The risk of radiocontrast nephropathy in patients with cirrhosis.

A retrospective case-control study was conducted to determine whether liver cirrhosis might be a risk factor for radiocontrast induced nephropathy as has been suggested. Data from 72 patients with cirrhosis and 72 patients without cirrhosis who all received 100-150 ml of low osmolality radiocontrast medium for abdominal or chest computerized tomography scan were reviewed. Blood urea nitrogen and creatinine were recorded before and 48-72 h after the administration of an intravenous radiocontrast agent. Acute renal failure developed in two patients with cirrhosis (2.8%) and one patient in the control group (1.4%). This difference was not significant. There was no significant change in blood urea nitrogen and creatinine in either group after radiocontrast injection. Both of the cirrhotic patients who developed radiocontrast induced nephropathy had received high-dose diuretics and were hypovolemic. We conclude that hepatic cirrhosis per se may not be a risk factor for radiocontrast-induced nephropathy.

Life-threatening hyperkalemia after intravenous labetolol injection for hypertensive emergency in a hemodialysis patient.

Intravenous labetolol, a nonselective alpha- and beta-blocking drug, is commonly used to treat severe hypertension. Nonselective beta-blockers can cause hyperkalemia, especially in patients with renal failure. One series reported 3 renal transplant patients who had hyperkalemia after labetolol infusion, but none of these patients developed any serious complication. We report a case of life-threatening hyperkalemia (serum [K+] 9.9 mEq/l) with ventricular tachycardia and hypotension in a patient on maintenance hemodialysis who received labetolol for a hypertensive emergency. Physicians should be aware of this potentially lethal complication, which is easily preventable.

Symptomatic atrial arrhythmias in hemodialysis patients.

BACKGROUND/AIMS: Cardiac arrhythmias are frequent in hemodialysis patients and can interrupt treatment. However, the frequency and risk factors have remained unclear because previous reports of arrhythmias in dialysis patients have usually been continuous-monitoring studies that looked at all cardiac ectopy regardless of its seriousness. METHODS: We reviewed retrospectively only symptomatic atrial arrhythmias in a population of 106 maintenance hemodialysis patients over three years, in order to estimate their actual frequency and any risk factors. RESULTS: Ten patients, seven men and three women, required treatment for atrial arrhythmias (9.4%): four for supraventricular tachycardia, three for atrial flutter, and three for atrial fibrillation. Their mean age was 53.7 +/- 6.1 years; five of them were < or = 40 years. Seven arrhythmias were new, three were recurrences. All but one occurred between 3 and 4 hours of hemodialysis, and dialysis had to be stopped in nine instances. There was no pattern of hypotensive episodes preceding the arrhythmias. Mean serum K+ drawn at the time of the arrhythmias was 3.8 +/- 0.2 mEq/L. Mean plasma intact parathormone was 1128 +/- 417 pg/mL, compared to 454 +/- 58 pg/mL for our entire hemodialysis population (p = .0036). Subsequent echocardiograms showed abnormalities in 9/10 patients: five had left ventricular hypertrophy, six had left atrial enlargement, five had valvular lesions (four mitral regurgitation; one aortic incompetence), and three had ejection fractions <50%. There were four deaths in these patients over the next 14 months, but probably only one was cardiac. CONCLUSIONS: Serious atrial arrhythmias are common in a hemodialysis population. Risk factors for symptomatic atrial arrhythmias in hemodialysis patients may include hyperparathyroidism and echocardiographic findings of chamber enlargement, valvular lesions, or ventricular dysfunction.

A simple estimate of the effect of the serum albumin level on the anion Gap.

