Renal failure in liver disease

Progressive renal failure in cirrhosis and fulminant liver disease remains an adverse prognostic factor. Irrespective of the type of renal functional impairment which ranges form "prerenal failure" to "hepatorenal syndrome" and "acute tubular necrosis", renal hypoperfusion, as a consequence of either reduced perfusion pressure or increased renal vascular resistance, is an important pathomechanism. Awareness of the risk of renal failure and avoidance of nephrotoxic agents and of brisk reductions in effective circulating volume are important for prevention. Plasma volume expansion, on the other hand, is mandatory in trying to reverse incipient renal functional impairment. Pharmacological attempts to improve renal hemodynamics by lowering renal and increasing extrarenal vascular resistance have so far largely been disappointing. However, increasing knowledge about mediators and synthesis of specific agonists and antagonists, such as those against endothelin or antidiuretic hormone, may add promising treatment options in the near future. TIPS is another therapeutic tool of potential interest in the management of renal failure in liver disease which needs further evaluation. Renal replacement therapy, preferentially in the form of continuous procedures, may be life-saving in those patients awaiting liver transplantation or spontaneous recovery of their hepatic function.     

Adrenal dysfunction in patients with renal amyloid

Amyloidosis is a multi-system disease. Renal involvement often leads to end-stage renal failure, which carries a poor prognosis. This paper reports the adrenal status of 22 patients with renal amyloid who were considered for or who had been commenced on renal replacement therapy. Twelve patients were considered or found to have AA amyloid and the remaining 10 had AL amyloid. Of 16 patients tested, seven demonstrated an abnormal response to a synacthen test. Four patients died at Addisonian crisis and hypo-adrenalism probably contributed to the deaths of a further two patients. Amyloid deposition was found in the adrenal glands in seven patients who died of systemic amyloidosis and renal failure. It is recommended that all patients with renal amyloid should have an assessment of adrenal function performed and if abnormal replacement steroid therapy should be commenced.     

Use of sucralfate in renal failure

OBJECTIVE: To assess the potential for the development of aluminum toxicity in patients with renal insufficiency or chronic renal failure who are taking sucralfate. DATA SOURCES: Clinical literature accessed through MEDLINE (1966-December 1999) and International Pharmaceutical Abstracts (1970-December 1999). Key search terms included sucralfate, renal failure, renal insufficiency, and end-stage renal disease. DATA SYNTHESIS: Urinary excretion is an important route of elimination for systemically absorbed aluminum. Accumulation of aluminum in patients with impaired renal function may lead to significant toxicity. A potential source of aluminum is the antiulcer medication sucralfate. Studies and case reports evaluating the use and toxicity of sucralfate in patients with normal renal function, as well as those with renal failure or renal insufficiency, were reviewed. CONCLUSIONS: Aluminum accumulation and toxicity have been reported with the use of sucralfate in patients with compromised renal function. The risk of toxicity most likely represents a long-term complication of sucralfate use in this patient population. Toxicity may be enhanced by concurrent use of other aluminum-containing medications, such as phosphate binders or antidiarrheal preparations. These medications, in addition to sucralfate, should be avoided if possible in patients with end-stage renal disease. Patients with renal failure or renal insufficiency who are undergoing prolonged sucralfate therapy should be monitored for potential signs of aluminum toxicity.     

The hepatorenal syndrome

The onset of renal failure in a patient with cirrhosis or acute liver failure is alarming because it raises the possibility of the hepatorenal syndrome (HRS). Periodic surveillance of renal function is helpful in patients with severe liver disease to detect HRS early and to help correct reversible contributing factors. Once established, HRS responds relatively poorly to medical management, although recent advances have brought hope for an improved prognosis. In this article the diagnosis, pathophysiology, and management of HRS are discussed in detail, with an emphasis on recent diagnostic and therapeutic advances.     

