Renal failure in otherwise uncomplicated acute viral hepatitis.

Twelve patients with otherwise uncomplicated acute viral hepatitis (two were HBsAg-positive) developed renal failure. Apart from dehydration due to repeated vomiting in one patient, no factor responsible for precipitating renal failure could be identified. The clinical course was characterised by renal failure with plasma urea concentrations reaching maximum values of 26-69 mmol/l (175-416 mg/100 ml). Ten patients needed dialysis for up to two weeks. Seven patients recovered completely, while the other five died from sepsis. The types of renal failure were similar to those described in fulminant hepatic failure and cirrhosis--namely, functional renal failure in five patients and acute tubular necrosis in seven. Two of the patients with functional renal failure later developed tubular necrosis. The mechanism responsible for renal failure in acute viral hepatitis is uncertain, though endotoxaemia may contribute.     

Should patients with renal failure associated with myeloma be dialysed?

In a study of renal function in multiple myeloma seven patients presented with renal failure and three developed it 16-106 months after diagnosis. All were dialysed. Infection with dehydration was a precipitating factor in all seven cases of acute or acute on chronic renal failure. Of these, two patients recovered normal renal function and one other was left with permanent renal impairment but no longer required dialysis. Results from the seven patients with acute renal failure and for the three with more chronic features support the practice of dialysis for all patients who present with renal failure. Dialysis is not indicated for those patients with progressive myelomatous disease. The study showed no evidence that chemotherapy permitted recovery from established renal failure. The prognosis in this elderly group is heavily dependent on the presence of cardiovascular or other degenerative disease.     

肾后性急性肾衰诊治临床探讨

目的分析60例肾后性急性肾功能衰竭患者的诊治。方法对60例肾后性急性肾功能衰竭患者的诊治效果进行回顾性分析。结果解除梗阻后,22例患者肾功能恢复正常,38例未完全恢复正常,其中19例行维持性血液透析。结论影象学检查是明确诊断的主要方法,梗阻程度和时间是影响肾功能恢复的关键因素。     

Carbon monoxide poisoning and nonoliguric acute renal failure.

Carbon monoxide poisoning in a 37-year-old man was complicated by neurologic damage, skin changes, muscle necrosis and nonoliguric renal failure. The relation between nontraumatic rhabdomyolysis and acute renal failure in carbon monoxide poisoning is reviewed. Recognition of the acute renal failure in such cases is important, for this complication can be fatal; the prognosis is excellent, however, if proper medical management is provided.     

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.     

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.     

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.     

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.     

Renal Failure in Acute Pancreatitis

In three patients with acute pancreatitis complicated by renal failure recovery followed dialysis and treatment of associated complications. The records of cases of pancreatitis treated at Addenbrooke''s Hospital, Cambridge, suggest that renal failure is a grave and not infrequent complication of acute pancreatitis.     

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.     

Serum Folate and Vitamine B12 Levels in Acute and Chronic Renal Disease. Effect of Peritoneal Dialysis

Serum folate and vitamin B₁₂ levels have been measured in 32 patients with renal failure. The initial mean serum folate level was raised above normal in seven patients with acute renal failure whereas the mean level in eight patients severely ill from chronic renal failure was significantly lower than normal. Serum folate levels fell during peritoneal dialysis and rose between dialyses in all these patients and also in one patient who was dialysed for acute pancreatitis.The mean serum B₁₂ level was raised in patients with both acute and chronic renal failure, but there was no consistent change in serum B₁₂ level during dialysis.Hypersegmented polymorphs were present in the peripheral blood film of most of the patients with acute or chronic renal failure. Their presence bore no relation to the clinical state, blood urea, serum folate, or serum B₁₂ level of the patients.     

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.     

Bilateral peripheral facial nerve palsy in acute poisoning with ethylene glycol

Acute poisonings with polyethylene glycol become more and more frequent. The acute poisoning with polyethylene glycol leads to a considerable metabolic acidosis and acute renal failure. Usually there is no peripheral nervous system involvement. Two cases of the bilateral facial nerve palsy in patients with renal failure due polyethylene glycol poisoning are presented. It seems that it is the first report on the lesions to facial nerve involvement in the course of the acute polyethylene glycol poisoning.     

