Christos P. Carvounis

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

Intravenous labetolol, a nonselective α- and β-blocking drug, is commonly used to treat severe hypertension. Nonselective β-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.

Role of the endogenous kallikrein-kinin system in modulating vasopressin-stimulated water flow and urea permeability in the toad urinary bladder.

This study investigates the endogenous kallikrein-kinin systems role as a modulator of vasopressin action in the toad urinary bladder. Kalli-krein inhibition by aprotinin, which results in decreased kinin production, significantly increased both vasopressin and 8-Br-cyclic (c) AMP-stimulated water flow. Kinin potentiation by the kininase II inhibitor captopril (SQ 14225) significantly decreased vasopressin and 8-Br-cAMP-stimulated water flow. In contrast to water flow, vasopressin-stimulated urea permeability was decreased by aprotinin and increased by captopril. We conclude that the endogenous kallikrein-kinin system represents a significant modulator of vasopressin action and it permits separate control of vasopressin-stimulated water flow and solute transport.

Screening for microalbuminuria simplified by urine specific gravity.

Background: The albumin-to-creatinine ratio and the 24-hour urine collection to measure microalbuminuria are inconvenient and expensive. The newer rapid and less expensive dipstick methods for screening of microalbuminuria estimate only albumin and are subject to errors caused by variation in volume. We determined the relation between urine-specific gravity (Usg) and urine creatinine (Ucr) so that Ucr can be derived from Usg to correct for albumin concentration in the urine which is influenced by urine volume. Methods: We randomly included 42 consecutive patients from the primary care clinic, and 34 patients from the diabetic clinic. Results: We found that a very good correlation existed between Usg and Ucr in the 42 patients from the primary care clinic (Ucr = 11.4 × Usg –11,509, r = 0.83, p < 0.001). Patients from the diabetic clinic who had well-controlled blood sugar (n = 21) showed a similar trend (Ucr = 10.82 × Usg –10,882, r = 0.87, p < 0.001). However, this was not the case with uncontrolled diabetics (Ucr = 2.53 × Usg –2,513, r = 0.26, NS). Using simple arithmetic, we derived a simplified formula where Ucr can be predicted from Usg. Using multiple regression to incorporate the urinary glucose level by dipstick, a more generic formula was obtained for estimating urinary creatinine. Conclusion: Usg can be used instead of Ucr to normalize for the varied urine concentration while screening for microalbuminuria. Poorly controlled diabetics should be screened after their blood sugars are well controlled or use the more generic formula that incorporates urinary glucose. Thus, by measuring spot urine albumin and specific gravity by dipsticks one gets an easy, immediate and accurate estimation of microalbuminuria in an office setting.

Renal involvement in the systemic inflammatory reaction syndrome

Uncontrolled infection quite often leads to systemic inflammatory reaction syndrome (SIRS) and multiorgan dysfunction (MOD) syndrome. Thirty-five consecutive patients (19 males) fulfilling strict diagnostic criteria for SIRS were enrolled in two multicenter prospective double-blind trials involving new therapies for SIRS. The patients were followed prospectively up to day 28 after the enrollment. In the 35 patients with SIRS, males predominated in the age group below 40 (10/12, 83%) compared to the older group (nine males out of 23, 39%). Out of 16 females presenting with SIRS, only two were below the age of 40. This distribution was statistically different than our general MICU population. The serum albumin in these patients was uniformly low, with a mean of 22.5 gm/L. The bulk of SIRS patients (22/35; 63%) went on to develop acute renal failure (ARF). Although statistically not different, skin and peritoneal infections were more common in ARF group while pulmonary infections in non-ARF group. The majority of blood-cultures grew gram-positive organisms. Resolution of SIRS occurred within first 3 days in greater number of non-ARF survivors than ARF survivors (6/9, 66.7% vs. 6/16, 37.5%). Of the 22 ARF patients, 17 showed improvement in their renal function; the five who did not, died before day 28. The overall mortality (about 32%) was similar in both groups. Patients who developed both ARF and ARDS did not survive. In conclusion. SIRS occurs mostly in elderly patients, almost always in patients with low albumin levels. Premenopausal women seem to be protected. Blood cultures isolated a gram-positive organism in the majority of cases. Improvement in serum creatinine suggests good prognosis. The mortality in ARF and non-ARF groups is similar.

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.

