A 25-year-old lady presented with hypertensive encephalopathy. She also had chronic refractory hypertension for the past 7 years. Workup revealed persistent hypokalaemia with metabolic alkalosis suggesting hyperaldosteronism. Hyperaldosteronic states such as renal artery stenosis, Conn's syndrome and Liddle's syndrome were ruled out. Her plasma renin activity was high. Contrast-enhanced CT of the abdomen showed a 1.9×2 cm heterogeneously enhancing lesion in the anterior aspect of the right kidney suggesting a possibility of reninoma. The benign tumour was resected by a nephron-sparing surgery. Histopathology suggested a juxtaglomerular cell tumour. Anti-hypertensive drugs were completely withdrawn postoperatively.

Background:

Pathophysiologic changes after brain death can lead to acid-base disturbances. The primary aim of this study was to clarify the acid-base state and its source in brain dead donors using Stewart's approach. Additionally, we investigated whether the presence of metabolic acidosis affected the number of organs retrieved from donors.

Methods:

A retrospective review of electronic medical records was performed for brain dead donors who had undergone organ harvesting during the past 5 years in a tertiary medical center. The parameters related to acidbase disturbance and the number of organs retrieved from the donors was assessed.

Results:

Sixty one brain dead donors were evaluated in this study. Twenty three (37.7%) of these patients had metabolic acidosis at the initial diagnosis of brain death. Metabolic acidosis resulted from hyperchloremia and a large strong ion gap. The severity of metabolic acidosis was masked by hypernatremia and hypoalbuminemia. In addition, donors without metabolic acidosis also showed mixed acid-base disturbances in which metabolic acidosis induced by significant hyperchloremia was combined with metabolic alkalosis caused by hypoalbuminemia and hypernatremia. Although more organs were retrieved from the donors without metabolic acidosis than those with metabolic acidosis (P=0.012), serum albumin level (P=0.010) and donor age (P<0.001), rather than metabolic acid-base disturbances, significantly correlated with the number of organs retrieved in multivariate regression analysis.

Conclusion:

Most brain dead donors exhibited metabolic acid-base disturbances. However, rather than metabolic acidosis, serum albumin level and donor age were well correlated with the number of organs retrieved.

Dehydration is a common presentation to any emergency department with symptoms ranging from lethargy, confusion, oliguria as well as those specific to the underlying cause. In this case we describe a young patient who following a short history of vomiting and abdominal pain developed carpopedal spasm and distal parasthesia on a background of Gitelman syndrome. Biochemical blood analysis showed a marked hypokalaemia, hypomagnesaemia and mild metabolic alkalosis in addition to a prolonged QTc interval of 592 ms seen on ECG. Following fluid replacement and electrolyte correction his clinical symptoms resolved along with QTc normalisation. This case demonstrates a patient with a rare and interesting renal disorder who presented with typical biochemical and ECG abnormalities in addition to tetany in the presence of normal plasma calcium.

Acid-base disturbances caused by environmental factors and physiological events including feeding have been well documented in several fish species, but little is known about the impact of dietary electrolyte balance (dEB). In the present study, we investigated the effect of feeding diets differing in dEB ( - 100, 200, 500 or 800 mEq/kg diet) on the growth, nutrient digestibility and energy balance of Nile tilapia. After 5 weeks on the test diet, the growth of the fish was linearly affected by the dEB levels (P< 0·001), with the lowest growth being observed in the fish fed the 800 dEB diet. The apparent digestibility coefficient (ADC) of fat was unaffected by dEB, whereas the ADC of DM and protein were curvilinearly related to the dEB levels, being lowest and highest in the 200 and 800 dEB diets, respectively. Stomach chyme pH at 3 h after feeding was linearly related to the dEB levels (P< 0·05). At the same time, blood pH of the heart (P< 0·05) and caudal vein (P< 0·01) was curvilinearly related to the dEB levels, suggesting the influence of dEB on postprandial metabolic alkalosis. Consequently, maintenance energy expenditure (MEm) was curvilinearly related to the dEB levels (P< 0·001), being 54 % higher in the 800 dEB group (88 kJ/kg0·8 per d) than in the 200 dEB group (57 kJ/kg0·8 per d). These results suggest that varying dEB levels in a diet have both positive and negative effects on fish. On the one hand, they improve nutrient digestibility; on the other hand, they challenge the acid-base homeostasis (pH) of fish, causing an increase in MEm, and thereby reduce the energy required for growth.

