Mannitol-induced acute renal failure

Mannitol is widely used to reduce intracranial pressure and is protective against ischemic and nephrotoxic acute renal failure. However, the capacity of this seemingly innocuous agent to produce acute renal failure is not well recognized. We report herein the clinical course of 8 cases of mannitol-induced acute renal failure. In addition, we reviewed all previously reported cases of mannitol-induced renal failure. In the present series, acute oliguric renal failure developed within 3.5 +/- 1.1 (mean +/- SD) days after receiving daily and total mannitol doses of 189 +/- 64 g and 626 +/- 270 g, respectively, over 3.5 +/- 1.5 days. The peak serum creatinine was 5.7 +/- 2.7 mg/dl and peak osmolal gap was 74 +/- 39 mOsm/kg water. Renal tubular epithelial cells containing vacuoles were seen in the urinary sediments of 6 patients. Renal function improved rapidly upon discontinuation of mannitol and/or removal of mannitol by hemodialysis. In those previously reported cases in which the baseline renal function was normal, acute renal failure developed after receiving total mannitol doses of 1171 +/- 376 g. The peak osmolal gap was 107 +/- 17. In contrast, in those with underlying renal compromise, renal function worsened after a total mannitol dose of 295 +/- 143 g. The pathogenesis of mannitol-induced renal failure is not yet established but may be associated with renal vasoconstriction produced by high concentrations of mannitol. This may be averted in clinical practice by monitoring the osmolal gap, rather than serum osmolality alone, when using mannitol infusions for the treatment of intracranial hypertension.     

利福平致急性肾功能衰竭的临床病理特点及其机制初探

目的 初步探讨利福平引起急性肾功能衰竭的临床病理特点及其可能的发病机理。方法 对4例因应用利福平或主要含利福平成份药物所致的急性肾功能衰竭病人的临床特点、肾脏病理特征进行分析,并采用血清学抗人球蛋白试验方法检测病人的抗利福平抗体类型。结果 利福平引起急性肾衰病例占同期住院急性肾衰的1．98％。4例病人均有前驱感染史,临床主要表现为（尤其是再次用药后出现）发热、乏力、胃肠道症状,短期内出现少尿或无尿,化验可见溶血性贫血、血小反减低及肾功能损害,部分伴有肝功能损害。肾活检3例为急性肾小管坏死,1例为急性间质性肾炎。4例的血清抗利福平抗体检测均为阳性。结论 利福平引起的急性肾衰临床并不少见,尤其常见于再次用药的病人,对此类病人在用药过程中应加强对肾功能的监测,血清抗利福平抗体的检测有助于确诊。     

Hemolytic uremic syndrome by Streptococcus pneumoniae

Hemolytic uremic síndrome (HUS) is an acute disease characterized by microangiopathic hemolytic anemia, thrombocytopenia, and acute renal failure, usually,but not always, associated with the prodrome of diarrhea. A 2-year-6-month old boy with pneumonía caused by Streptococcus pneumoniae developed the third day after admission oliguric acute renal failure, anemia, and thrombocytopenia. The patient needed veno-venous hemodiafiltration/ hemofiltration during ten days. He received five packed red blood cell, and one platelet transfusions, and was treated with plasma infusions during six days. Renal function was normal at discharge. HUS caused by Streptococcus pneumoniae has more morbility and mortality that classic HUS, although they usually recovery renal function. In those cases of atypical HUS, different from others, blood transfusions that contains IgM should be avoided,because they can increase antigen-antibody reaction and cellular damage. The low incidence of HUS by Streptococcus pneumoniae and the systemic infectious component difficult the early diagnosis. Taking into account the different transfusion approach in these cases, it is necessary to be aware for diagnosing HUS by Streptococcus pneumoniae in all patients with systemic infection and sudden renal function deterioration.     