The Clinical Spectrum of Renal Insufficiency During Acute Glomerulonephritis in the Adult

Twenty-seven adults with acute poststreptococcal glomerulonephritis were divided into two groups according to the severity of reduction in renal function: (1) 14 patients with mild depression of renal function, and (2) 13 patients with more severe renal insufficiency. In the first group the outcome was favourable, with complete clinical recovery in 11 patients. Only two patients in the second group have recovered. Five have died of renal failure and in six the chronic stage has developed. The most notable histopathological lesion observed in this group of patients was severe proliferative glomerulonephritis with a large number of epithelial crescents. According to the mode of development and time of onset of renal failure, these 13 patients could be divided into three sub-groups: (1) early renal failure without oliguria (three patients), (2) early renal failure with severe oliguria or anuria (three patients) and (3) delayed renal failure (seven patients).Although there are exceptions, the development of renal insufficiency in an adult patient suffering from acute glomerulonephritis is usually associated with a guarded prognosis.     

犬、猫肾功能衰竭的中西医结合疗法

本文介绍了中医的肾脏生理功能理论、阐述了目前西兽医及中兽医对犬猫急性肾功能衰竭、慢性肾功能衰竭发病原因的认识,分析了肾功能衰竭的中医辨证分型和急性肾功能衰竭、慢性肾功能衰竭的治疗原则。     

Mechanism-based therapeutic approaches to rhabdomyolysis-induced renal failure

Rhabdomyolysis-induced renal failure represents up to 15% of all cases of acute renal failure. Many studies over the past 4 decades have demonstrated that accumulation of myoglobin in the kidney is central in the mechanism leading to kidney injury. However, some discussion exists regarding the mechanism mediating this oxidant injury. Although the free-iron-catalyzed Fenton reaction has been proposed to explain the tissue injury, more recent evidence strongly suggests that the main cause of oxidant injury is myoglobin redox cycling and generation of oxidized lipids. These molecules can propagate tissue injury and cause renal vasoconstriction, two of the three main conditions associated with acute renal failure. This review presents the evidence supporting the two mechanisms of oxidative injury, describes the central role of myoglobin redox cycling in the pathology of renal failure associated with rhabdomyolysis, and discusses the value of therapeutic interventions aiming at inhibiting myoglobin redox cycling for the treatment of rhabdomyolysis-induced renal failure.     

Value of renal biopsy in acute intrinsic renal failure.

Eighty-four patients presented with acute renal failure and features suggesting a diagnosis of intrinsic renal disease other than "acute reversible renal failure." Renal biopsy proved valuable in establishing the diagnosis, in indicating the reversibility of the lesion, and in helping to decide on treatment.     

低剂量多巴胺对急性心衰合并肾功能不全患者的影响

目的:探讨低剂量多巴胺能否通过利尿作用改善急性左心衰患者的充血症状以及肾功能。方法:将2013年9月至2013年12月我院收治的80例急性心衰合并肾功能不全的患者随机分为对照组和治疗组,每组各40例。对照组给予常规治疗,治疗组在常规治疗的基础上加用小剂量多巴胺静脉泵入48小时。观察和比较两组患者48小时内的总尿量及血清胱抑素C的变化、充血症状、肾功能及临床疗效的差异。结果:与对照组相比,治疗组48小时总尿量、血清胱抑素C的变化、体重变化、BNP变化、肌酐变化、进展性心衰发生率、死亡率、治疗失败患者比例均无明显差异(P0.05)。结论:低剂量多巴胺不能在利尿治疗基础上减轻急性心力衰竭并发肾功能不全患者的充血症状或改善肾功能。     

Renal involvement following near-drowning in the sea

1. The metabolic changes in rats following introduction of sea water directly into the stomach were studied. The results were compared with those of a human case report of acute renal failure following swallowing of sea water. 2. In both rats and man, acute renal failure appeared within the first 24 hr. A slight improvement was found five days later. 3. There was an acute hypocalcemia. This was supposedly due to the large magnesium content of the sea water. 4. It is probable that water entering the alimentary canal, dry drowning, affects the kidneys by the initial flow of water to the intestines. This results in hemo-concentration and reduced kidney function. The abnormality is a transient one and could be due to a partial anoxia due to shrinking of the erythrocytes. 5. It is concluded that an apparently uneventful swallowing of sea water can turn into secondary drowning with transient acute renal failure.     

Acute renal failure in tropical Africa.

Between 1972 and 1975, 55 adult patients with acute renal failure were admitted to the renal unit of Korle Bu Hospital. Fourteen patients died, giving an overall death rate of 25%. Massive intravascular haemolysis after a short febrile illness was the commonest cause of acute renal failure. Clinically these patients presented with blackwater fever but in only one could Plasmodium falciparum malaria be confidently diagnosed. In half the patients various bacterial and viral infections (especially typhoid) could be incriminated as causing this blackwater fever syndrome. The incidence of glucose-6-phosphate dehydrogenase deficiency was 22.5%, but we could not confirm the impression of a greater predisposition to acute renal failure in patients with this enzyme defect.