BACKGROUND: The serum anion gap (serum [Na(+)]-Cl(-)]-[CO(2)]) is still the first-line approach to metabolic acidosis. However, while it is generally acknowledged that hypoalbuminemia mandates a downward adjustment of the expected anion gap, a specific correction factor for the anion gap in the face of low serum albumin has never been demonstrated. METHODS: We reviewed initial laboratory data from 432 consecutive patients admitted or transferred to the medical intensive care unit at Nassau County Medical Center over a 6-month period and correlated the serum albumin with the anion gap and the serum [tCO(2)] using multivariate analysis. We looked at the anion gap as a function of delta (albumin), the difference between normal and actual serum albumin, defined as 4.0 - measured serum albumin g/dl. We also assessed [tCO(2)] as an independent variable. RESULTS: For patients with normal or high serum tCO(2), the ratio of change in anion gap (delta anion gap) to delta (albumin) was 1.46 and 1.45, respectively. For patients with serum tCO(2) <22 mEq/l this ratio was 1.89. In the latter group, anion gap was best predicted taking both delta (albumin) and serum tCO(2) into account: anion gap = 36.2 - serum tCO(2) - 2.3 x delta (albumin) (r = 0.71, p < 0.0001). CONCLUSION: For intensive care patients with normal or high serum tCO(2) (>21 mEq/l) a simple bedside adjustment of the anion gap by subtracting 1.5 times the difference between measured serum albumin and the 'normal' level of 4.0 g/dl gives a close estimate of the actual anion gap. For intensive care patients with serum tCO(2) <22 mEq/l, correction of the anion gap is well predicted by adding about twice the Delta (albumin) to the calculated gap.

Use of 'locked-in' antibiotic to treat an unusual gram-negative hemodialysis catheter infection.

A 37-year-old woman on maintenance hemodialysis for 3 years had multiple vascular access failures due to antiphospholipid syndrome. She was dialyzed via a tunneled left subclavian catheter, but after 1 year developed chills and fever during each dialysis session. Blood cultures grew out Xanthomonas maltophilia sensitive to ceftazidime and ciprofloxacin. Intravenous administration of both antibiotics failed to eradicate infection. We added 'locked-in' ceftazidime, instilling it daily into the catheter along with heparinized saline for 3 weeks. Within 24 h the patient was dialyzed uneventfully, and all subsequent blood cultures have been negative. This case shows the successful use of a 'locked-in' antibiotic to treat an unusual gram-negative catheter infection. Two prior series have reported similar good results in infections with more common organisms. Such treatment may permit continued use of tunneled hemodialysis catheters for longer periods.

Prediction of acute renal failure by "bedside formula" in medical and surgical intensive care patients.

BACKGROUND: Prediction of which intensive care unit (ICU) patients are likely to develop acute renal failure (ARF) would be useful. However, scoring systems such as APACHE have been disappointing in this regard. We previously developed a bedside formula to predict ARF using only 3 parameters: serum albumin, urine osmolality, and presence of sepsis. METHODS: We prospectively evaluated 115 consecutive medical ICU (MICU) patients, comparing the bedside formula to APACHE II AND APACHE III as predictors of ARF or death and looking at nutritional parameters such as iron binding capacity, triceps skin fold, mid-arm circumference, and total lymphocyte count. We then evaluated 123 additional consecutive MICU and 98 consecutive surgical ICU (SICU) patients, comparing the bedside formula to APACHE II. RESULTS: The bedside formula was consistently more accurate than APACHE II in predicting ARF or in-hospital death in MICU patients. However, in SICU neither formula predicted ARF, and APACHE II predicted in-hospital death slightly better. No nutritional parameter other than albumin correlated with ARF. CONCLUSION: The bedside formula appears superior to APACHE II in predicting ARF or death in MICU but not SICU. This suggests that these two ICU populations are different.

Changes in venous histology in chronic hemodialysis patients.

