Encephalopathy uremic

Uremic encephalopathy occurs as a result of the effects of uremia on the central nervous system and is associated with symptoms including alterations in consciousness, thinking, memory, speech, psychomotor behavior, and emotion. Sensory and motor function may be altered, particularly affecting leg nerves, resulting in leg cramps and restless leg syndrome. Uremic encephalopathy is less common because of earlier initiation of dialysis in patients with Stage 5 CKD. 

The presenting symptoms of uremia are similar to many other encephalopathic states. The differential diagnosis is even more complex, since patients with renal failure are subjected to other intercurrent illnesses that may also induce other encephalopathic effects. In patients with renal failure, treatment with dialysis will restore more normal body fluid composition. Despite the possibility that multiple causes of encephalopathy might occur simultaneously, uremic encephalopathy may be successfully differentiated in most instances by means of the usual clinical methods. 

If the patient with kidney failure also has cirrhosis or some other form of hver failure, this additional ammonia load may present a stress that cannot be adequately handled by the diseased liver. The result may be increased blood and central nervous system ammonia levels with development of encephalopathy (Fraser Arieff, 1985). Thus, patients with cirrhosis and end-stage kidney disease are at particular risk for developing encephalopathy since both conditions act synergistically to increase both blood and central nervous system ammonia. It should also be noted that plasma urea and serum creatinine do not always adequately reflect renal function in patients with severe liver disease. Recent studies suggest that many patients who have cirrhosis, ascites, and normal plasma urea and creatinine may in fact have severe renal functional impairment (Gines et al., 1988 Papadakis Arieff, 1987 Takabatake et al., 1988). In such individuals, differentiation of hepatic from uremic encephalopathy on clinical grounds may be difficult. 

Although there are many factors that contribute to uremic encephalopathy, most investigations have shown no correlation between encephalopathy and any of the commonly measured indicators of renal failure. In recent years, there has been considerable discussion of the possible role of PTH as a uremic toxin. There is a substantial amount of evidence to suggest that PTH may exert an adverse effect on the central nervous system (Cogan et al., 1978 Cooper et al., 1978 Guisado et al., 1975 Mahoney Arieff, 1982). 

Arieff AI, Guisado R Massry SG. (1975). Uremic encephalopathy Studies on biochemical alterations in the brain. Kidney Int 7, S194-S200. 

Mahoney CA Arieff AI. (1982). Uremic encephalopathies Cliniceil, biochemiceil and experimented features. Amer J Kidney Dis 2, 324—336. 

Mahoney CA, Samacki P Arieff Al. (1984). Uremic encephalopathy Role of brain energy metabolism. Am J Physiol 247 (Reneil Fluid Electrolyte Physiol. 16), F527-F532. 

Uremic and dialysis encephalopathies. Patients with renal failure continue to manifest neuropsychiatric symptoms despite significant advances in therapeutics and management. Patients with renal failure who are not yet on dialysis develop an array of symptoms, including clouding of consciousness, disturbed sleep patterns, tremor and asterixis that may progress to coma and death. 

The major population at risk for aluminum loading and toxicity consists of individuals with renal failure. In a study by Alfrey (1980), 82% of nondialyzed uremic patients and 100% of dialyzed uremic patients had an increased body burden of aluminum. The decreased renal function and loss of the ability to excrete aluminum, ingestion of aluminum compounds to lessen gastrointestinal absorption of phosphate, the aluminum present in the water used for dialysate, and the possible increase in gastrointestinal absorption of aluminum in uremic patients can result in elevated aluminum body burdens. The increased body burdens in uremic patients has been associated with dialysis encephalopathy (also referred to as dialysis dementia), skeletal toxicity (osteomalacia, bone pain, pathological fractures, and proximal myopathy), and hematopoietic toxicity (microcytic, hypochromic anemia). Pre-term infants may also be particularly sensitive to the toxicity of aluminum due to reduced renal capacity (Tsou et al. 1991)... 

Thrombotic thrombocytopenic purpura is a rare acute or subacute disease in adults, rather similar to the hemolytic uremic syndrome in children, in which there is systemic malaise, fever, skin purpura, renal failure, hematuria and proteinuria. Hemorrhagic infarcts caused by platelet microthrombi occur in many organs in the brain they may cause stroke-like episodes (Matijevic and Wu 2006) although more commonly there is global encephalopathy. The blood film shows thrombocytopenia, hemolytic anemia and fragmented red cells. The differential diagnosis includes infective endocarditis, idiopathic thrombocytopenia, heparin-induced thrombocytopenia with thrombosis, systemic lupus erythematosus, non-bacterial thrombotic endocarditis and disseminated intravascular coagulation. 

