normotensive patients. The pattern of PRSC was similar in the groups of patients but with a marked individual variation. ES was slightly lower in the hypertensives than in the normotensives but the difference was not statistically significant. Multiple regression analysis demonstrated a significant correlation between mean BP, the natural logarithm of PRC and ES, but the effect of ES was negligible. PRC was negatively correlated to ES in all patients, including the hypertensives. These results strongly suggest that the renin-angiotensin system is the most important factor involved in the pathogenesis of hypertension in end-stage renal disease, when sodium balance is adequately controlled. A clinical application of the predictive value of PRC concerning the effect of bilateral nephrectomy on hypertension is outlined.

Effect of Bilateral Nephrectomy on Serum Gastrin Concentration, Gastric Histamine Content, Histidine Decarboxylase Activity, and Acid Secretion in the Rat

Nephrectomy caused a marked increase in the concentration of circulating gastrin immunoreactivity but did not increase basal acid secretion. In normal rats, both histamine and pentagastrin stimulated gastric acid output, but after nephrectomy only histamine was effective. Histidine decarboxylase in the oxyntic mucosa was greatly activated following nephrectomy. Thus, in the nephrectomized rat gastrin (and pentagastrin) no longer evoked acid secretion, whereas it retained its ability to activate gastric histidine decarboxylase. The results suggest that the kidney is important for metabolism and excretion not only of gastrin but of humoral antagonists of gastrin-induced acid secretion as well.

Proceedings: Effect of bilateral nephrectomy on serum gastrin concentration, gastric histamine content, histidine decarboxylase activity and acid secretion in the rat.

In the nephrectomized rat gastrin (and pentagastrin) does not evoke acid secretion but retains its ability to activate gastric hirtidine decarboxylase. The results suggest that the kidney is important for metabolism and excretion not only of gastrin but of humoral antagonists of gastrin-induced acid secretion as well.

Clinical effects of bilateral nephrectomy : Stenzel KH, Cheigh JS, Sullivan JF, Tapia L, Riggio RR, Rubin AL: Am J Med 58: 69–75, 1975

Clinical effects of bilateral nephrectomy : Stenzel KH, Cheigh JS, Sullivan JF, Tapia L, Riggio RR, Rubin AL: Am J Med 58: 69–75, 1975

Effect of Bilateral Nephrectomy and Bilateral Ureteral Ligation on Serum Gastrin Levels in the Rat

Serum gastrin activity was determined in rats 48 hr after bilateral nephrectomy or bilateral ureteral ligation. Although both groups of rats became equally azotemic as determined by serum urea nitrogen levels, serum gastrin levels were elevated only in the rats with bilateral nephrectomies, above the levels observed in normal or sham-operated control rats. These data (1) suggest that hypergastrinemia of renal failure is related to the loss of normal functioning renal mass and is not a result of the uremic state per se, and (2) provide additional evidence supporting the role of the kidney as a major site of degradation of endogenous gastrin in the rat.

Possible contribution of renal gluconeogenesis to the development of n-monomethylacetamide-induced hyperglycemia in the rat.

The gluconeogenic capacity of the rat kidney cortex in the experimental diabetes induced by N-monomethylacetamide (NMMAA) was studied. Renal cortical slices from NMMAA diabetic rats synthesized glucose at an accelerated rate from pyruvate, α-ketoglutarate or fructose, but not from glutamine. In contrast, NMMAA added to the incubation medium inhibited glucose production by slices from normal rats, irrespective of the substrate used. To evaluate the role of renal gluconeogenesisin vivo, the effect of bilateral nephrectomy on the development of NMMAA-induced hyperglycemia was studied. The hyperglycemic effect of NMMAA was markedly blunted in nephrectomized rats. On the other hand, ureteral ligation after NMMAA administration did not prevent a normal rise in blood glucose. These data are consistent with the view that the stimulated renal gluconeogenesis in the NMMAA diabetic rat represents a significant proportion of total carbohydrate production in the body, and contributes to the elevation of the blood glucose level.