Because most hemodialysis access fails at the venous side, we studied samples of brachial vein obtained during access creation in 15 patients with end-stage renal disease who gave consent. Veins were examined by computer-assisted histomorphometry, and the results correlated with the patients' clinical data. The mean venous medial width was 239 +/- 31 microm, and mean intimal width was 6.0 +/- 0.9 microm. Mean venous medial width was 358 +/- 74 microm and mean venous intimal width was 9.2 +/- 1.2 microm in the 4 patients who had been undergoing dialysis more than 6 months, compared with 196 +/- 23 microm and 4.9 +/- 0.8 microm, respectively, in the 11 patients undergoing dialysis less than 6 months (P < 0.01). The number of months undergoing hemodialysis correlated well with venous medial width (r = 0.79; P < 0.001). Correlation between number of months undergoing dialysis and intimal width did not reach statistical significance. Medial and intimal widths of the 4 patients with diabetes were not significantly different from those of the patients without diabetes. Serum parathyroid hormone level did not correlate with either medial or intimal venous width. We conclude there may be changes in the veins of hemodialysis patients with time that cause thickening of layers, even in veins not directly used for access. This may affect the creation or survival of subsequent vascular accesses.

Tubulointerstitial nephritis associated with minimal self reexposure to rifampin.

We report the case of a 27-year-old Asian man who self-medicated with two capsules of rifampin 1 year after completing a continuous course of chemotherapy for tuberculosis that included that drug. He developed flank pain and edema and presented with uremia requiring dialysis; despite this, he had a serum potassium of only 3.5 mEq/L. Renal biopsy showed interstitial infiltrate with inflammation of the tubules. Renal function began to improve after a 3-week course of prednisone. This case is remarkable for the severity of the renal failure despite such a minimal self-exposure.

Serum creatinine and blood urea nitrogen over a six-year period in the very old. Creatinine and BUN in the very old.

In a population of 141 very elderly subjects, there was a small but significant decline in BUN and creatinine at 3 years, which persisted at 6 years although partially attenuated. A similar pattern of falling BUN and creatinine was seen in the 31 subjects who began the study with mild azotemia. There was no significant change in the subjects' mean Body Mass Index during the 6-year period of observation. The azotemic subjects had a rate of death or dropout from the study similar to that of the entire cohort. Mean systolic blood pressure fell by 5.4 mm Hg (p < 0.05) and diastolic blood pressure by 2.1 mm Hg (p = NS) by 6 years. Users of diuretics or NSAID had a mean BUN and creatinine comparable to those not taking these medications. We conclude that BUN and serum creatinine do not necessarily increase with time in the old old, even in those with mild azotemia, hence, several determinations of these parameters may be needed to ensure accuracy. While renal function in the elderly probably does not improve with time, it may stabilize due to improvement in blood pressure. Use of diuretics and NSAID by functioning elderly individuals is not necessarily associated with worsening azotemia.

Effect of oral L-carnitine on serum myoglobin in hemodialysis patients.

Oral L-carnitine has been reported to lower the elevated serum myoglobin of renal failure in chronic peritoneal dialysis patients, and intravenous L-carnitine can improve muscle fatigue and cramps in chronic hemodialysis patients. In this study oral L-carnitine, 1.98 g/day, was administered to 6 chronic hemodialysis patients for 8 weeks. Serum levels of myoglobin, creatine kinase, and aldolase, as well as skeletal muscle symptoms (cramps during dialysis, fatigue, and weakness) were monitored biweekly for 12 weeks. Mean baseline serum myoglobin level was 337 +/- 34 ng/mL. By 6 and 8 weeks mean serum myoglobin was 234 +/- 39 and 233 +/- 40 ng/mL, significantly lower by the Friedman test (p < 0.05). Four weeks after carnitine was discontinued, mean serum myoglobin had risen to 320 +/- 118 ng/mL. Serum creatine kinase and aldolase levels were normal throughout the study. All 6 patients noted improvement in muscular symptoms, with maximal effect at 8 weeks, although 2 patients did not improve until 2 to 4 weeks after carnitine was stopped. We conclude that oral L-carnitine may lower serum myoglobin and improve muscle cramps and weakness in hemodialysis patients. The maximal effect of carnitine on myoglobin occurs 2 weeks before the maximal improvement in muscular symptoms.

Recurrent membranous lupus nephritis after renal transplantation: a case report and review of the literature.