婴幼儿先天性心脏病术后急性肾功能衰竭的腹膜透析治疗

目的探讨腹膜透析（PD）对小儿先天性心脏病（先心病）术后急性肾功能衰竭（ARF）的治疗效果。方法对2例2008年于我院在体外循环下行先心术术后出现急性肾功能衰竭行腹膜透析的临床数据进行分析。结果2例病儿均在低体温体外循环下行先心病根治术,术后均出现肾功能不全并行腹膜透析治疗,分别在3-5天内肾功能恢复。结论对于婴幼儿先天性心脏病术后并发急性肾功能不全,尽早应用腹膜透析是一种较为安全、有效的治疗方法,可以有效改善患者预后。     

Acute renal failure following drip infusion pyelography

Acute renal failure is a well-known complication of intravenous pyelography in patients with diabetes mellitus or multiple myeloma.We describe 10 patients in whom acute renal failure developed after drip infusion pyelography (DIP). Of these patients, only four were diabetic and none had multiple myeloma.All patients had preexisting renal disease. Serum creatinine was higher than 1.5 mg/dl in eight. Proteinuria, vascular disease, dehydration and fluid overload were all seen in the group. An increase in serum creatinine was noted in all patients within 48 hours following DIP. Urine volume decreased in eight patients within 24 hours after the examination. Renal function returned to the levels pre-DIP in three patients in periods ranging from eight to 10 days. In five others, serum creatinine decreased almost to the prestudy levels but remained elevated by 0.7 to 1.4 mg/dl at the time of the last observation. No patient died of acute renal failure.The data indicate that (1) preexisting renal insufficiency in the setting of systemic disease is the most prevalent predisposing factor to acute renal failure after DIP; (2) renal hypoperfusion of various types seemed to render these patients susceptible to acute renal failure after DIP; (3) in some patients, acute renal failure was not typical of acute tubular necrosis; and (4) recovery of renal function toward base line after a short period of oliguria frequently occurred.In 10 patients acute renal failure developed after drip infusion pyelography (DIP). Six had neither diabetes mellitus nor multiple myeloma. All patients had preexisting renal disease. Proteinuria, vascular disease, fluid overload and volume contraction were noted. All patients had elevated serum creatinine levels and eight were oliguric. Return of renal function toward base line was frequently seen. The prevalent predisposing cause of acute renal failure after DIP was preexisting renal disease on a background of systemic disease.     

Intravascular hemolysis and renal insufficiency after bone marrow transplantation

Renal disease has not been considered a major late complication of bone marrow transplantation. Of 31 evaluable pediatric patients undergoing allogeneic or autologous bone marrow transplantation for neuroblastoma or acute lymphoblastic leukemia, 14 developed a hemolytic anemia, microscopic hematuria, and renal insufficiency at a median of 5 months (range, 3 to 7 months) posttransplant. Renal biopsies were performed in two patients at the onset of kidney disease and showed mesangiolysis with intraglomerular capillary aneurysm formation, mesangial proliferation, and focal thickening and splitting of the glomerular basement membranes. The clinical presentation, time to onset of renal disease, and biopsy material are consistent with a diagnosis of radiation nephritis, a previously uncommon finding in this patient group. The high incidence of this syndrome in the current report may have been due to the combination of intensive chemotherapy and total- body irradiation in the conditioning regimens.     

Endothelin is an important determinant of renal function in a rat model of acute liver and renal failure

BACKGROUND AND AIMS: Renal failure occurs in approximately 55% of patients with acute liver failure. We have previously shown that plasma endothelin 1 concentrations are elevated in patients with acute liver failure and the hepatorenal syndrome. There are few reported satisfactory animal models of liver failure together with functional renal failure. In this study, a rat model of acute liver failure induced by galactosamine that also develops renal failure was first characterised. This model was used to investigate the hypothesis that endothelin 1 is an important mediator involved in the pathogenesis of renal impairment that occurs in acute liver failure. METHODS: Acute liver failure was induced in male Sprague-Dawley rats by intraperitoneal injection of galactosamine together with treatment with the endothelin receptor antagonist Bosentan. Twenty four hour urine collections were made using a metabolic cage. Renal blood flow was measured in anaesthetised animals. RESULTS: This model developed renal failure and liver failure in the absence of any significant renal pathology, and with an accompanying fall in renal blood flow. Plasma concentrations of endothelin 1 were increased twofold following the onset of liver and renal failure (p<0.05), and there was significant upregulation of the endothelin receptor A (ET(A)) in the renal cortex (p<0.05). Administration of Bosentan prevented the development of renal failure when given before or 24 hours after the onset of liver injury (p<0.05) but had no effect on liver injury itself, or on renal blood flow. CONCLUSIONS: This study demonstrates that this animal model has many of the features needed to be regarded as a model of renal failure that occurs in acute liver failure. The observation that plasma levels of endothelin 1 and ET(A) receptors are increased and upregulated, and that renal failure is prevented by an endothelin antagonist supports the hypothesis originally put forward that ET(A) is important in the pathogenesis of renal failure that occurs in patients with acute liver failure.     