Hypokalaemia is a common clinical disorder, the cause of which can usually be determined by the patient's clinical history. Gitelman syndrome is an inherited tubulopathy that must be considered in some settings of hypokalaemia. We present the case of a 60-year-old male patient referred to our nephrology department for persistent hypokalaemia. Clinical history was positive for symptoms of orthostatic hypotension and polyuria. There was no history of drugs consumption other than potassium supplements. Complementary evaluation revealed hypokalaemia (2.15 mmol/l), hypomagnesaemia (0.29 mmol/l), metabolic alkalosis (pH 7.535, bicarbonate 34.1 mmol/l), hypereninaemia (281.7 U/ml), increased chloride (160 mmol/l) and sodium (126 mmol/l) urinary excretion and reduced urinary calcium excretion (0.73 mmol/l). Renal function, remainder serum and urinary ionogram, and renal ultrasound were normal. A diagnosis of Gitelman syndrome was established. We reinforced oral supplementation with potassium chloride and magnesium sulfate. Serum potassium stabilised around 3 mmol/l. The aim of our article is to remind Gitelman syndrome in the differential diagnosis of persistent hypokalaemia.

INTRODUCTION:

Coexistent respiratory failure and metabolic alkalosis is a common finding. Acidotic diuretics cause a fall in pH that may stimulate respiration.6p

OBJECTIVE:

The purpose of the study was to evaluate the effectiveness of short-term treatment with acetazolamide for combined respiratory failure and metabolic alkalosis.6p

METHODS:

A randomized placebo-controlled and double-blind parallel group trial where oral acetazolamide 250 mg three times a day for five days were administered to patients hospitalized for respiratory failure due to a pulmonary disease (Pa O2 ≤8 kPa and/or Pa CO2 ≥7 kPa) who had concurrent metabolic alkalosis (base excess (BE) ≥8 mmol/L). Pa O2 after five days was the primary effect variable. Secondary effect variables were Pa CO2 , BE and pH on day five, and the total number of days in hospital.

RESULTS:

Of 70 patients enrolled (35 in each group) data from 54 were analyzed per protocol, while last observation carried forward was used for the remaining 16. During five days' treatment, Pa O2 increased on average 0.81 kPa in the placebo group and 1.41 kPa in the acetazolamide group. After adjustment for baseline skewness, the difference was statistically significant (adjusted mean difference 0.55 kPa, 95% confidence interval 0.03 to 1.06). Pa CO2 decreased in both groups, but the difference was not statistically significant. As expected, pH and BE decreased markedly in the acetazolamide group.

CONCLUSION:

Acetazolamide may constitute a useful adjuvant treatment, mainly to be considered in selected patients with respiratory failure combined with prominent metabolic alkalosis or where non-invasive ventilation is insufficient or infeasible.

TRIAL REGISTRATION:

ClinicalTrials.gov: NCT00222534.

The quantitative effect of strong electrolytes, pCO2 , and plasma protein concentration in determining plasma pH and bicarbonate concentrations can be demonstrated with the physicochemical approach. Plasma anion gap (AG) and strong ion gap (SIG) are used to assess the presence or absence of unmeasured anions.The physicochemical approach is useful for detection and explanation of acid-base disorders in horses with colitis. AG and SIG accurately predict hyperlactatemia in horses with colitis.Fifty-four horses with acute colitis and diarrhea.Retrospective study. Physicochemical variables were calculated for each patient. ROC curves were generated to analyze sensitivity and specificity of AG and SIG for predicting hyperlactatemia.Physicochemical interpretation of acid-base events indicated that strong ion metabolic acidosis was present in 39 (72%) horses. Mixed strong ion acidosis and decreased weak acid (hypoproteinemia) alkalosis was concomitantly present in 17 (30%) patients. The sensitivity and specificity of AG and SIG to predict hyperlactatemia (L-lactate > 5 mEq/L) were 100% (95% CI, 66.4-100; P < .0001) and 84.4% (95% CI, 70.5-93.5 P < .0001). Area under the ROC curve for AG and SIG for predicting hyperlactatemia was 0.95 (95% CI, 0.86-0.99) and 0.93 (95% CI, 0.83-0.99), respectively.These results emphasize the importance of strong ions and proteins in the maintenance of the acid-base equilibria. AG and SIG were considered good predictors of clinically relevant hyperlactatemia.