Recurrent lupus nephritis in transplanted kidneys is rare. To the best of our knowledge, we report only the second case of recurrent membranous lupus nephritis in an allograft 8 years after transplantation. Unlike the first case, our patient received a transplant from a living-related donor rather than a cadaver. Disease "burn-out," the use of immunosuppressive drugs, and treatment of recurrence as rejection have all been offered as possible explanations for the rarity of recurrence. The majority of cases represent recurrence of the proliferative lesions, although a variety of histologic patterns and transformations have been reported.

Poisoning by amatoxin-containing mushrooms in suburban New York--report of four cases.

We report four cases of poisoning with amatoxin-producing mushrooms in suburban Long Island. All occurred when amateur mushroom hunters picked mushrooms from neighboring lawns. Two patients presented 30 hours post ingestion with evidence of acute hepatic dysfunction. One survived, after treatment with charcoal and penicillin; the other, a 90-year-old woman with prior cardiac disease soon developed shock and subsequently died. The other two patients were admitted 18 hours after ingestion of Lepiota chlorophyllum and received prompt charcoal hemoperfusion. Both did well, although one had a mild elevation of transaminases. Although most reports of amatoxin poisoning originate in Europe, these cases confirm that amatoxin-producing mushrooms, including Lepiota chlorophyllum, may be found in northeastern American suburbs. Such patients who present prior to 24 hours after ingestion should receive charcoal hemoperfusion if a lethal dose (> 50 g of mushroom) has been eaten.

A prospective study of urine and serum myoglobin levels in patients with acute rhabdomyolysis.

Serum and urine myoglobin levels, measured by radioimmunoassay, were determined prospectively in eight patients with acute rhabdomyolysis, within 24 hours of admission. Five patients had urine myoglobin concentrations greater than 1,000 ng/ml (normal < 5 ng/ml); four of these patients subsequently developed acute renal failure. In three patients whose urinary myoglobin levels ranged from 19 to 275 ng/ml, acute renal failure did not occur. This difference in the occurrence of acute renal failure between the two patient groups was statistically significant (p < 0.05). Mean peak serum creatinine was significantly higher in the patients with high urine myoglobin (6.4 +/- 1.3 mg/dl) compared to those with low urine myoglobin (2.2 +/- 0.3 mg/dl), p < 0.02. There was no statistical correlation between level of serum creatine phosphokinase and serum or urine myoglobin, although the serum and urine myoglobin levels correlated well with each other. These findings suggests that among other factors, urine myoglobin may need to reach a critical level in order for myoglobinuric renal failure to ensue.

Interstitial nephritis in a patient receiving adoptive immunotherapy with recombinant interleukin-2 and lymphokine-activated killer cells.

A patient receiving adoptive immunotherapy with recombinant interleukin-2 (IL-2) and lymphokine-activated killer (LAK) cells for metastatic melanoma developed acute renal insufficiency out of proportion to the decrease in her renal perfusion after 4 days of receiving IL-2. On the 8th day of IL-2 and the 3rd day of LAK cell infusion she expired suddenly from an acute intra-abdominal hemorrhage due to rupture of a metastasis. Postmortem examination of the kidneys showed an interstitial infiltrate consisting largely of lymphocytes and concomitant tubulitis. Immunoperoxidase staining of the infiltrating cells with a panel of lymphocyte-specific monoclonal antibodies showed the majority of cells to be T lymphocytes (70-75%), with a more focal infiltrate of B lymphocytes (25-30%) and rare monocytes, granulocytes and natural killer cells. This patient represents the first reported case of acute interstitial nephritis associated with IL-2 immunotherapy. Our finding is consistent with the hypothesis that the acute renal failure that accompanies this therapy may sometimes be due to intrinsic renal disease as well as the usual pre-renal failure. Nephritis may be caused by IL-2-mediated effects on lymphocytes, resulting in renal parenchymal infiltration.

