Theophylline-induced protection in myoglobinuric acute renal failure: further characterization

We have reported previously that aminophylline has an ameliorating effect on the course and severity of glycerol-induced myoglobinuric acute renal failure in rats. Since aminophylline dissociates into theophylline in biological fluids and since theophylline is an adenosine receptor antagonist, we attributed the ameliorating effects to antagonism of the hemodynamic effects of endogenous adenosine. However, theophylline blocks tubuloglomerular feedback and produces natriuresis, and either of these effects might have accounted for the beneficial effects in acute renal failure. Therefore, this study was designed to further characterize the effects of theophylline in glycerol-induced acute renal failure in rats. Aminophylline had dose-dependent beneficial effects, as judged by the peak serum creatinine during the 3 days following induction of acute renal failure, by the number of animals with peak serum creatinine greater than 1 mg/dL, and by the mortality rate. Both furosemide and theophylline block tubuloglomerular feedback and produce natriuresis, but aminophylline had protective effects, whereas furosemide actually increased mortality, compared with aminophylline, following induction of myoglobinuric acute renal failure. Therefore, aminophylline's protective effects are independent of tubuloglomerular feedback and natriuresis. These results offer further support for the hypothesis that adenosine-induced hemodynamic changes play a pathogenic role in glycerol-induced acute renal failure in rats.     

Survival of Rats Undergoing Continuous Bile Drainage Depends on Maintenance of Circadian Rhythm of Bile Secretion

It is very difficult to collect bile secretions from animals for extended periods of time. We compared the use of saline or water as drinking fluids to sustain the animals, which were being continuously drained of bile. Complete bile drainage was performed in 16 male Wistar rats by surgical intervention. After surgery, 8 rats were given tap water, and the other 8 were given normal saline for water. The rats that received water rapidly lost weight after bile drainage, and all died within 8 days after the operation. In contrast, all rats that drank saline maintained their body weight and survived 14 days or longer after surgery. Serum biochemistry of the rats with water intake on the third day after bile drainage revealed hyponatremia, hypochloremia, and acute renal failure resulting in hyperkalemia. In contrast, electrolyte balance and renal function were normal in the rats with saline intake, and bile was secreted continuously with a circadian rhythm. These results clearly demonstrate that saline as drinking water is essential to the replacement of lost fluids and loss of electrolytes due to bile drainage. Further, saline proved efficacious for sustaining experimental animals undergoing continuous bile collection.     

Survival of rats undergoing continuous bile drainage depends on maintenance of circadian rhythm of bile secretion

It is very difficult to collect bile secretions from animals for extended periods of time. We compared the use of saline or water as drinking fluids to sustain the animals, which were being continuously drained of bile. Complete bile drainage was performed in 16 male Wistar rats by surgical intervention. After surgery, 8 rats were given tap water, and the other 8 were given normal saline for water. The rats that received water rapidly lost weight after bile drainage, and all died within 8 days after the operation. In contrast, all rats that drank saline maintained their body weight and survived 14 days or longer after surgery. Serum biochemistry of the rats with water intake on the third day after bile drainage revealed hyponatremia, hypochloremia, and acute renal failure resulting in hyperkalemia. In contrast, electrolyte balance and renal function were normal in the rats with saline intake, and bile was secreted continuously with a circadian rhythm. These results clearly demonstrate that saline as drinking water is essential to the replacement of lost fluids and loss of electrolytes due to bile drainage. Further, saline proved efficacious for sustaining experimental animals undergoing continuous bile collection.     

Body Water and Electrolyte Composition in Acute Renal Failure

Body water and electrolyte contents have been measured by means of muscle biopsy analysis in 11 patients with untreated acute renal failure and in one patient during the diuretic recovery phase of his illness. Patients with acute oliguric renal failure show two main types of imbalance. One group shows evidence of a reduction in extracellular sodium and chloride with normal intracellular water and electrolytes. These findings are thought to be due to a combination of excess urinary salt loss during the development of oliguric renal failure, and inadequate replacement of extrarenal electrolyte losses. A second group shows overhydration of both extra- and intracellular phases, associated with an excess of sodium and chloride. The intracellular potassium concentration is reduced, owing to the intracellular water excess. The patient studied during the diuretic recovery phase of acute renal failure showed a marked loss of sodium and chloride, which emphasizes the necessity to replace urinary electrolyte losses at this stage of the illness. It is often extremely difficult to assess fluid and electrolyte balance in patients presenting with acute renal failure, and muscle biopsy analysis or isotope dilution studies may be required before accurate replacement therapy is possible.     