Risk Factors to Predict Renal Failure and Death in the Medical Intensive Care Unit

The ability to predict outcomes based on admission criteria has important implications, both prognostically and for assessing interventions on comparable groups. Use of severity of disease scoring systems such as the APACHE II score for predicting mortality has become widespread. There is no comparable formula for acute renal failure. We prospectively evaluated 115 consecutive admissions to the medical intensive care unit to define risk for renal failure from admission data and to assess the impact of admission hypoalbuminemia levels on outcome. Diagnosis, age, serum creatinine and albumin levels, urinary electrolyte concentrations and osmolality, daily serum creatinine levels, and urine output were recorded. Admission APACHE II score was calculated. Admission hypoalbuminemia (57% of patients) was associated with both acute renal failure and death (odds ratios, 16.19 and 8.06, respectively). The Glasgow coma score distinguished between patients in whom acute renal failure developed and in those it did not. Low urine osmolality (<400 mOsm/kg) was the most significant factor in predicting mortality (odds ratio, 9.87). Mortality was lowest in the normal albumin group (2%), intermediate in the low albumin/no renal failure group (12%), and highest in the low albumin/acute renal failure group (53%). The APACHE II score was accurate in 3 of 14 deaths in the hypoalbuminemic population and in the one normal albumin patient who died. We conclude that at admission, hypoalbuminemia, urinary hypo-osmolality, and abnormal creatinine levels are predictive of acute renal failure and death, diagnosis, and mental status impact on the risk for acute renal failure. APACHE II lacks predictive value in hypoalbuminemic patients.

UNMEASURED CATIONS: PROBABLE CAUSE OF RELATIVELY LOW ANION GAP IN CHRONIC RENAL FAILURE

It is commonly believed that the electrolyte pattern in the patients with chronic renal failure (CRF) is associated with high anion gap (AG) and low serum bicarbonate (HCO3). However it was seen in many clinical studies that the AG is normal or only minimally increased in such patients. It is also known that organic cations, in particular guanidines, also increase in the serum of patients with CRF. We thus postulated that the relatively small increase in AG could be, in part, explained by the coexistent increase in unmeasured cations. If this is true, one may expect that the serum osmolality measured directly will be higher than the estimated one, leading to an osmolar gap (OG). Previous studies have shown that indeed OG exists in patients with CRF. We proceeded to determine SMA-7, AG, and OG simultaneously in ambulatory, undialyzed CRF patients with serum creatinine between 4 and 12 mg/dL. These investigations were also done on nine patients, after dialysis, who went on to have dialysis. The patients were divided into the normal AG (AG ≤ 14) and a high AG (AG > 14) groups. There was no correlation of serum bicarbonate with degree of renal dysfunction. Serum AG influenced HCO3 only in the patients with high AG group (bicarbonate = 23.85 − 0.69 (ΔAG), r2 = 0.45). In patients with normal anion gap there was a good correlation between ΔAG and OG (ΔAG = 3.4 − 0.15 OG, r = 0.46, r2 = 0.21, p < 0.05). Thus serum bicarbonate appears to be controlled by both AG and OG. Following dialysis, OG decreased from 15.5 ± 1.06 to 6.08 ± 1.71, p < 0.01. We conclude that OG must be made up of unmeasured cations of low molecular weight as it normalizes the AG, and gets cleared after dialysis. These low molecular weight substances could be guanidines, such as guanidosuccinic acid and methylguanidine, which are increased by one hundred fold in CRF.

Does Timing of Dialysis in Patients with ESRD and Acute Myocardial Infarcts Affect Morbidity or Mortality

BACKGROUND AND OBJECTIVES Patients with ESRD have an increased incidence of coronary events with a relatively higher risk for mortality after acute myocardial infarction (AMI). We evaluated whether it is safer to delay dialysis in AMI or if delay poses separate risks. DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS We conducted a retrospective review of 131 long-term hemodialysis patients who had AMI and were admitted between 1997 and 2005 at three New York City municipal hospitals. Patients were separated into three groups on the basis of time between cardiac symptoms and first dialysis (<24 h, 24 to 48 h, and >48 h). RESULTS A total of 17 (13%) patients died, 10 (59%) of whom had either hypotension or an arrhythmia during their first cardiac care unit dialysis. Although these groups were comparable in acuity and cardiac status, there were no findings of increased morbidity (26, 36, and 20%, respectively) or mortality (11, 18, and 13%, respectively), despite differences in the timing of each groups dialysis. We found that previous cardiac disease, predialysis K+, DeltaK+ after dialysis, and APACHE scores were significantly higher in patients with peridialysis morbidity. CONCLUSIONS We conclude that there is no increased morbidity with early dialysis in AMI, but rather close attention needs to be paid to the rate of decrease in serum potassium in patients with ESRD and their level of acuity when undergoing dialysis.