In all patients with chronic renal insufficiency, strict supervision of total aluminium intake is vital. The administration of aluminium should be stopped as soon as the serum concentration exceeds 150 pg/ml or at the appearance of the first symptoms of encephalopathy (81). According to current recommendations, dia-lysate solutions should contain less than 10 pg/l of aluminium (82). There is some controversy about the view that aluminium-containing medications used to control serum phosphate concentrations in uremic subjects should be replaced by calcium-containing phosphate binders (83). Another approach used to reduce the toxic risks of aluminium hydroxide may be to tailor doses to the phosphate concentration in serum, that is individualizing aluminium gel therapy (SED-12, 515). 

Campistol JM, Cases A, Botey A, Revert A. Acute aluminum encephalopathy in an uremic patient. Nephron I989 5I(I) I03-6. 

Geyer J, Hoffler D, Demers HG, Niemeyer R. Cephalosporin-induced encephalopathy in uremic patients. Nephron 1988 48(3) 237. 

Pascual J, Liano F, Ortuno J. Cefotaxime-induced encephalopathy in an uremic patient. Nephron 1990 54(1) 92. 

Arik N, Cengiz N, Bilge A. Metronidazole-induced encephalopathy in a uremic patient a case report. Nephron 2001 89(l) 108-9. 

Over the years, problems have arisen as a result of the presence of significant amounts of aluminium in parenteral nutrition solutions in particular they have been held responsible for hypercalciuria and its consequences (54). Parenterally administered aluminium bypasses the gastrointestinal tract, which normally serves as a protective barrier to aluminium entry into the blood. In the past, aluminium contamination of casein hydrolysate, which was used as a source of protein in parenteral nutrition solutions, was associated with low-turnover osteomalacia and with encephalopathy in uremic patients. Premature infants are still at risk of aluminium accumulation as a result of prolonged parenteral nutrition (as are patients receiving plasmapheresis with albumin contaminated in its preparation with aluminium). Metabolic bone disease can result (54). 

Other complications may include lethargy, delirium, seizure, encephalopathy, hemolytic-uremic syndrome, septicemia, Reiter syndrome, hepatitis, rectal prolapse, myocarditis, and toxic mega colon. 

In addition to the consequences of reduced excretory, regulatory, and endocrine function of the kidneys, the uremic syndrome has several systemic manifestations—among them pericarditis, pleuritis, disordered platelet and granulocyte function, and encephalopathy— that have been difficult to explain. 

The dose of ammonium chloride can be calculated on the basis of the chloride deficit using the same method as for HCl, using the conversion of 20 g ammonium chloride providing 374 mEq of H . However, only half of the calculated dose of ammonium chloride should be administered so as to avoid ammonia toxicity. Ammonium chloride is available as a 26.75% solution containing 100 mEq in 20 mL, which should be further diluted prior to administration. A dilute solution may be prepared by adding 100 mEq of ammonium chloride to 500 mL of normal saline and infusing the solution at a rate of no more than 1 mEq/min. Improvement in metabolic stams is usually seen within 24 hours. CNS toxicity, marked by confusion, irritability, seizures, and coma, has been associated with more rapid rates of administration. Ammonium chloride must be administered cautiously to patients with renal or hepatic impairment. In patients with hepatic dysfunction, impaired conversion of ammonia to urea may result in increased ammonia levels and worsened encephalopathy. In patients with renal failure, the increased urea synthesis may exacerbate uremic symptoms. ... 

Furthermore, certain factors may increase intestinal aluminum absorption. We have previously described severe hyperaluminemia resulting in an acute rapidly fatal encephalopathy in four uremic patients who had been taking aluminum hydroxide and Shohl s solution, an alkalinizing buffer of sodium citrate and citric acid. The encephalopathy resembled the earlier dialysis dementia of the 1970s, but was much more acute, culminating in death within 3 weeks (B4, B5). 

B5. Bakir, A. A., Hryhcrczuk, D. O., Berman, E., and Dunea, G., Acute fatal hyperaluminemic encephalopathy in undialyzed and recently dialyzed uremic patients. Trans. Am. Soc. Artif. Intern. Org. 32, 171-176 (1986). 

Bakir AA, Hryhorczuk DO, Berman E, Dunea G. Acute fatal h3 raluminemic encephalopathy in undialyzed and recently dialyzed uremic patients. Trans Am Soc Artif Intern Organs (1986) 32,171-6. 

In patients who have other medical problems such as advanced liver disease with hepatic insufficiency, it is often difficult to differentiate whether the encephalopathy is due to hepatic or renal causes. In patients with renal failure, the major route for elimination of urea is not available thus, there is an ino-ease in blood urea. The amount of urea that enters the colon is ino-eased because of the elevated plasma urea. Urea is then acted on by colonic bacteria and mucosal enzymes in a manner similar to that of protein and amino acids. This leads to inCTeased ammonia production in uremic subjects that may either increase plasma ammonia levels or lead to misinterpretation of this test. 

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