早期发生急性肾衰竭与急性心肌梗死后心源性休克患者预后的关系

目的了解急性心肌梗死后心源性休克患者早期发生急性肾衰竭与其预后的关系.方法回顾性分析解放军总医院1993～2003年间,因急性心肌梗死或冠心病心绞痛住院,并出现心源性休克的病例,以24h内是否出现急性肾衰竭为标准,比较其住院期间死亡率,并采用多元Logistic回归分析,评估早期发生急性肾衰竭对患者预后的影响.结果符合统计分析标准的患者共172例,其中51例(30%)于24h内出现急性肾衰竭.有无早期发生急性肾衰竭的患者,其住院死亡率分别为90%(46/51)和56%(68/121).逐步回归分析表明,早期发生急性肾衰竭是影响急性心肌梗死后心源性休克患者预后的独立因素(OR=6.7,95%可信限2.5～18;P＜0.001).结论急性心肌梗死后心源性休克患者,早期发生急性肾衰竭,与其住院死亡率显著相关,可作为判断患者不良预后的指标.     

Thrombotic thrombocytopenic purpura/hemolytic uremic syndrome secondary to pancreatitis

Pancreatitis is a rare (～2.0%) complication of thrombotic thrombocytopenic purpura/hemolytic uremic syndrome (TTP/HUS). The opposite finding has rarely been reported. We present a case of an 18 years old obese male with alcohol associated pancreatitis (amylase 840 IU/L) who three days after onset, as the pancreatitis subsided (amylase 341 U/L), developed TTP/HUS. The TTP/HUS was marked by oliguria and severe renal failure (creatinine 1,326 μmol/L), was treated with daily plasma exchanges, obtained a complete response, and recovered renal function (creatinine 115 μmol/L). Similarly, in six of seven other cases from the medical literature the TTP/HUS occurred within 2–3 days of the onset of pancreatitis.     

Streptococcus pneumoniae purulent pleurisy and hemolytic uremic syndrome. A case report

A 22-month-old infant developed purulent pleurisy caused by Streptococcus pneumoniae and a hemolytic uremic syndrome. The diagnosis was suggested by the classical triad: hemolytic anemia, renal failure and thrombocytemia confirmed by renal biopsy which demonstrated extensive cortical necrosis. Renal involvement was severe, justifying an indication for renal transplantation.     

Postpartum hemolytic uremic syndrome: a rare entity and a treatment challenge

Hemolytic uremic syndrome (HUS) is a rare entity that in 7% of cases has been related to oral contraceptives, pregnancy and puerperium, In this clinical setting prognosis is worse and renal replacement therapy is usually needed. Different authors agree that plamapheresis is the treatment of choice, and has improved patient survival to 80-90%. We describe a case of a young woman that 10 days postpartum developed thrombocytopenia, microangiopathic hemolytic anemia and acute renal failure with nephrotic range proteinuria. With the suspicion of HUS she was started on plasmapheresis initially stopped due to an anaphylactic reaction to plasma and finally due to hyperhidratation with acute pulmonary edema needing mechanical ventilation. Renal biopsy confirmed the diagnosis. Clinical course was complicated with refractory hypertension and infectious complications In conclusion postpartum HUS is a rare clinical entity , that forces a differential diagnosis with hypertensive complications of pregnancy. It is associated to multiple complications difficult to handle during follow-up. Plasmapheresis treatment adds complexity to clinical care but is the only treatment of proven efficacy in order to improve survival and renal prognosis.     

