Acute hepatic failure and Hodgkin's disease]

We present the clinical outcome and imaging micro and macroscopic of a patient who died of e liver acute failure. Hodgkin disease with massive infiltration was found at necropsy. We offer a review of the liver complaint in this particular disease.     

Caring for a rehabilitation patient with chronic renal failure and end-stage renal disease

Patients with chronic renal failure and end-stage renal disease frequently suffer medical setbacks that necessitate a course of rehabilitation. Planning care for these patients requires special consideration if they are to attain a level of function close to what they enjoyed prior to the event that required them to be hospitalized. In this article, the author describes chronic renal failure, end-stage renal disease, types of dialysis and types of access, assessment upon admission to rehabilitation, and nursing care for patients with chronic renal failure and end-stage renal disease in a rehabilitation facility. This information can help nurses learn about what to look for and what questions to ask, common medications and laboratory values, dietary management, and the creation of a successful rehabilitation experience.     

High prevalence of pancreatic disease in chronic renal failure

Lymphocytes from the cervical lymph nodes of guinea pigs were incubated in medium 199 in the presence of cortizol in a concentration of 20 and 100 microng% for 24 hours. A determination was made of the lymphocyte survival and cortizol metabolism by them, and also (cytophotometrically) the nucleic acid content. In the intact and the sesitized guinea pigs progesterone in a concentration of 10-5 inhibited both the lytic action of coritizol and its metabolism There was observed a marked reduction of cortizol meta bolism by the lymphocytes from the 6th day after the sensitization, which was restored only by the 90th day. The cortizol-resistant lymphocyte population increased on the 17th--30th day. In a concentration of 100 microng% cortizol reduced the nucleic acid content in the lymphocytes of both the intact guinea pigs and sensitized ones on the 17th--30th day, when the cortizol-resistant population increased.     

Laparoscopic evaluation of liver disease in chronic renal failure prior to renal transplantation

It is not rare that controversial indications about the presence or the expression level of multidrug-resistant (MDR) proteins come out from different laboratories upon examination of identical tumor specimens. Distinct aspects, including the use of weakly discriminating monoclonal antibodies (MAbs) and/or unsuitable techniques and procedures, contribute in generating differences in the MDR phenotype evaluation of cancer cells. In this regard we describe here an innovative immunohistochemical approach for the determination of P-glycoprotein expression in cells and tissues. The method is based on the ability of phage-displayed peptides to mimic antibody epitopes. For this purpose we utilized the phage clone #55, which was affinity-purified from a phage-displayed random-peptide library using the MAb MM4.17 (specific for MDR1-P-glycoprotein) as previously described. This clone has been chosen since it clearly and undoubtedly reacts with its cognate MAb, as was determined by ELISA and dot blot tests. Inhibition of the MAb MM4.17 binding to MDR1-P-glycoprotein-expressing cells could be performed by adding a calibrated concentration of phage clone #55 particles, which mimic MDR1-P-glycoprotein antigen. This methodology can eliminate misleading interpretations concerning the presence and expression level of MDR1-P-glycoprotein and might well contribute in routine clinical determinations of MDR in tumor specimens, thus contributing to our understanding of the basis of the mechanisms of tumor cell resistance to drugs.     

Hyperleptinemia in chronic renal failure

To investigate the mechanism(s) of degradation of leptin, the protein product of ob (obese) gene, we measured serum leptin levels in 70 patients with chronic renal failure (CRF). The median of serum leptin concentrations of 36 male and 34 female patients with CRF were 7.3 ng/ml ranging from 0.5 to 39.0 ng/ml and 34.9 ng/ml from 1.1 to 76.1 ng/ml, respectively, while those of 29 male and 29 female healthy subjects were 5.8 ng/ml ranging from 0.5 to 37.7 ng/ml and 12.0 ng/ml from 2.0 to 45.2 ng/ml, respectively. The difference in male and female serum leptin concentrations between CRF group and the normal counterpart was statistically significant (p<0.005 and p<0.05, respectively). However, there was no significant correlation, either between serum creatinine or BUN, and serum leptin concentrations. These findings suggest that leptin is degraded and/or filtered in renal tissue.     

Conservative management of chronic renal failure

Failing kidneys can play havoc with other parts of the body. Specific treatment of these associated problems may help ward off uremia and preserve whatever renal function remains. Sodium levels may drop if too much water is mistakenly given to counteract kidney failure. Hyperkalemia can lead to cardiac arrest if potassium levels aren't reduced without delay. Acidosis also may reach life-threatening proportions, especially if diarrhea occurs. Almost all patients with chronic renal failure have a bleeding tendency and anemia, with the hematocrit dipping as low as 20 percent. Over half have decreased tolerance to carbohydrares, although severe hyperglycemia is rare. Disorders of calcium metabolism also are common, ranging from asymptomatic hypocalcemia to osteomalacia. The kidneys' impaired filtration ability should be kept in mind when drugs are prescribed. Dosages may need to be cut to avoid an adverse reaction.     

Glucose intolerance in chronic renal failure

It has been recognized that glucose intolerance is a common finding in patients with chronic renal failure (CRF). Insulin resistance and impaired insulin secretion contribute to the pathogenesis of glucose intolerance. The resistance to insulin action is commonly observed in chronic renal failure and mainly due to impaired glucose uptake by muscle. In contrast, insulin secretion in response to hyperglycemia is variable: increased, decreased and normal. Recent studies reported that high PTH levels impaired insulin secretion from pancreatic islets. In this review, we mention the mechanism of glucose intolerance in chronic renal failure.     