Metabolism and secretion of retinol transport complex in acute renal failure

Tissue uptake and distribution of retinol from circulatory vitamin A transport complex was studied in order to determine the origin of the increased serum retinol in rats with short-term acute renal failure. In rats with acute renal failure, serum retinol increased 37-70% within 2 h after surgery. After an injection of donor plasma containing 1.8 muCi of [3H]retinol in retinol transport complex, in rats with renal failure the ability to clear radioactivity was decreased 36% by 0.5 h and 57% by 2 h, as compared to sham-operated rats. The uptake and distribution of radioactivity by nonrenal tissues was similar in rats with acute renal failure and with intact kidneys. The lack of renal function did not alter hepatic cycling of [3H]retinol from the circulation and thus could not account for the increased serum retinol in renal failure. When hepatic release of retinol-retinol binding protein was blocked by colchicine, the up-regulation of serum retinol, normally observed in rats with acute renal failure, was abolished. Our studies provide strong evidence that kidney has an important role in maintaining serum retinol homeostasis by influencing the release of retinol-retinol binding protein from liver into circulation. Peripheral tissue uptake of circulatory retinol and hepatic cycling of nonutilized retinol are not directly influenced by the kidney.     

Effect of retinoic acid and apo-RBP on serum retinol concentration in acute renal failure

We recently demonstrated a rapid up-regulation of serum retinol-retinol binding protein-transthyretin concentration in rats with short-term acute renal failure. We examine the effect of retinoic acid and apo-retinol binding protein (apo-RBP) on the up-regulation of serum retinol in renal failure. Injection of retinoic acid (10 micrograms) into rats with acute renal failure or sham-operated rats increased circulatory retinoic acid concentration 29-fold within 2 h but did not influence serum retinol concentration in either group. Injection of a large dose of retinoic acid (100 micrograms) decreased serum retinol concentration in rats with acute renal failure (19%) and sham-operated rats (29%). These results suggest that changes in serum retinoic acid concentration within the near-physiological range have no effect on regulation of hepatic retinol release. Injection of a large dose of retinoic acid may depress serum retinol indirectly via a retinol sparing effect in target tissues. In rats with renal failure the serum retinol concentration, elevated 44-52% above that of sham-operated controls, was also increased to 70-164% above controls by the injection of 52-63 micrograms of apo-RBP. This suggests that circulatory apo-RBP can up-regulate serum retinol. Circulatory apo-RBP may be a positive physiological feedback signal from peripheral tissues for hepatic release of retinol.     

Drowning risks to epileptic children: a study from Hawaii.

The role of epileptiform seizures in causing drowning and near-drowning among children was studied by examining the case reports of all 140 childhood immersion accidents that occurred in an area of Hawaii over five years. Four of the 140 immersion accidents were caused partly by epileptiform seizures, but none were fatal. The combined results of the Hawaiian and Brisbane studies (total population studied over five years 1 600 000) showed that no epileptic children died from accidents in the sea or in swimming pools; and the 2.9% incidence of immersion accidents due to seizures in the Hawaiian study compares well with the incidence found in other series. If an epileptic child is mentally normal, well controlled with anticonvulsants, and supervised in the water then the risk of drowning is very small.     

Renal hypoxia and dysoxia after reperfusion of the ischemic kidney

Ischemia is the most common cause of acute renal failure. Ischemic-induced renal tissue hypoxia is thought to be a major component in the development of acute renal failure in promoting the initial tubular damage. Renal oxygenation originates from a balance between oxygen supply and consumption. Recent investigations have provided new insights into alterations in oxygenation pathways in the ischemic kidney. These findings have identified a central role of microvascular dysfunction related to an imbalance between vasoconstrictors and vasodilators, endothelial damage and endothelium-leukocyte interactions, leading to decreased renal oxygen supply. Reduced microcirculatory oxygen supply may be associated with altered cellular oxygen consumption (dysoxia), because of mitochondrial dysfunction and activity of alternative oxygen-consuming pathways. Alterations in oxygen utilization and/or supply might therefore contribute to the occurrence of organ dysfunction. This view places oxygen pathways' alterations as a potential central player in the pathogenesis of acute kidney injury. Both in regulation of oxygen supply and consumption, nitric oxide seems to play a pivotal role. Furthermore, recent studies suggest that, following acute ischemic renal injury, persistent tissue hypoxia contributes to the development of chronic renal dysfunction. Adaptative mechanisms to renal hypoxia may be ineffective in more severe cases and lead to the development of chronic renal failure following ischemia-reperfusion. This paper is aimed at reviewing the current insights into oxygen transport pathways, from oxygen supply to oxygen consumption in the kidney and from the adaptation mechanisms to renal hypoxia. Their role in the development of ischemia-induced renal damage and ischemic acute renal failure are discussed.     