Acute renal dysfunction during interleukin-2 treatment: suggestion of an intrinsic renal lesion.

Adoptive immunotherapy with interleukin-2 (IL-2) and lymphokine-activated killer (LAK) cells has been effective in treating some advanced malignancies in animals and humans. One complication of this treatment is a reversible, oliguric, acute renal failure, which has been ascribed to renal hypoperfusion and resultant prerenal azotemia. We serially studied renal function in 10 patients receiving high-dose regimens of recombinant interleukin-2 (rIL-2) to attempt to delineate further the nature of the renal dysfunction caused by IL-2 treatment. Renal plasma flow was computed from iodine 131 (I-131 Hippuran; Mediphysics, Paramus, NJ) orthoiodohippurate, excretion curves, and glomerular filtration rate (GFR) was determined by creatinine clearance. Studies done prior to and on day 4 of treatment showed that GFR fell in nine of 10 patients, with a mean decrease of 43% +/- 8%, and renal plasma flow fell in five of the 10 patients with a mean decrease of 5% +/- 10%. The average pretherapy filtration fraction was calculated to be 23% +/- 1% and after 4 days of treatment, decreased to a mean value of 15 +/- 2%. The BUN to creatinine ratio also declined in all patients. These findings collectively suggest that IL-2 nephrotoxicity may result from an intrarenal defect in addition to the previously described prerenal azotemia. Additionally, radionuclide studies of renal function are a reliable and reproducible noninvasive method of assessing these changes in renal function.

Sex differences in the subunits of glutathione-S-transferase isoenzyme from rat and human kidney.

Glutathione-S-transferase (GST) isoenzymes were purified from cytosolic preparations from kidneys of male and female rats and kidney cortical specimens from 2 male and 1 female human subjects. GST isoenzyme expression was analyzed by SDS-PAGE, measurement of catalytic activities with specific substrates and determination of their subunits by ELISA and Western blotting using specific antibodies. GST from female rat kidneys showed a preponderance of subunits 3 and 4; levels of these isoenzymes were 3-4 times greater in females than in males. Levels of subunits 1 and 2 were 1.5-2 times greater in the male rat kidneys. Additional minor bands at 24 and 22 kD were observed in GST preparations from both male and female rat kidneys while a band at 25.3 kD was observed only in the male rat kidney. These bands did not react with antibodies to GST 1-1, GST 2-2 or GST 3-4. Both male and female human kidney samples contained GST isoenzymes comparable to the near-neutral (25-5 kD) and basic forms (25 kD) of GSTs found in human liver. In addition a 28-kD band was present in GST preparations from both male and female human kidneys. Additional bands at 29 and 25.2 kD were present only in male human kidneys. Both the kidney cytosol and the total GSTs prepared from female rats shared 2- to 4-fold greater activity with 1,2-dichloro-4-nitrobenzene, ethacrynic acid and trans-4-phenyl-3-buten-2-one than those from males. The measurement of specific subunit amounts by ELISA were in agreement with these results.(ABSTRACT TRUNCATED AT 250 WORDS)

Renal microradiography of experimental ureteral obstruction in the rabbit.

Microradiography of nephrons in kidneys perfusion-fixed with glutaraldehyde permits examination of large numbers of nephrons. This technique was applied to rabbits between one and 14 days following unilateral ureteral ligation. Kidneys without ureteral occlusion served as controls. By two days after ureteral obstruction there was dilatation of the ducts of Bellini and papillary collecting ducts. At three to four days there was splaying and tortuosity of the loops of Henle. By eight to 10 days the proximal straight tubules were noted to be dilated and helically twisted. After two weeks of ureteral obstruction there was dilatation of Bowman's space with encroachment on the glomerular capillary tuft. At this time many proximal convoluted tubules began to show atrophic changes. These morphologic alterations may due in part to back pressure on the nephrons, with retrograde progression as the duration of urinary tract obstruction is increased. The distal convoluted tubule and the descending limb of the loop of Henle were not noted to be abnormal during the study.