Anti-RNA polymerase III antibodies in the diagnosis of scleroderma renal crisis sine scleroderma.

We describe the use of antibodies to RNA polymerase III in the diagnosis of scleroderma in 2 patients who presented with renal crisis without other clinical features of the condition. Both presented with accelerated hypertension, rapidly progressive acute renal failure, microangiopathic hemolytic anemia, and thrombocytopenia. One patient developed digital infarcts in the course of his initial illness. Neither showed evidence of skin thickening at presentation. Nailfold capillaroscopy was normal in one patient and showed capillary dropout in the other. Renal biopsy showed findings consistent with thrombotic microangiopathy and both had anti-RNA polymerase III antibodies.     

Acute renal failure,hemolytic anemia and skin rash associated with captopril therapy

In a 71 year old white man with renovascular hypertension, a skin rash, Coombs' positive hemolytic anemia, peripheral eosinophilia and acute renal failure with eosinophiluria developed 47 days after the start of captopril therapy. The skin rash, eosinophilia and acute renal failure resolved promptly after the discontinuation of captopril therapy but the hemolytic anemia and positive Coombs, test persisted for eight weeks.     

Pulmonary hypertension, hemolytic anemia, and renal failure. A mitomycin-associated syndrome

After treatment with mitomycin C, a patient developed pulmonary hypertension with interstitial infiltrates, microangiopathic hemolytic anemia, systemic hypertension, and renal failure with the nephrotic syndrome. Open lung biopsy documented intracapillary fibrin thrombi in the pulmonary vasculature. Renal biopsy documented glomerular and arteriolar changes that were most consistent with a thrombotic-thrombocytopenic-like process. Treatment with corticosteroids, fresh-frozen plasma, and total plasma exchange was ineffective. The patient died six months after the onset. When mitomycin-C therapy is given, the clinician should be aware of the pulmonary, renal, and microangiopathic changes that can be associated with such therapy.     

Thrombotic thrombocytopenic purpura associated with von Willebrand factor-cleaving protease (ADAMTS13) deficiency in children

The physiopathology of thrombotic thrombocytopenic purpura (TTP) has been clarified since 1998, when it was shown that TTP in adults was most often associated with an acquired deficiency of von Willebrand factor-cleaving protease (ADAMTS13) due to autoantibodies, whereas TTP in children was most often associated with a hereditary autosomal recessive severe deficiency of ADAMTS13. The hereditary form of TPP (Upshaw-Schulman syndrome) is a very rare but life-threatening disease if adequate treatment (plasma therapy) is not administered. First manifestations occur before age 10 in two thirds of cases and as soon as birth in most cases. The subsequent course is characterized by recurrent hemolytic and thrombocytopenic crises, with intervals between relapses from every 3 to 4 weeks in two thirds of cases to several months or years in one third of cases. TTP crises are associated with cerebral vascular accidents in at least 30% of patients, with a risk of neurologic sequelae in approximately 20% of patients. Renal involvement includes frequent acute renal failure due to hemoglobinuria and/or thrombotic microangiopathy during hemolytic crisis and progressive renal deterioration in approximately 50% of cases, leading to chronic or end-stage renal failure in approximately 20% of patients. The clinical phenotype may vary from the typical congenital recurrent TTP. Some mild forms are limited to a fluctuating thrombocytopenia and may be misdiagnosed as idiopathic thrombocytopenic purpura. Phenotypic variability may be observed within a single family, which suggests a role of modifier genes. Fresh frozen plasma (FFP) replaces active ADAMTS13. Ten milliliters per kilogram FFP every 2 to 4 weeks suffices to maintain remission. FFP infusions are best used preventively, given that rescue infusions may not prevent central nervous system and renal involvement. It is hoped that plasmatic or recombinant purified ADAMTS13 will be available in the years to come.     

