Prevention of postoperative acute renal failure

Postoperative acute renal failure (PO-ARF) is a serious complication resulting in a prolonged stay and high mortality. Patients may be at risk for this problem because of an underlying medical illness, nature of surgery, nephrotoxin exposure, or combinations of these factors. An increase in the intra abdominal pressure above 20-mm Hg is associated with an increase in the incidence of PO-ARF. Based on many clinical studies in high-risk surgical patients and patients undergoing renal transplantation, the only proven management strategies for prevention of PO-ARF are adequate volume expansion and avoidance of hypovolaemia. Drugs known to be nephrotoxic should be avoided or used with caution. Three main pharmacological agents namely mannitol, frusemide and dopamine have been extensively tried in the prevention of PO-ARF. Mannitol has proven of value only in the presence of adequate volume expansion in attenuating renal dysfunction in transplant patients. Frusemide converts oliguric renal failure to non-oliguric renal failure. The bulk of the data, including that from prospective studies indicate dopamine is only a diuretic. Fenoldopam, a dopamine analogue, has shown early promise in reports. Calcium channel blockers have not been shown to improve the outcome in renal transplantation or help in the prevention of contrast-induced nephropathy. Atrial natriuretic peptide has not been proven to be of benefit in established renal failure and its role in prevention has not been assessed.     

Prevention of ischaemic acute renal failure with superoxide dismutase and sucrose

The preventive effects of intravenously administered superoxide dismutase (SOD) and of SOD combined with sucrose on acute renal failure were investigated in rat kidneys exposed to 45 min of warm ischaemia. Superoxide dismutase (20 mg) given just before primary ischaemia and in the early recirculation phase was found to ameliorate the red cell aggregation in the renal medulla, in particular, in the inner stripe of the outer zone the volume of trapped red cells decreased from 11.2 +/- 1.6% in untreated animals to 0.02 +/- 0.001%, thus allowing improved restoration of medullary blood flow. This was also accompanied by an expected restoration of the urine osmolality reaching almost 400 mOsm kg-1 after administration of SOD + sucrose. Superoxide dismutase also restored the capillary macromolecular permeability as evidenced by normalization of plasma to lymph transport of proteins. Micropuncture studies showed that in ischaemically damaged but untreated kidneys the tubules were obstructed and that the proximal tubular pressure rose to such a level that the net driving force for filtration approached zero. This explains the marked decrease in glomerular filtration rate (GFR) from a normal value of about 1 ml min-1 to 0.01 +/- 0.02 ml min-1. After treatment with SOD the tubules were still largely obstructed, resulting in a depression of the net driving force and a decrease in single nephron glomerular filtration rate (SNGFR) to about 11 nl min-1, that is, to only 25% of the normal SNGFR. The total filtration was 0.09 +/- 0.04 ml min-1.(ABSTRACT TRUNCATED AT 250 WORDS)     

维拉帕米对缺血性急性肾功能衰竭的保护作用

目的：观察维拉帕米对缺血性急性肾功能衰竭是否具有保护作用。方法：以维拉帕米灌注切除右肾的成年雄性ＳＤ大鼠之左肾，５ｍｉｎ后夹闭左肾动脉４５ｍｉｎ，对照组则灌注生理盐水。再灌注２４ｈ后，观察左肾血流量（ＬＲＢＦ），尿量（ＵＶ），血尿素氮（ＢＵＮ），血肌酐，肌酐清除率（ＣＣｒ），左／右肾重量之比，肾脏组织学评分ＨＳＫ，尿中Ｎ＿乙酰氨基葡萄糖苷酶（ＮＡＧ）和丙氨酸氨基肽酶（ＡＡＰ）活性的变化。结果：与对     

Outer medullary circulatory defect in ischemic acute renal failure.

Changes in medullary circulation may contribute significantly to the pathogenesis of ischemic acute renal failure. The microcirculation of the outer medulla of the rat kidney was studied by morphometry, carbon injection, and scanning electron microscopy of vascular casts after temporary renal ischemia. Morphometry showed a markedly reduced vascular area and an increased tubular epithelial cell area in the outer stripe of the medulla 2 hours after blood reflow. Maximum diminution in vascular area occurred 24-48 hours after reflow, with swollen and later necrotic tubular epithelium compressing the surrounding vascular compartment. Outflow blockade of venous vasa recta in the outer stripe caused congestion of the inner stripe. Carbon injection and scanning electron microscopy of vascular casts confirmed the perfusion defects of the outer stripe. These results suggest that decreased blood reflow to the outer stripe of the medulla secondary to tubular epithelial cell swelling and necrosis plays a significant role in the pathogenesis of ischemic acute renal failure in the rat.     