Management of hepatorenal syndrome

Hepatorenal syndrome is a form of acute or sub-acute renal failure which develops in patients with chronic liver disease. In contrast to other forms of acute renal failure it may be reversible using pharmacological agents. The pathogenesis involves splanchnic vasodilatation and intense renal vasoconstriction. Increasing intravascular volume and prolonged treatment with vasoconstrictor drugs reverses renal failure in a significant proportion of patients. Agents currently used include the vasopressin analogues terlipressin and the alpha1-adrenoceptor agonist midodrine. The somatostatin analogue octreotide has been used in combination therapy but is ineffective as monotherapy. Intravenous albumin is an important adjunctive treatment both in the prevention and treatment of hepatorenal syndrome. Increasing intravascular volume using TIPS (transjugular intrahepatic stent shunt) is effective in some patients and may be useful in maintaining patients who have initially responded to pharmacological therapy. Despite improvements in survival, long term prognosis is still poor and generally depends on the degree of reversibility of the underlying liver disease or access to liver transplantation.     

Acute Renal Failure due to Bacterial Pyelonephritis

Five patients who presented with acute renal failure in associationwith urinary tract infection are reported. Renal function improvedrapidly on antibacterial therapy and no alternative cause foracute renal failure could be Identified. None had previouslybeen known to have renal disease but three of the five had takenconsiderable amounts of analgesics. The unusual severity of renal functional impairment resultingfrom urinary tract infection in these patients is unexplainedbut may relate to previous analgesic abuse and/or delay in treatment.Since acute non-obstructive pyelonephritis may result in severereversible renal failure, this diagnosis must be consideredin patients presenting with acute uraemia.     

Chronic pain management in older people

Successful management of chronic pain in older people is dependent on a careful history and physical examination as it is in young adults. However, detailed attention must also be paid to the effects of co-morbidity on the pain and its treatment, on communication strategies with patients who often have sight and hearing impediments, and on the feasible range of functional outcomes for each patient. Drug interactions are common in older people as they take more medications and have reduced ability to clear most analgesic and adjuvant medications. This suggests a larger than usual role for non-pharmacological management strategies. However, simple analgesics and narcotics are safe to use in older people without overt liver and renal disease, providing the lowest dose compatible with functional improvement is sought; the goal of therapy is to maintain optimum function rather than cure the pain. In general the outcome is positive for both the patient and the practitioner as patients usually respond to medical, physical, psychosocial and cognitive behavioural programmes as well as young adults if given an appropriate milieu, adequate time and empathy.     

Acute renal failure

Acute renal failure occurs in 5 percent of hospitalized patients. Etiologically, this common condition can be categorized as prerenal, intrinsic or postrenal. Most patients have prerenal acute renal failure or acute tubular necrosis (a type of intrinsic acute renal failure that is usually caused by ischemia or toxins). Using a systematic approach, physicians can determine the cause of acute renal failure in most patients. This approach includes a thorough history and physical examination, blood tests, urine studies and a renal ultrasound examination. In certain situations, such as when a patient has glomerular disease, microvascular disease or obstructive disease, rapid diagnosis and treatment are necessary to prevent permanent renal damage. By maintaining euvolemia, recognizing patients who are at increased risk and minimizing exposure to nephrotoxins, physicians can decrease the incidence of acute renal failure. Once acute renal failure develops, supportive therapy is critical to maintain fluid and electrolyte balances, minimize nitrogenous waste production and sustain nutrition. Death is most often caused by infection or cardiorespiratory complications.     

Acute renal failure due to bacterial pyelonephritis.

Five patients who presented with acute renal failure in association with urinary tract infection are reported. Renal function improved rapidly on antibacterial therapy and no alternative cause for acute renal failure could be identified. None had previously been known to have renal disease but three of the five had taken considerable amounts of analgesics. The unusual severity of renal functional impairment resulting from urinary tract infection in these patients is unexplained but may relate to previous analgesic abuse and/or delay in treatment. Since acute non-obstructive pyelonephritis may result in severe reversible renal failure, this diagnosis must be considered in patients presenting with acute uraemia.     