Hemorrhagic cardiac tamponade in critically ill patients with acute renal failure

PURPOSE: The purpose of this study was to report the development, management, and follow up of tamponading uremic pericardial effusion in critically ill patients with acute renal failure. SETTING: The setting for this study was an adult, 24-bed tertiary multidisciplinary intensive care unit (ICU) of a university hospital. PATIENTS: The subjects were 5 critically ill patients with multiple organ failure including acute renal failure (ARF) that was slow to resolve. RESULTS: Renal involvement was attributed to renal hypoperfusion, sepsis and myoglobinuria. Continuous veno-venous hemofiltration (CVVH) was instituted early during hospitalization in 4 cases and lasted for 35 to 48 days; renal replacement therapy was not used in 1 case. Tamponade developed late in the course of ARF, after CVVH was discontinued in the 4 cases and was effectively managed with percutaneous pericardiocentesis under echocardiography and continuous catheter drainage of the pericardial sac for 48 to 72 hours. Hemorrhagic fluid (Hb 2.2-5.9 g/dL) with lymphocyte predominance was detected. Transient constrictive-like pericarditis findings were present in all patients after the procedure. All patients were discharged from the hospital in a good condition with normal serum and creatinine levels; 1-year follow up showed a normal echocardiogram. CONCLUSION: Awareness for the possibility of hemorrhagic pericarditis and cardiac tamponade is needed in ICU patients with ARF slow to resolve. Transient constrictive-like pericarditis may present after pericardiocentesis.     

Interstitial nephropathies induced by meticillin: demonstration of distal tubule functional anomalies

Renal tubular dysfunction was investigated in two patients with meticillin-induced interstitial nephritis. Some degree of renal failure persisted after the acute episode in both cases. The first patient was investigated 10 weeks after the onset of the nephropathy. Nephrogenic diabetes insipidus and distal tubular acidosis were demonstrated. The second patient was investigated 7 months after the onset of the nephropathy. A major impairment in urinary concentration ability was demonstrated. Neither patient had proximal tubular dysfunction. These data show that meticillin-induced interstitial nephritis may be responsible for distal tubular abnormalities, namely nephrogenic diabetes insipidus and distal tubular acidosis, which may persist long after the onset of the nephropathy.     

A sporadic case of acute Hantavirus nephropathy in The Netherlands

A 32-yr-old man presented with acute renal failure preceded by a viral-like disease with high fever, bilateral loin pain, nausea, headache and slight thrombocytopenia. Renal biopsy revealed only minor tubulointerstitial abnormalities. Renal function completely normalised within 10 days after hospitalisation. The diagnosis of acute Hantavirus nephropathy was proved by serological examinations.     

Repeated daclizumab administration to delay the introduction of calcineurin inhibitors in heart transplant patients with postoperative renal dysfunction

Daclizumab is an interleukin-2 receptor antagonist which is used for induction therapy in heart transplant patients. It has few side effects and is associated with a low infection rate. Postoperative renal failure after heart transplantation is common and potentially fatal. The administration of calcineurin inhibitors in the postoperative period can aggravate the situation. We report the cases of six patients who underwent heart transplantation and developed acute renal failure in the immediate postoperative period. All were administered daclizumab weekly to avoid the introduction of calcineurin inhibitors and to facilitate recovery of renal function. Calcineurin inhibitors were introduced only once renal function had improved. Renal function recovered in all cases and there was a low complication rate. The administration of repeated doses of daclizumab to patients who experience acute postoperative renal failure after heart transplantation may provide an alternative therapeutic approach that enables calcineurin inhibitors to be avoided and, consequently, renal function to recover.Full English text available from:www.revespcardiol.org     

Acute renal failure due to ciprofloxacin

Acute renal failure developed in three patients within a few days of starting ciprofloxacin hydrochloride therapy. An allergic interstitial nephritis was suggested by fever and eosinophiluria in one patient and by erythema multiforme in another. A kidney biopsy specimen confirmed this diagnosis in one patient. Renal function improved shortly after withdrawal of the drug in all three patients. Literature survey revealed an additional three patients with a similar complication. Allergic manifestations, such as fever or rash, were a feature in most reported cases. In view of this potential complication, renal function should be closely monitored in patients receiving ciprofloxacin therapy, especially if other potentially nephrotoxic drugs are prescribed concomitantly.