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Query: UMLS:C0032285 (pneumonia)
 54,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The symptoms and clinical course of chronic hypokalemic nephropathy are described in 21 patients with longstanding potassium deficiency. In 14 patients (group A) the potassium depletion was caused by malnutrition and/or abuse of laxatives and/or diuretics. 7 patients (group B) suffered from primary (6 cases) or secondary (1 case) aldosteronism. The average duration of potassium depletion was 8.8 years in group A and 3.4 years in group B. Depending on the duration of potassium depletion, chronic renal disease develops which may end in terminal renal failure. Urinalysis is non-specific or negative. The clearance of creatinine slowly decreases. Metabolic alkalosis is a constant finding and in group A occurs with a tendency to hyponatremia and hypochloremia, with the development of metabolic acidosis only in advanced renal insufficiency. In contrast to patients of group B, patients of group A have normal or low blood pressures converting to hypertension, if at all only in the late phase. The cases of group A had secondary aldosteronism (and, correspondingly, a hyperplastic juxtaglomerular apparatus). Although urinary tract infection is a regular finding in advanced stages, the clinical, radiological and histological evidence suggests that bacterial pyelonephritis, if occurring at all, is rather a complication than the cause of the disease. In 5 patients 7 instances of acute renal failure of unknown origin were observed which was lethal in one case. Another patient died from terminal renal failure, a third from an intercurrent pneumonia. Renal histology obtained from 13 patients showed the picture of diffuse chronic abacterial interstitial nephritis.
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PMID:Symptoms and course of chronic hypokalemic nephropathy in man. 87 Feb 67

Cystic fibrosis was diagnosed in two female infants, respectively nine months old (Case 1) and six months old (Case 2). Clinical presentation of these two infants showed frequent episodes of pneumonia, dehydration and poor weight gain, despite fair intake of food since birth. Hyponatremic, hypochloremic metabolic alkalosis had been found during their previous hospitalizations. In Case 1, stool fat was positive with negative trypsin test. Both cases had abnormal findings on chest X-ray films, but the pancreas showed no remarkable cystic changes from sonography. Plastic-bag method of sweat test showed Na/Cl: 155/185 nmol/L in Case 1, Na/Cl: 127/135 nmol/L in Case 2. A family history was suggested, since each one had an elder brother who had died in early infancy with similar clinical presentations. Both patients were put on special diet therapy as well as chest physical therapy. Case 1 died suddenly at 16 months of age. Autopsy revealed mucusplugged dilated ducts with atrophy of the exocrine portion of the pancreas. DNA analysis in Case 2 showed abnormal mutation point at 1898+5 G-->T on chromosome 7.
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PMID:Cystic fibrosis in two Chinese infants in Taiwan. 821 63

We undertook the present study to examine the acid-base and electrolyte disturbances in relation to hydration status in patients with diabetic ketoacidosis (DKA). A total of 40 insulin-dependent diabetes mellitus patients (22 male, 18 female), aged 18-61 years with DKA admitted to our hospital during the last 2 years, were studied. The duration of diabetes averaged 9 +/- 2 years. In all cases a detailed investigation of the acid-base status and electrolyte parameters was performed. Twenty-one patients had a pure metabolic acidosis with an increased serum anion gap, seven had DKA combined with hyperchloremic metabolic acidosis, nine had DKA coexisting with metabolic alkalosis, while three had DKA with a concurrent respiratory alkalosis. Hydration status as evidenced by the ratio of urea/creatinine seems to play an important role in the development of mixed acid-base disorders (detected by changes in the ratios delta anion gap/delta bicarbonate (delta AG/delta HCO3) and sodium/chloride (Na/Cl)). In fact, hyperchloremic acidosis developed in the patients with the better hydration status. However, contradictorily, the severely dehydrated patients who experienced recurrent episodes of vomiting developed DKA with a concurrent metabolic alkalosis. Finally, patients with pneumonia or gram-negative septicemia exhibited DKA combined with a primary respiratory alkalosis. We conclude that patients with DKA commonly develop mixed acid-base disorders, which are partly dependent on patients' hydration status.
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PMID:Acid-base and electrolyte disturbances in patients with diabetic ketoacidosis. 896 87

The case of a 74-year-old woman with past history of hypertension and cerebrovascular accident admitted with pneumonia, dehydration, hypernatremia and severe hypokalemic alkalosis is presented. After correction of the hypertonic dehydration, the hypokalemia and alkalosis persisted in spite of aggressive potassium supplementation and the patient became hypertensive. Mineralocorticoid excess was suspected and excluded after extensive endocrinological testing. The use of aldactone failed to revert the abnormalities. Triamterene administration corrected the electrolytes and acid base aberrations, and dramatically improved the blood pressure control. This clinical picture is compatible with the diagnosis of Liddle's syndrome. Our patient exemplifies the unique occurrence of hypokalemic metabolic alkalosis in association with volume contraction at the start of the hospitalization and volume expansion later on her course.
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PMID:Saline-resistant metabolic alkalosis, severe hypokalemia and hypertension in a 74-year-old woman. 1066 85

