Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers: what to do if the serum creatinine and/or serum potassium concentration rises.

Introduction Guidelines governing the optimal treatment of blood pressurein patients with chronic renal failure emphasize the need formore stringent blood pressure control and the use of drugs thatinterfere with the renin–angiotensin system [1,2]. Asthis approach is adopted, physicians will commonly encounterpatients where blood pressure control is accompanied by an increasein the serum creatinine concentration and patients who develophyperkalaemia. How physicians respond to these events is ofconsiderable importance. In the patient with an increase in serum creatinine concentration,decreasing the dose of antihypertensive medications and allowingblood pressure to increase will cause the serum creatinine concentrationto return to the original baseline. Unfortunately, such an approachis not optimal for the long-term preservation of renal functionand should be discouraged. Small and non-progressive increasesin the serum creatinine concentration accompanying better bloodpressure control do not reflect structural     

The Marmara earthquake: admission laboratory features of patients with nephrological problems.

BACKGROUND: Earthquakes are major causes of morbidity and mortality. North-western Turkey was struck by a devastating earthquake in August 1999, which caused several thousand deaths. Among the most important morbid events in survivors were acute nephrological problems. METHODS: Within the first week of the disaster, specific questionnaires asking about 63 clinical and laboratory parameters were sent to 35 reference hospitals that were treating the victims. Of the registered 639 victims, 423 were admitted within the first 3 days of the disaster; the admission laboratory data of these 423 patients are the subject of this analysis. RESULTS: In the 423 patients (233 males, mean age 31.3+/-14.4 years), time under the rubble was 10.7+/-10.4 h. Mean values at admission were as follows: serum potassium 5.4+/-1.3 mEq/l, creatine phosphokinase 58205+/-77889 IU/l, albumin 2.6+/-0.7 g/dl, phosphorus 5.2+/-1.8 mg/dl, haematocrit 35.0+/-9.3%, leukocyte count 14945+/-6614/mm(3), platelet count 183975+/-134012/mm(3), blood urea nitrogen 55.1+/-28.9 mg/dl, and creatinine 3.9+/-2.3 mg/dl. Serum potassium above 6.5 mEq/l was noted in 91 patients (22.7%), an alarming finding for risk of fatal arrhythmias. Non-survivors were characterized by higher figures of serum potassium (P=0.001), as well as lower haematocrit (P=0.028), platelets (P<0.001), and serum albumin (P=0.003). In a multivariate analysis model of admission laboratory parameters, serum creatinine (P<0.001, o.r.=2.19), potassium (P=0.001, o.r.=3.64), and phosphorus (P=0.004, o.r.=1.78) predicted dialysis needs, whereas serum albumin (P=0.028, o.r.=0.23) and creatinine (P=0.039, o.r.=0.60) were related to mortality. CONCLUSIONS: Admission laboratory data may be useful for predicting dialysis needs and survival chance of disaster victims. High incidences of some life-threatening abnormalities dictate the need for empirical therapy even in the field.     

Beta-adrenoceptor blockade and suxamethonium-induced rise in plasma potassium

The effects of beta-adrenergic blockade on the suxamethonium-induced rise in arterial plasma potassium were studied in patients who presented for open heart surgery. No potentiation of the immediate rise in plasma potassium was observed.     

Tumour Lysis Following Hydrocortisone Prior to a Blood Product Transfusion in T-Cell Acute Lymphoblastic Leukaemia

The acute tumour lysis syndrome is a well recognised complication of chemotherapy for lymphoid malignancies. There are few reports, however, of this complication after corticosteroid therapy alone. We report a case of T-cell acute lymphoblastic leukaemia who developed the biochemical picture of tumour lysis after two doses of hydrocortisone given prior to platelet transfusion. Prophylactic corticosteroids prior to blood product infusion should be reserved for patients who have experienced febrile or allergic reactions in the past and it is suggested that they should only be administered to patients with active lymphoid malignancies with due caution.     