高频喷射通气治疗海水淹溺肺水肿兔肺AKP活性变化的图像定量分析

用海水灌注的方法诱发海水淹溺肺水肿（ＰＥＳＷＤ）,采取高频喷射通气（ＨＦＪＶ）治疗之。以细胞化学反应和图像定量分析为手段从碱性磷酸酶（ＡＫＰ）角度研究其病理生理变化机理。结果表明,海水灌注后ＡＫＰ产物数量和密度显著增加,ＨＦＪＶ治疗后均回落至接近正常水平。推测ＰＥＳＷＤ引起ＡＫＰ活性代偿性升高,ＨＦＪＶ后,肺部氧供应改善可能是导致ＡＫＰ活性下降的原因     

Needle biopsy of the kidneys; studies of two cases of lower nephron nephrosis due to toxic solvents

In two cases of "lower nephron nephrosis" or acute renal failure, needle biopsies of the kidney were performed. The first case developed in a 46-year-old woman following inhalation of vapors from an insecticide spray and a cleaning fluid. The second case was due to ingestion of carbon tetrachloride. Histologic study of the human kidney during toxic nephrosis showed changes confined mainly to the epithelium of the proximal tubules, confirmed the diagnosis, and illuminated the clinical course. Needle biopsy of the kidney during acute renal failure did not influence the course of the disease unfavorably. It was easy, and entailed no complications. Needle biopsy of kidneys may prove as informative and valuable as needle biopsies of the liver by aiding in the prognosis as well as in the diagnosis of various renal diseases.     

Salmon lice, Lepeophtheirus salmonis, infestation as a causal agent of premature return to rivers and estuaries by sea trout, Salmo trutta, juveniles

A field experiment conducted in the River Lønningdalselven in spring 1992 supports the hypothesis that salmon lice, Lepeophtheirus salmonis, infestations may cause premature return of sea trout, Salmo trutta, juveniles, either to estuaries or to rivers. When lice infested (exposed) and uninfested (control) sea trout juveniles (post smolts) were released simultaneously into the sea, exposed fish returned to the estuarine area earlier compared with controls. Within the following two days, exposed sea trout migrated further into freshwater. At that time they were infested with a median of 62.5 lice, dominated by chalimus larvae and late juveniles. Exposed sea trout suffered from an osmoregulatory failure in sea water and this is considered one reason for infested fish returning to brackish water. While only a few control fish returned to the estuary on the day of release, some more returned to freshwater the following four days. During this time they had become heavily infested with copepodids, and carried a median of 150.0 lice. It is suggested that physiological stress and high infection pressure in the sea results in sea trout juveniles returning to estuaries and freshwater.     

Effect of propranolol on glycerol induced acute renal failure in rats

The effect produced by propranolol, administered for a prolonged period of time and in large doses, on renal function in rats has been studied, as well as the modifications induced by this treatment in an experimental model of acute renal failure, and the effects of a single dose of propranolol given 1 hour before provoking failure. Propranolol, administered chronically, causes sodium and water retention and increases creatinine clearance. Acute renal failure induced by glycerol in rats treated for 7 days with propranolol is less severe than the one produced in untreated animals. In this ARF model, a single dose of propranolol does not seem to have a protective effect.     

Role of glomerular nitric oxide in glycerol-induced acute renal failure

Myoglobinuric acute renal failure remains one of the least understood clinical syndromes and the mediators involved remain obscure. The aim of the present study was to assess the role of nitric oxide in glycerol-induced acute renal failure under normal conditions and after uninephrectomy. Acute renal failure was induced in rats by injection of 50% glycerol (10 mL x kg(-1) body weight). Half of the animals were subjected to uninephrectomy two days before glycerol injection. Two days after the induction of acute renal failure, glomeruli from some animals were isolated and glomerular nitrite production was measured. Another group of animals was used for acute clearance studies. In this case, the effect of infusing either L-NAME or L-arginine was assayed. Glomerular nitrite production was significantly decreased in glycerol-induced acute renal failure. Glomeruli from uninephrectomized animals showed an increase in nitrite production, both in normal conditions and after glycerol injection, as compared with glomeruli from non-nephrectomized animals. L-NAME infusion worsened renal function in all the study groups, but more slowly in animals with glycerol-induced acute renal failure than in control rats. In uninephrectomized animals L-NAME reduced renal function more than in animals with two kidneys. In conclusion, in this model of acute renal failure the decrease in glomerular nitric oxide production plays an important role in the decrease in renal function. After uninephrectomy, an increase in glomerular nitric oxide synthesis plays a protective role against glycerol-induced acute renal failure.     