Acute kidney injury requiring renal replacement therapy occurs in up to 10% of all intensive care unit patients. Those who are hemodynamically unstable are often treated with continuous renal replacement therapy requiring continuous anticoagulation of the extracorporeal circuit. This is usually achieved by infusion of unfractionated heparin, which subsequently increases the risk of bleeding. To avoid systemic anticoagulation for continuous renal replacement therapy, regional anticoagulation with citrate has been introduced. We studied safety and efficacy of regional citrate anticoagulation for continuous venovenous hemodialysis in surgical patients requiring high dialysis doses. This was an observational prospective study in a 40-bed surgical intensive care unit at a university hospital. During a 12-month study period, all consecutive critically ill patients with high risk of bleeding requiring continuous renal replacement therapy continuous renal replacement therapy were treated with citrate anticoagulation for continuous venovenous hemodialysis. Prescribed dialysis dose was 45 mL/kg per h with a 10% increase for expected downtime. We studied filter lifetime, delivered dialysis dose, control of acid-base status, bleeding episodes, and adverse effects, that is, citrate intolerance. The total number of filters analyzed in 75 patients was 100. Mean (± standard deviation) filter running time was 78 ± 25 h. Fifty-one circuits had to be renewed because of extended filter running time (96 ± 18 h), 33 discontinued for reasons not related to renal replacement therapy (62 ± 19 h), and 13 due to filter clotting (58 ± 18 h). The mean dialysis dose during the first 72 h was 49 ± 14 mL/kg per h. Overall, acid-base status after 72 h was well controlled in 62% of patients, metabolic alkalosis (pH > 7.45) occurred in 29%, and metabolic acidosis (pH < 7.35) in 9%. In one patient, treatment was stopped because of citrate accumulation. Citrate intoxication or overt bleeding episodes were not observed. Regional citrate anticoagulation for continuous venovenous hemodialysis is a safe and effective method to deliver a high dialysis dose in critically ill patients with a high risk of bleeding. Filter patency was excellent, acid-base status was well controlled, and clinically relevant adverse effects were not observed. Therefore, citrate anticoagulated continuous venovenous hemodialysis is a useful treatment option for patients with acute kidney injury requiring high dialysis doses and at risk of bleeding.

Bartter's syndrome is a heterogeneous disorder characterized by deficient renal reabsorption of sodium and chloride, and hypokalemic metabolic alkalosis with hyper-reninemia and hyperaldosteronemia. Bartter syndrome type III (BS type III), due to mutations in the CLCNKB gene, is highly variable. The aim of our study was to describe the clinical presentation in a Chinese girl with BS type III and to explore mutations or SNPs of CLCNKB gene in her family.The clinic data of the patient was collected. Mutations or SNPs were investigated by sequencing of the exon of CLCNKB gene. The clinic analysis confirmed the diagnosis of BS type III. The coexistence of 13 reported SNPs and 11 novel SNPs of CLCNKB gene were found in the patient and her parent. a novel heterozygous C to G transition at nucleotide 2471 in exon 20 of CLCNKB gene harbored uniquely by the patient were revealed.A novel heterozygous C to G mutation at nucleotide 2471 of CLCNKB gene and some new SNPs were identified in a Chinese girl with BS type III having persistent hypokalemia. The novel mutation and SNPs make the genetic background of the patient more complicated.