Current therapy of chronic renal failure

The course of chronic renal failure is generally progressive and mediated by several factors that operate in combination. Several extrarenal events which may cause transient or permanent deterioration of renal function, are important, because their correction may slow the progression of renal disease e.g. volume disorders, infection, nephrotoxic agents. In progression of chronic renal disease leading factors are hypertension, proteinuria and high protein/phosphorus intake. Number of evidence suggests that ameliorating hypertension, reducing proteinuria slow the progression of chronic renal failure. Clinical studies in diabetic nephropathy demonstrated that the renoprotective effect of ACE inhibitors was independent of their effect of systemic blood pressure. In ESRD patients access for renal replacement therapy should be obtained as early as possible. An A-V fistula may take several weeks to mature especially in diabetic or elderly patients. Early dialysis has been advocated in diabetic patients. In general, patients can start ESRD therapy when residual kidney function drops to 5-10% of normal value. High quality of dialysis should be provided to the uremic patient with respect of successful renal transplantation.     

Free phenols in chronic renal failure

Serum total free phenols are elevated in chronic renal failure, acute renal failure and hepatic coma. Being partly protein-bound, phenols behave during dialysis in a similar manner to considerably larger molecules which are not protein-bound. In view of their potential toxicity they should be considered as an alternative to 'middle molecules'. Patients on regular hemodialysis have retention of phenols if their post-dialysis serum creatinine is above 6-7 mg/dl. Patients on short time dialysis have high pre-dialysis neutral phenol levels. Such levels are sufficiently high to suggest a role in the genesis of neurological symptoms, anemia and bone disease. Certainly pre-dialysis free phenols reflect adequacy of dialysis.     

Dialysis treatment of chronic renal failure

Of the patients with chronic renal replacement therapy in Germany, only 27% are living with a functioning graft, while the other 73% are dialysis patients. At the end of 1990, there were about 30,000 patients on regular dialysis treatment in Germany. Without selection for chronic dialysis, the average age of newly accepted patients is 61 years. More than 30% of the new dialysis patients are diabetics. Intermittent haemodialysis (89.5%), intermittent haemofiltration (4.5%), and peritoneal dialysis (6%) are the different methods of chronic dialysis treatment in Germany. The 5-year-survival rate with regular haemodialysis treatment is 67%, for 50 years old patients without diabetic nephropathy (EDTA, Europe).     

The electroretinogram in chronic renal failure

Fifty-nine enterococci isolated from 18 patients in an intensive care unit (ICU) and 21 patients in general wards (GW) at Royal Perth Hospital (RPH) during a period of 14 months were examined for antibiotic resistance by susceptibility testing and DNA polymorphism by pulsed-field gel electrophoresis. The study showed that penicillin-resistant Enterococcus faecium is a common nosocomial isolate in ICU. The DNA patterns of various strains of E. faecium and E. faecalis were closely related in most consecutive isolates from the same patients but were generally different for isolates from different patients. Thirty two different DNA patterns were identified for 59 isolates from 39 patients. Identical or similar DNA patterns were also identified for some isolates from different patients, suggesting that cross-infection had occurred between patients in ICU and GW. These data suggest that cross-infection occurred more commonly in ICU than in GW and are consistent with the known higher risk of ICU patients for nosocomial infection.     

Estrogen-stimulated neurophysin in chronic renal failure

Estrogen-stimulated neurophysin (ESN) was determined by radioimmunoassay in three groups of patients with chronic renal failure: predialysis patients, patients on hemodialysis and patients on continuous ambulatory peritoneal dialysis. ESN levels were significantly elevated in all patients. ESN of these patients is undistinguishable from highly purified pituitary ESN. Immunological and physicochemical analyses of ESN in patients with renal failure suggest that the elevated plasma level is due to a failure of renal clearance. In addition, heterogeneity of urinary ESN, revealed by multiple immunoreactive peaks after gel filtration, indicates altered renal metabolism.     

Serum lipids in chronic renal failure

The serum lipids and lipoprotein patterns in 100 adult patients with nonnephrotic chronic renal failure were analyzed retrospectively. Hypertriglyceridemia was found in 43% of these patients. Forty-nine of the 100 had a normal lipoprotein pattern, whereas 42 had type IV hyperlipoproteinemia. This abnormal lipoprotein pattern could not be correlated with the degree of renal impairment, the type of renal disease, or with the patient's age, sex, weight, or diet.     

Oxalosis and chronic renal failure after intestinal bypass

A 45-year-old man underwent a jejunoileal shunt procedure for obesity. Twenty months later he developed severe oxalosis and chronic renal failure, which required maintenance hemodialysis. The sequential observation of two biopsy specimens and the necropsy (over a span of 39 months) suggests that oxalate deposition caused tubular obstruction and destruction with subsequent atrophy of nephrons. This indicates that patients undergoing intestinal bypass are at risk for developing irreversible renal failure due to enteric hyperoxaluria.     

Fluid therapy in acute and chronic renal failure

Fluid therapy is one of the mainstays of treatment for renal failure, and rehydration is the primary goal. In those patients with ARF or "acute on chronic" decompensated CRF, induction of a diuresis to facilitate renal excretory function is important. Measurement of urine production in these patients helps guide fluid and electrolyte therapy. In oliguric renal failure, retention of water and electrolytes is likely, whereas in nonoliguric ARF as well as CRF, loss of water and electrolytes is the primary concern.