Monophasic synovial sarcoma presenting as a primary ileal mass: a case report and review of the literature

Introduction

Iliocaval fistulas can complicate an iliac artery aneurysm. The clinical presentation is classically a triad of hypotension, a pulsatile mass and heart failure. In this instance, following presentation with multiorgan failure, management included the immediate use of an endovascular stent graft on discovery of the fistula.

Case presentation

A 62-year-old Caucasian man presented to our tertiary hospital for management of iatrogenic trauma due to the insertion of a central venous line into his right common carotid artery, causing transient ischemic attack. Our patient presented to a peripheral hospital with fever, nausea, vomiting, acute renal failure, acute hepatic dysfunction and congestive heart failure. A provisional diagnosis of sepsis of unknown origin was made. There was a 6.5 cm×6.5 cm right iliac artery aneurysm present on a non-contrast computed tomography scan. An unexpected intra-operative diagnosis of an iliocaval fistula was made following the successful angiographic removal of the central line to his right common carotid artery. Closure of the iliocaval fistula and repair of the iliac aneurysm using a three-piece endovascular aortic stent graft was then undertaken as part of the same procedure. This was an unexpected presentation of an iliocaval fistula.

Conclusion

Our case demonstrates that endovascular repair of a large iliac artery aneurysm associated with a caval fistula is safe and effective and can be performed at the time of the diagnostic angiography. The presentation of an iliocaval fistula in this case was unusual which made the diagnosis difficult and unexpected at the time of surgery. The benefit of immediate repair, despite hemodynamic instability during anesthesia, is clear. Our patient had two coronary angiograms through his right femoral artery decades ago. Unusual iatrogenic causes of iliocaval fistulas secondary to previous coronary angiograms with wire and/or catheter manipulation should be considered in patients such as ours.     

Renal sympathetic nerve regulation to heating is altered in rats with heart failure

Heart failure (HF) alters the regulation of basal sympathetic nerve discharge (SND); however, the effect of HF on SND responses to acute stress is not well established. In the present study, renal SND responses to hyperthermia were determined in chloralose-anesthetized HF rats and in sham controls. Whole body heating (colonic temperature increased from 38 to 41 degrees C) was used as an acute stressor because increased internal body temperature provides a potent stimulus to the sympathetic nervous system. Left ventricular end-diastolic pressure and the right ventricular wt-to-body wt ratio were increased (P < 0.05) in HF compared with sham rats. The following observations were made: 1) renal sympathoexcitatory responses to heating were significantly reduced in HF compared with sham rats, 2) renal blood flow remained unchanged from control levels during heating in HF rats but was significantly reduced in sham rats, and 3) renal SND responses to heating were significantly higher in HF rats with bilateral lesions of the hypothalamic paraventricular nucleus (PVN) compared with sham PVN-lesioned HF rats. These results demonstrate a marked attenuation in the responsiveness of renal SND to heating in HF rats and suggest that HF alters the organization of neural pathways mediating SND responses to heating.     

Oligaemia,Renal Failure,and Jaundice Associated with Acute Pustular Psoriasis

An episode of acute pustular psoriasis in a middle-aged man was associated with cholestatic jaundice and followed by acute tubular necrosis. It is suggested that renal failure was due to oligaemia after the loss of albumin into and from the skin. Fluid balance, central venous pressure, and arterial blood pressure should be monitored in patients with acute pustular psoriasis.     