Transfusions of CPDA-1 red blood cells stored for up to 28 days decrease donor exposures in very low-birth-weight premature infants

The goal of this research was to study the safety and the efficacy of transfusing citrate-phosphate-adenine anticoagulant-preservative (CPDA-1) RBC stored for up to 28 days to reduce donor exposures in premature infants. A prospective randomized two-group study was conducted with very low-birth-weight premature infants that received at least one RBC transfusion during hospital stay. Neonates randomly assigned to Group 1 (26 infants) were transfused with CPDA-1 RBC stored for up to 28 days; those assigned to Group 2 (26 infants) received CPDA-1 RBC stored for up to 3 days. Demographic and transfusion-related data were collected. Neonates from both groups showed similar demographics and clinical characteristics. The number of transfusions per infant transfused was 4.4 +/- 4.0 in Group 1 and 4.2 +/- 3.1 in Group 2, and the number of donors per infant transfused was 1.5 +/- 0.8 (Group 1) and 4.3 +/- 3.4 (Group 2), P < 0.001. RBC transfusions containing 29.7 +/- 18.3 mmol L(-1) of potassium (RBC stored for up to 28 days) did not cause clinical or biochemical changes and reduced donor exposures by 70.2%, compared to transfusions containing 19.8 +/- 12.3 mmol L(-1) of potassium (RBC stored for up to 3 days), P < 0.001. In conclusion, RBC stored for up to 28 days safely reduced donor exposures in premature infants.     

Molecular insights from dysregulation of the thiazide‐sensitive WNK/SPAK/NCC pathway in the kidney: Gordon syndrome and thiazide‐induced hyponatraemia

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'Near-miss' hyperkalaemic cardiac arrest associated with rapid blood transfusion

A case is presented in which a relatively modest blood transfusion resulted in acute hyperkalaemia with a 'near-miss' cardiac arrest. While transfusion-related hyperkalaemia usually occurs in association with massive transfusions, several factors may have increased the risk of such an acute reaction. A high index of suspicion is required, especially in patients with risk factors. Anaesthetists should not be lulled into a false sense of security simply because modest volumes of blood are being transfused.     

Renal effects of cyclo-oxygenase-2 inhibition

SUMMARY: The renal cyclo-oxygenase (COX)-2 isoenzyme has an important role in the maintenance of renal homeostasis, particularly in the setting of reduced renal perfusion. Selective inhibition of COX-2 in the kidney has significant effects on renal physiology, most marked when COX-2 expression is induced. the clinical risk of renal impairment, salt and water retention, and electrolyte disturbance should be considered carefully when prescribing a COX-2 inhibitor in this setting.     

K+ balance in humans during exercise

Onset of exercise leads to a sudden increase in [K⁺] in venous plasma from the exercising muscles. Delayed by about 10 s, the arterial [K⁺] rises nearly at the same rate as the venous concentration. At exercise intensities below 100% of Vo _{2 max}, both venous and arterial [K⁺] stabilize at a steady-state value. At higher intensities, venous and arterial plasma [K⁺] continue to rise until exhaustion. During the first 5 min of exercise the contracting muscles always lose K⁺, with a peak in loss rate after 1–2 min. During steady state, the loss rate is minimized or may even be reduced to zero. The loss is caused by an exercise-induced efflux of K⁺ from the contracting cells which exceeds the exercise-induced influx mediated by the Na, K pump. The Na, K pump is stimulated by catecholamines in vitro and in resting tissue in vivo. However, the loss rate of K⁺ from steady-state exercising muscles does not show any increase during β-adrenergic blockade or decrease during β-adrenergic stimulation. This is probably due to a compensatory change in intracellular [Na⁺]. During low exercise intensity, arterial [K⁺] does not increase after 1–2 min, while the exercising muscles lose K⁺, showing that the extracellular pool of K⁺ is redistributed. During β-adrenergic blockade this redistribution is impaired so that the rise in plasma [K⁺] is accentuated. Conversely α-adrenergic blockade reduces the exercise-induced hyperkalaemia. Hence, the adrenergic system plays an important role in regulation of whole-body K⁺ balance during exercise, but its significance in exercising muscles is not clear.