肝肾联合移植的适应证及时机

背景：肝肾联合移植以来,肾功能不全甚至肾功能衰竭已不再是肝脏移植的禁忌症。目的：探寻肝肾联合移植适应证及移植时机,以利合理应用稀缺的实体器官供体。方法：收集接受肝肾联合移植患者15例,回顾性分析其移植前状态与移植后移植肾及原肾恢复情况间的状态。结果与结论：入组15例肝肾联合移植患者均手术顺利,至今存活,随访1.5-8（3.6±1.2）年。入组患者中出现移植肾功能延迟恢复1例,行床旁连续性肾脏替代治疗治疗2周后肾功能逐渐恢复;1例移植前行连续性肾脏替代治疗治疗4周的肝肾综合征患者,移植后2个月行肾图检查提示原肾功能恢复正常;另2例移植前连续性肾脏替代治疗超过6周的肝肾综合征患者,移植后行肾图提示原肾功能未恢复;伴有原发肾病的终末期肝病患者移植前24h尿蛋白〉500mg、肾小球滤过率〈30mL/min或经穿刺活检证实肾小球硬化率〉30%,肝肾联合移植后行肾图提示原肾逐渐失功。移植前行连续性肾脏替代治疗治疗超过6周的肝肾综合征患者,需施行肝肾联合移植;移植前伴有原发肾病的终末期肝病患者,如果24h尿蛋白〉500mg、肾小球滤过率〈30mL/min或经活检证实肾小球硬化率〉30%,需施行肝肾联合移植。     

Cirrhosis and chronic liver failure: part I. Diagnosis and evaluation

Cirrhosis and chronic liver failure are leading causes of morbidity and mortality in the United States, with the majority of preventable cases attributed to excessive alcohol consumption, viral hepatitis, or nonalcoholic fatty liver disease. Cirrhosis often is an indolent disease; most patients remain asymptomatic until the occurrence of decompensation, characterized by ascites, spontaneous bacterial peritonitis, hepatic encephalopathy, or variceal bleeding from portal hypertension. Physical examination of patients with cirrhosis may reveal a variety of findings that necessitate a hepatic- or gastrointestinal-based work-up to determine the etiology. Some patients already may have had laboratory or radiographic tests that incidentally uncovered signs of cirrhosis and its comorbidities. No serologic or radiographic test can accurately diagnose cirrhosis. A significant correlation has been demonstrated between persistently elevated liver function tests and biopsy-proven underlying hepatic disease; thus, a more targeted serologic work-up is indicated in patients whose liver function test results are persistently abnormal. Unnecessary medications and surgical procedures should be avoided in patients with cirrhosis. Referral for liver biopsy should be considered only after a thorough, non-invasive serologic and radiographic evaluation has failed to confirm a diagnosis of cirrhosis; the benefit of biopsy outweighs the risk; and it is postulated that biopsy will have a favorable impact on the treatment of chronic liver disease.     

Treatment of Wilson's disease with zinc. XVIII. Initial treatment of the hepatic decompensation presentation with trientine and zinc

We have treated 9 patients who presented with hepatic decompensation resulting from Wilson's disease with a combination of trientine and zinc, generally for at least 4 months, followed by transition to zinc maintenance therapy. All of these patients had hypoalbuminemia, all but 1 had hyperbilirubinemia, and 7 had ascites. All of these patients would have been candidates for liver transplantation on the basis of their initial Child-Turcotte-Pugh (CTP) scores. The minimal listing criteria for transplant candidates is a score greater than 7. Eight of the 9 patients had demonstrated a CTP score of 10 or higher. The other scoring system that has been used in Wilson's disease to determine need for transplantation is the prognostic index of Nazer, in which a score over 6 indicates that the patient is unlikely to survive without a transplant if treated with penicillamine. Two of our patients had Nazer scores higher than 6. With our medical therapy, all 9 of these patients have recovered normal liver function as reflected by normalization of their CTP scores to 5. Because of coexisting neurologic disease, 1 of our 9 patients was initiated on a neurologic protocol and by chance randomized to receive tetrathiomolybdate (TM) and zinc after 2 weeks of trientine/zinc treatment. This patient's liver function recovered much more rapidly than did that of the other 8 patients, all of whom were treated with trientine/zinc, suggesting that TM therapy offers a further advantage. In summary, we were able to take 9 patients who presented with liver failure -8 of whom had CTP scores indicating a potential need for liver transplantation and 2 of whom had Nazer prognostic scores indicating that they were not likely to survive if treated only with penicillamine - and treat them medically, with recovery in all 9. We believe the trientine/zinc combination therapy should be the standard for initial treatment of liver failure in Wilson's disease because its efficacy is equal or slightly superior to that of penicillamine and because it has a much lower incidence of side effects. Moreover, TM warrants study to determine whether therapy for hepatic Wilson's disease can be further improved.     