Persistent oxidative stress following renal ischemia-reperfusion injury increases ANG II hemodynamic and fibrotic activity

ANG II is a potent renal vasoconstrictor and profibrotic factor and its activity is enhanced by oxidative stress. We sought to determine whether renal oxidative stress was persistent following recovery from acute kidney injury (AKI) induced by ischemia-reperfusion (I/R) injury in rats and whether this resulted in increased ANG II sensitivity. Rats were allowed to recover from bilateral renal I/R injury for 5 wk and renal blood flow responses were measured. Post-AKI rats showed significantly enhanced renal vasoconstrictor responses to ANG II relative to sham-operated controls and treatment of AKI rats with apocynin (15 mM, in the drinking water) normalized these responses. Recovery from AKI for 5 wk resulted in sustained oxidant stress as indicated by increased dihydroethidium incorporation in renal tissue slices and was normalized in apocynin-treated rats. Surprisingly, the renal mRNA expression for common NADPH oxidase subunits was not altered in kidneys following recovery from AKI; however, mRNA screening using PCR arrays suggested that post-AKI rats had decreased renal Gpx3 mRNA and an increased expression other prooxidant genes such as lactoperoxidase, myeloperoxidase, and dual oxidase-1. When rats were infused for 7 days with ANG II (100 ng·kg(-1)·min(-1)), renal fibrosis was not apparent in sham-operated control rats, but it was enhanced in post-AKI rats. The profibrotic response was significantly attenuated in rats treated with apocynin. These data suggest that there is sustained renal oxidant stress following recovery from AKI that alters both renal hemodynamic and fibrotic responses to ANG II, and may contribute to the transition to chronic kidney disease following AKI.     

Effects of atrial natriuretic factor on renal handling of water and electrolytes in rats

The intravenous injection of an extract of atrial myocardium into anesthetized rats during a hypotonic diuresis resulted in an increase in the renal excretion of water, sodium, potassium, calcium, magnesium, and phosphate. There was an increase in urine concentration which was probably a result of the secretion of vasopressin since it did not occur in Brattleboro (di/di) rats. A transient increase in glomerular filtration rate and renal plasma flow occurred during the first five minutes with a more sustained rise in filtration fraction. Injection of atrial extract also caused a partial inhibition of solute-free water formation in Brattleboro rats subjected to water diuresis and a partial inhibition of solute-free water reabsorption in rats subjected to maximal antidiuresis by infusing vasopressin. In neither case was the degree of inhibition as profound as that observed after injecting furosemide in a dose which caused a comparable natriuretic response. A large dose of furosemide blocked the natriuretic response to atrial extracts whereas, when a comparable level of sodium and water output was produced by massive infusions of saline, the natriuretic response to atrial extract was increased. It is suggested that atrial natriuretic factor might inhibit sodium transport in nephron segments beyond the medullary thick ascending limb. Furosemide might also act at the same tubular site or inhibit tubular secretion of the atrial natriuretic factor.     

Leptin blockade attenuates sodium excretion in saline-loaded normotensive rats

Previous investigations in normotensive animals have demonstrated a marked natriuretic and diuretic response following the acute administration of supraphysiologic doses of synthetic leptin. However, the importance of endogenous leptin in the regulation of renal sodium and water balance is not yet defined. This study examined the hemodynamic and renal excretory effects of circulating leptin blockade with a specific polyclonal antibody in groups of normotensive, chronically saline-loaded Sprague-Dawley rats. In the experimental group (n = 10), leptin antibody significantly decreased urinary sodium excretion and urinary flow by approximately 30% compared to the control rats (n = 10). Mean arterial pressure remained unchanged. Collectively, these results are interpreted to suggest that leptin is an important renal sodium-regulating factor under conditions of mild sodium and volume expansion.     

A cervical ligamentum flavum cyst in an 82-year-old woman presenting with spinal cord compression: a case report and review of the literature

Introduction

Legionnaires' disease is recognized as a multi-systemic illness. Afflicted patients may have pulmonary, renal, gastrointestinal tract and central nervous system complications. However, renal insufficiency is uncommon. The spectrum of renal involvement may range from a mild and transient elevation of serum creatinine levels to anuric renal failure requiring dialysis and may be linked to several causes. In our present case report, we would like to draw attention to the importance of the pathological documentation of acute renal failure by reporting a case of a patient with acute tubulointerstitial nephritis complicating Legionnaires' disease.

Case presentation

A 55-year-old Caucasian man was admitted to our hospital for community-acquired pneumonia complicated by acute renal failure. Legionella pneumophila serogroup type 1 was diagnosed. Although the patient's respiratory illness responded to intravenous erythromycin and ofloxacin therapy, his renal failure worsened, he became anuric, and hemodialysis was started. A renal biopsy was performed, which revealed severe tubulointerstitial nephritis. After initiation of steroid therapy, his renal function improved dramatically.

Conclusions

This case highlights the importance of kidney biopsies in cases where acute renal failure is a complicating factor in Legionnaires' disease. If the presence of acute tubulointerstitial nephritis can be confirmed, it will likely respond favorably to steroidal treatment and thus irreversible renal damage and chronic renal failure will be avoided.