Volume adjustment by renal medullary cells in hypo- and hyperosmolal solutions containing permeant and impermeant solutes.

1. The changes in the volumes of cells in slices (thickness 0-3-0-4 mm) of rat renal outer and inner medulla have been investigated during aerobic incubation for 20 min at 37 degrees C in Krebs phosphate-bicarbonate Ringer modified by the addition of urea or sucrose in order to produce a range of media hypo- and hyperosmolal with respect to the calculated tissue fluid osmolalities in these regions. 2. On the assumption that under these conditions the measured inulin space approximates to the true extracellular space (ECS), it was found that osmotic swelling or shrinkage of cells was not accompanied by any significant variation in the absolute size of the ECS. 3. Calculated cell volume changes in both regions were minimal when slices were incubated in urea-containing media iso-osmolal with tissue fluids in that region. In sucrose-containing media minimal cell volume changes occurred when media were hypo-osmolal in relation to tissue fluids by a factor of approximately 0-68. 4. In all except the most hypo-osmolal media studied, calculated cell volume changes (as percentage of initial volume) were linearly related to the reciprocal of the incubation media osmolalities. The points of interception of the regression lines on the cell volume axis were dependent upon both the region studied and the composition of the incubation medium (urea or sucrose). 5. These changes were accompanied by variations in slice solute concentrations. Slice [Na] was greatest, and slice [K] least, following incubation in those media producing the greatest percentage changes in cell volume. 6. The volume of distribution [14-C]sucrose within the inner medulla was 61-7 plus or minus 2-5 mul./100 mg wet weight of tissue (mean plus or minus S.E., n equals 6) after 10 min incubation. The increase to 70-8 plus or minus 4-2 mul./100 mg (n equals 6) after 100 min was not significant (0-1 greater than P greater than 0-05). The volume of distribution within the outer medulla rose markedly during this period, from 38-1 to 58-2 mul./100 mg.     

Effects of aging on expression of ischemic acute renal failure in rats

Ischemic acute renal failure is principally a disease of the elderly, but the effect of aging on renal susceptibility to ischemic damage has not been defined. To address this issue, adolescent (3-4 months), mature (12-13 months), and aged (24-25 months) rats underwent base-line renal functional assessments, and then they were subjected to a standardized ischemic event (37-minute, bilateral renal artery occlusion). The loss of renal function [assessed by azotemia and creatinine clearance, (Ccr)] and the severity of tubular damage (necrosis, casts) were determined 24 hours later. Base-line functional assessments indicated no significant differences in Ccr/100 gm body weight between the groups, but urinary protein excretion increased with age (p less than 0.001). In response to renal artery occlusion, the adolescent, mature, and aged rats lost 59 +/- 4, 82 +/- 4, and 94 +/- 1% of their base-line Ccr (p less than 0.01), respectively. Among the proteinuric rats, no correlation was noted between percent loss Ccr and urinary protein excretion. Despite the large differences in postischemic renal function, the extent of tubular morphologic damage did not differ among the groups. The percent loss Ccr did not correlate with necrosis (r = -0.02) or casts (r = 0.07). Although focal glomerulosclerosis and mild tubular atrophy were noted in the aged kidneys these lesions were minimal to absent in the mature rats. We conclude that aging increases susceptibility to severe ischemic acute renal failure in the rat, an effect that is apparent even during a transition from the adolescent to the mature state. This finding cannot be simply ascribed to increasing proteinuria, a loss of renal functional reserve, or to increased tubular morphologic damage. The data are most consistent with the view that underlying age-related glomerular/hemodynamic changes lead to an exaggerated functional decline in response to ischemic renal injury.     