Amyloidosis in Crohn disease. Case reports and review of the literature

A review of the literature on Crohn's disease with secondary amyloidosis and four own case reports are presented. At least 1% of patients with Crohn's disease develop amyloidosis. The extent of the inflammatory bowel disease seems to have an influence on the occurrence of amyloidosis. The survival time of 40 out of 72 patients was 2.1 years after the onset of diagnosis. The complications induced by the amyloidosis determine the fate of the patients. Therefore the periodical protein determination in urine and the Congo-red-colouring of rectal mucosa after rectoscopy are justified. After the diagnosis of amyloidosis in patients with Crohn's disease the inflammation should be treated consequently, according to the principles of the treatment of the underlying disease. But the resection of the inflammatory bowel should be avoided if the renal function is still sufficient, because frequently there occurs a postoperative renal failure. In the case of renal amyloidosis with a creatinin-clearance of more than 10 ml/min, a therapeutic attempt should be made with 1.0 to 1.5 mg/day of colchicin or 10 g/day dimethylsulphoxid (DMSO) for at least six months. During existing renal failure the proceeding of amyloidosis in other organs is to be expected. The secondary amyloidosis disposes the fate of the patients.     

The importance of associated extra-renal vascular disease on the outcome of patients with atherosclerotic renovascular disease

Atherosclerotic renovascular disease (ARVD) is a disease of ageing. It is usually a manifestation of widespread vascular disease and although it may be symptomless, many patients with ARVD present with the effects of extra-renal vascular disease, such as peripheral vascular (PVD), coronary heart (CHD) and cerebrovascular disease. ARVD is a common cause of hypertension and chronic renal failure (CRF), and it is one of the most common renal diagnoses in elderly patients accepted on to dialysis programmes with end-stage renal failure (ESRF). The cause of renal impairment in these patients is still a matter of debate. Patients with ARVD have a high mortality, especially those with renal failure. In this review we examine the relationships between ARVD and co-morbid extra-renal vascular disease, and the impact of these associated vascular pathologies upon renal functional and mortality outcomes is considered. The latest evidence concerning the likely pathogenesis of renal dysfunction in patients with ARVD is also reviewed.     

Rapidly progressive glomerulonephritis with extensive glomerular crescent formation

Thirty-nine patients with severe crescentic glomerulonephritis and rapidly progressive renal failure were reviewed. Nineteen patients had a focal necrotizing glomerulonephritis, they usually presented with signs of multi-system disease, and eight had histologically-proven microscopic polyarteritis. A second group of 20 patients presented with an acute nephritic syndrome, often with nephrotic features, and had only minor prodromal symptoms. Renal biopsy material showed various forms of proliferative glomerulonephritis in addition to crescents. The most important prognostic feature at admission was renal function: only four of 21 patients who required dialysis recovered any renal function. The prognosis was worse for those with necrotizing glomerulonephritis, of whom two-thirds had oliguria on admission. All patients who were not oliguric, and some with oliguria, were treated with high doses of corticosteroids, usually accompanied by azathioprine and anticoagulants. Seventeen of 18 patients who were not oliguric initially retained or regained renal function, although three subsequently went into renal failure, and three others died of non-renal causes. At the most recent review, 25 of the 39 patients were either dead (16 patients) on dialysis or transplanted (nine patients). Ten were alive with diminished renal function, one had normal renal function but persisting proteinuria, and three were well. Prompt treatment may have contributed to these favourable results in a very severe disease.     