We report a case of a 40-year-old man presenting with relapsing encephalopathy 4 years post-intestinal transplantation. Each episode was preceded by symptoms suggestive of subacute intestinal obstruction, marked dehydration, and, on one occasion, grade 4 encephalopathy. Physical examination revealed hypertonia, clonus, and hyperreflexia. Biochemistry was consistent with renal impairment, metabolic alkalosis, hyperammonaemia, and normal liver function. Plain radiographs and abdominal computed tomography revealed dilated proximal small bowel loops, and barium radiography demonstrated a strictured distal anastomosis. Hydrogen breath testing indicated bacterial overgrowth. Following rehydration and antibiotic therapy, the patient recovered fully between episodes. Further episodes of encephalopathy did not recur following resection of the distal anastomotic stricture and resolution of bacterial overgrowth. Unfortunately, one year later the patient died of pneumonia. To the best of our knowledge, encephalopathy secondary to intestinal transplant related porto-caval shunt and bacterial overgrowth in strictured bowel has not been previously reported but might have implications for the management of future patients.
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PMID:Relapsing encephalopathy following small bowel transplantation. 1282 21

We describe here the interesting case of a 73-year-old hypertensive man with pseudoaldosteronism. He had been taking glycyrrhizin at a dose of 75 mg/day for 12 years because of mild liver damage, but had never experienced any previous symptoms associated with hypokalemia. He was referred to our hospital because of hypokalemic tetraparesis and rhabdomyolysis. At that time, we noted mineralocorticoid excess characterized by hypokalemia due to urinary K loss, exacerbation of hypertension due to increased tubular Na reabsorption, metabolic alkalosis, and suppression of both plasma renin activity and plasma aldosterone concentration. His urinary free cortisol excretion rate and the urinary ratio of free cortisol to free cortisone were markedly elevated. Thus we diagnosed pseudoaldosteronism that was related to the long-term use of glycyrrhizin. When he developed pseudoaldosteronism, he also contracted pneumonia, and exhibited elevated levels of serum cortisol and creatinine clearance (CCr) as well as hypouricemia, hypocalcemia, and hypophosphatemia. All normalized after the recovery from pneumonia and the administration of spironolactone. The extracellular volume expansion associated with increased tubular Na reabsorption by the aldosterone-sensitive distal nephron and the resulting increase in CCr caused an inhibition of proximal tubular reabsorption of uric acid, Ca, and inorganic phosphate, leading to their renal loss and therefore hypouricemia, hypocalcemia, and hypophosphatemia, respectively. In this patient, the increased circulating cortisol associated with the stress of inflammation caused by pneumonia triggered the development of pseudoaldosteronism.
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PMID:Pseudoaldosteronism with increased serum cortisol associated with pneumonia, hypouricemia, hypocalcemia, and hypophosphatemia. 2097 51

Ensuring adequate nutrition in children with chronic kidney disease whilst avoiding hyperkalaemia can be a difficult balance to achieve. Pre-treatment of feeds, whether milk, formula or enteral nutrition, with sodium polystyrene sulfonate (SPS) is practiced in some paediatric centres internationally. Such treatments are purported to avoid the potentially serious complications of direct administration of SPS, such as intestinal necrosis, aspiration pneumonitis and metabolic alkalosis to name but a few. Although described some 45 years ago, this study by Palma et al. is only the second retrospective study to describe the clinical consequence of pre-treating feeds with SPS with the majority of earlier studies describing only the in vitro effects of this method. Whilst effective in reducing serum potassium, the authors justifiably highlight the high incidence of complications, such as hypokalaemia (31.6%) and hypernatraemia (26.3%). We have further highlighted this with a summary of the available literature on this subject demonstrating the gross alterations of the electrolyte composition of feeds following SPS pre-treatment and clinical complications in its application. We heartily agree and support the conclusion by Palma et al. that where this therapy is practiced, close monitoring of electrolytes is essential and much more work is needed to identify those patient cohorts for which this can indeed be considered a safe and effective intervention.
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PMID:Let food be thy medicine and medicine be thy food? 2999 17

A 23-year-old woman was referred to the tertiary centre with acute kidney injury and severe metabolic alkalosis following an accidental ethylene glycol poisoning. The patient had been treated with continuous haemodiafiltration and regional citrate anticoagulation, and a tracheostomy was performed due to pneumonia. Besides severe metabolic alkalosis and hypernatremia, the laboratory tests revealed total protein of 108 g/L on admission to the tertiary centre. The haemodiafiltration with regional citrate anticoagulation continued with parallel correction of the alkalosis and normalisation of the total plasma protein. The tracheostomy was decannulated and the patient was discharged to the district hospital. The case demonstrates the usefulness of regional citrate anticoagulation even in severe metabolic alkalosis which was likely related to the method setting prior to admission and to an overcompensation of the initial severe metabolic acidosis. The unusual hyperproteinaemia might be interpreted with the aid of the Stewart-Fencl model of the acid-base regulation.
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PMID:A Rare Case of Severe Metabolic Alkalosis with Unusual Hyperproteinemia Treated with Continuous Renal Replacement Therapy and Regional Citrate Anticoagulation. 3019 2