缺血性急性肾功能衰竭下丘脑精氨酸加压素表达的变化

目的：探讨精氨酸加压素(AVP)在急性肾功能衰竭发病过程中的作用。方法：将SD大鼠随机分成对照组、术后2d和术后4d急性肾功能衰竭模型组,取脑,行精氨酸加压素的免疫组织化学反应,比较下丘脑阳性区域的灰度值。结果：急性肾功能衰竭模型组的下丘脑阳性区域的灰度值低于对照组,术后4d急性肾功能衰竭模型组的灰度值最小。结论：在急性肾功能衰竭的发生发展中,下丘脑精氨酸加压素分泌增加并参与了缺血性肾功能损伤。     

Effects of verapamil in models of ischemic acute renal failure in the rat

This study was designed to determine whether verapamil protects renal function in experimental ischemia in the rat and, if so, whether the protection is mediated by verapamil's vasodilatory action or by an effect on renal cells independent of vascular perfusion. Inulin clearance (CIn) was examined for 3 h subsequent to 40 min of unilateral intrarenal infusion of norepinephrine (0.75 microgram X kg-1 X min-1) and 3 and 48 h subsequent to 40 min of unilateral renal pedicle clamp. In norepinephrine-induced ischemia CIn fell to 0.8 +/- 0.4% of preischemic values in saline-treated kidneys and 0.5 +/- 0.3% in verapamil post-treated kidneys. By contrast, CIn fell only to 52.3 +/- 6.5% of preischemic values in verapamil-pretreated kidneys. Verapamil pretreatment significantly counteracted the intrarenal vasoconstriction produced by norepinephrine, sustaining renal blood flow during the norepinephrine infusion. In pedicle clamp-induced ischemia verapamil pre- and posttreatment had no beneficial effect on preservation of glomerular filtration rate, whereas mannitol pretreatment was beneficial. Parallel studies in the isolated perfused rat kidney confirmed the in vivo observations. In conclusion, verapamil exerts no protective effect on renal function at 3 or 48 h when ischemia is induced by renal pedicle clamp. Likewise, verapamil administration subsequent to norepinephrine-induced ischemia is ineffective in preserving renal function. Verapamil pretreatment in norepinephrine-induced ischemia preserves renal function probably by attenuating the vasoconstrictive ischemic insult due to norepinephrine.(ABSTRACT TRUNCATED AT 250 WORDS)     

Primary renal non-Hodgkins lymphoma presenting with acute renal failure

Primary renal lymphoma (PRL) has been reported in medical literature. Its occurrence is rare and controversial, the kidney being an extranodal organ. We report a case of primary renal lymphoma presenting with acute-on-chronic renal failure and unilateral involvement of the left kidney without obstruction and with minimal peripheral organ involvement. Definitive diagnosis was made from histologic examination of the mass postoperatively. Renal function became stabilized after the removal of the tumor.     

老年急性肾功能衰竭的特点

目的：老年急性肾功能衰竭（Acute renal failure,ARF）随着老年化的进程而逐年上升,且病情复杂,并发症多见,预后险恶。由于老年肾脏结构功能的退行性变及其机体整体功能的下降,致使老年急性肾功能衰竭有其自身的特点,现就此作一综述。     

Prevention of acute renal failure: role of vaso-active drugs, mannitol and diuretics

Evidence exists that acute renal failure (ARF) independently increases mortality risk in critically-ill patients. Therefore prevention of ARF seems of paramount importance. Preservation of renal blood flow and (sufficient) perfusion pressure favourably influences the prevention of renal function deterioration in the critically-ill septic patient. The first step to achieve this is infusion of fluids, either crystalloids or colloids, with the aim of optimal fluid resuscitation. Although "optimal fluid resuscitation" is poorly defined, in clinical practice it can be considered as the point where a certain preload is obtained, after which no further increase of cardiac output is observed with further fluid infusion. Vasoactive drugs can be added to this regimen in case of insufficient restoration of flow and especially perfusion pressure. The addition of norepinephrine can be of value if high doses of dopamine fail to restore perfusion pressure. No evidence exists that low-dose dopamine prevents renal failure and, therefore, dopamine should not be given for this indication. The use of diuretic agents can be harmful, as indicated by observational and cohort studies. Although mannitol flushes out intratubular casts and increases tubular flow, which is favorable in myoglobinuria or hemoglobinuria, so far no well designed clinical studies have demonstrated its efficacy in ARF In conclusion, there is currently no convincing evidence for any benefit from diuretic agents and/or (low dose) dopamine in the prevention of ARF. High quality intensive care and avoidance of harm is, therefore, the current standard of the prevention of ARF.