A new look at renal dysfunction in the cirrhotic patient

Hepatorenal syndrome (HRS) is a pre-renal azotemia-like acute renal failure occurring in patients with end-stage cirrhosis. HRS results from arteriolar vasodilatation, arteriolar underfilling, and intense renal vasoconstriction. By definition, it is not responsive to volume expansion, and the prognosis is especially poor even with the use of terlipressin or albumin dialysis or both. It may be difficult, on the basis of the current criteria, to clearly differentiate HRS from other causes of acute renal failure in cirrhosis. In addition, patients with HRS frequently have underlying chronic kidney changes that may not be reversible after transplantation. In the previous issue of Critical Care, a group of experts proposed a new classification of acute, acute-on-chronic, or chronic renal impairment in cirrhosis on the basis of the RIFLE (Risk, Injury, Failure, Loss, and End-stage kidney disease) criteria. The group proposed the term 'hepatorenal disorder' to define patients with advanced cirrhosis and kidney dysfunction at an earlier stage, regardless of the mechanisms. As stated by the authors, more data are needed to clearly identify, by non-invasive means, those with a potential for improvement with liver transplantation and those who can undergo a combined liver and kidney transplantation.     

Preventing acute renal failure in patients with chronic renal insufficiency: nursing implications

The kidneys can withstand substantial loss of functional tissue before showing signs of insufficiency that may lead to a life on dialysis. Situations that lead to reduced renal perfusion or exposure to nephrotoxic agents in patients with chronic renal insufficiency can cause acute renal failure and quicken a downhill course to end stage renal disease if preventive measures are not employed. The nurse's role in prevention of acute deterioration of renal function in renal insufficiency includes knowledge of risk factors and nephrotoxins, awareness of fluid volume status, and an appropriate teaching plan.     

How do we optimize the management of chronic renal failure?]

Optimization of the management of chronic renal failure (CRF) is aimed at decreasing morbidity and mortality risks of CRF patients, due to the progression of CRF toward end-stage renal disease (ESRD), and to CRF-related complications with functional or life-threatening consequences. The so-called spontaneous progression of CRF toward ESRD depends on factors related to the primary renal disease, and on non-specific factors mainly related to hypertension and renal functional adaptations to nephron loss. Secondary prevention of CRF needs: early identification of primary renal disease, in order to start specific therapies; the treatment of hypertension; dietary advice on protein intake; prevention of events and drug toxicity potentially harmful to renal function. Clinical events appear late in the course of CRF, following several disorders often present for a long time: hypertension, dyslipidemia, phosphocalcic disorders, anaemia, malnutrition). These disorders should be screened for, and treated, as a part of tertiary prevention measures. When dialysis becomes unavoidable, early information and medical preparation of the patient are mandatory, giving the best chances of success to the applied dialysis method. Unfortunately, most CRF patients are referred at a late stage of the disease, when the effects of therapeutic interventions are limited; this results in increased length of hospital stays, increased risk of early dialysis complications, and decreased capacity to be treated at home.     

Systemic diseases with renal manifestations

This article discusses the epidemiology, recognition, screening, and management of six systemic diseases that commonly present with renal manifestations: diabetic nephropathy, lupus nephritis, congestive heart failure, HIV, liver disease, and dysproteinemias. Diabetic nephropathy remains the leading cause of end-stage renal disease in the United States. The outlook for patients who have lupus nephritis and HIV-associated nephropathy has improved in the last decade. Kidney disease is common in patients who have advanced liver disease, and creatinine-based methods do not provide an accurate estimation of renal function in this population. Dysproteinemias are associated with protean renal manifestations, and renal disease may be the presenting manifestation.