Disturbances in fluid and electrolytes are among the most common clinical problems encountered in the intensive care unit (ICU). Recent studies have reported that fluid and electrolyte imbalances are associated with increased morbidity and mortality among critically ill patients. To provide optimal care, health care providers should be familiar with the principles and practice of fluid and electrolyte physiology and pathophysiology. Fluid resuscitation should be aimed at restoration of normal hemodynamics and tissue perfusion. Early goal-directed therapy has been shown to be effective in patients with severe sepsis or septic shock. On the other hand, liberal fluid administration is associated with adverse outcomes such as prolonged stay in the ICU, higher cost of care, and increased mortality. Development of hyponatremia in critically ill patients is associated with disturbances in the renal mechanism of urinary dilution. Removal of nonosmotic stimuli for vasopressin secretion, judicious use of hypertonic saline, and close monitoring of plasma and urine electrolytes are essential components of therapy. Hypernatremia is associated with cellular dehydration and central nervous system damage. Water deficit should be corrected with hypotonic fluid, and ongoing water loss should be taken into account. Cardiac manifestations should be identified and treated before initiating stepwise diagnostic evaluation of dyskalemias. Divalent ion deficiencies such as hypocalcemia, hypomagnesemia and hypophosphatemia should be identified and corrected, since they are associated with increased adverse events among critically ill patients.
Central Nervous System ; Critical Illness ; Dehydration ; Delivery of Health Care ; Electrolytes ; Hand ; Hemodynamics ; Humans ; Hyperkalemia ; Hypernatremia ; Hypocalcemia ; Hypokalemia ; Hyponatremia ; Hypophosphatemia ; Intensive Care Units ; Perfusion ; Plasma ; Resuscitation ; Sepsis ; Shock, Septic ; Vasopressins ; Critical Care

Renal dysfunction in patients with chronic liver disease encompasses a clinical spectrum of hyponatremia, ascites, and hepatorenal syndrome. Clinical observation has suggested that patients with cirrhosis have hyperdynamic circulation, and recent studies strongly suggest that peripheral arterial vasodilatation and subsequent development of hyperdynamic circulation are responsible for disturbances in renal function. Arterial vasodilatation predominantly occurs in the splanchnic vascular bed, and seems to precede an increase in blood flow in the splanchnic circulation. Nitric oxide plays a central role in progressive vasodilatation, as evidenced by in vivo and in vitro studies. Renal dysfunction negatively affects the prognosis of patients with cirrhosis, as hyponatremia, ascites, and azotemia are associated with increased rate of complications and mortality. Recent advances in understanding the pathophysiology of renal dysfunction have enabled clinicians to develop new diagnostic criteria and therapeutic recommendations. Hepatorenal syndrome is regarded as a potentially reversible disorder, as systemic vasoconstrictors with concomitant albumin administration are emerging as a promising management option, especially in terms of providing bridging therapy for patients awaiting liver transplantation.
Ascites ; Azotemia ; Fibrosis ; Hepatorenal Syndrome ; Humans ; Hyponatremia ; Liver ; Liver Cirrhosis ; Liver Diseases ; Liver Transplantation ; Nitric Oxide ; Prognosis ; Splanchnic Circulation ; Vasoconstrictor Agents ; Vasodilation

No abstract available.
Skin*

Tuberculosis (Tb) is a common disease in the developing world and its incidence is slowly increasing in developed countries, where a resurgence has occurred subsequent to the acquired immunodeficiency syndrome epidemic. In addition, patients with end-stage renal disease who are on maintenance hemodialysis carry a high risk for Tb; reported incidence varies from 6-16 times that of the general population. Extrapulmonary Tb constitutes a major part of Tb in dialysis patients. Isolated pancreatic Tb is a very rare occurrence in the setting of extrapulmonary Tb. It usually occurs as a complication of miliary Tb in immunodeficient individuals, particularly those with human immunodeficiency virus infection. There is no isolated pancreatic Tb in patients with end-stage renal disease. We recently experienced a case of isolated pancreatic Tb diagnosed by acid fast bacilli culture, Tb polymerase chain reaction from ultrasound-guided fine needle aspiration, and an excellent response after anti-Tb treatment in a 72-year-old patient with end-stage renal disease.
Acquired Immunodeficiency Syndrome ; Aged ; Biopsy ; Biopsy, Fine-Needle ; Developed Countries ; Dialysis ; HIV ; Humans ; Incidence ; Kidney Failure, Chronic ; Pancreas ; Polymerase Chain Reaction ; Renal Dialysis ; Tuberculosis

Transfusion support for hematopoietic stem cell transplantation (HSCT) is an essential part of supportive care, and compatible blood should be transfused into recipients. As leukocyte antigen (HLA) matching is considered first and as the blood group does not impede HSCT, major, minor, bidirectional, and RhD incompatibilities occur that might hinder transfusion and cause adverse events. Leukocyte reduction in blood products is frequently used, and irradiation should be performed for blood products, except for plasma. To mitigate incompatibility and adverse events, local transfusion guidelines, hospital transfusion committees, and patient management should be considered.

Chinese herb nephropathy (CHN) is characterized by progressive tubulointerstitial nephritis and development of renal failure in a couple of years after diagnosis. Aristolochic acid (AA) is believed to be associated with the development of CHN. The authors report a case of CHN in which AA in the herb regimen was identified by high-performance liquid chromatography (HPLC). A 32-year-old female presented with nausea, vomiting and generalized weakness. She had been taking Chinese herbs for symptomatic care. Clinical and laboratory examinations revealed Fanconi syndrome, renal failure, and severe anemia. Renal biopsy showed severe tubulointerstitial nephritis with moderate tubular atrophy and interstitial fibrosis. She developed end-stage renal failure 4 months after diagnosis. The herb she had been taking was Aristolochia fangchi. HPLC technique was used to identify AA and to measure its concentration in the herb. From the clinical and laboratory data, the patient was diagnosed with CHN caused by aristolochic acid.
Adult ; Anemia ; Aristolochia* ; Aristolochic Acids ; Asian Continental Ancestry Group* ; Atrophy ; Biopsy ; Chromatography, High Pressure Liquid ; Chromatography, Liquid ; Diagnosis ; Fanconi Syndrome ; Female ; Fibrosis ; Humans ; Kidney Failure, Chronic ; Nausea ; Nephritis, Interstitial ; Renal Insufficiency ; Vomiting

BACKGROUND: Furosemide inhibit NaCl absorption in the thick ascending limb and produce an increase in distal delivery of Na+. We carried out semiquantitative immunoblotting and immunohistochemistry of rat kidneys to investigate whether chronic furosemide infusion is associated with compensatory increases in the abundance of Na+ transporters in distal nephron. METHODS: Osmotic minipumps were implanted into Sprague-Dawley rats to deliver 12 mg/day of furosemide(n=6) with simultaneous administration of 0.8% NaCl and 0.1% KCl in drinking water for 7 days. RESULTS: Compared with vehicle infused controls, urine volume and urine sodium amount were increased. However, there were no differences in body weight, serum aldosterone, and creatinine clearance. The abundance of Na+-K+-2Cl- cotransporter after furosemide infusion was increased in cortex (151+/-10 vs. 100+/-10%, p< 0.05) and outer medulla (122+/-5 vs. 100+/-3%, p< 0.01). In furosemide infusion group, the abundance of all three subunits of epithelial sodium channel (ENaC) was increased both in cortex (alpha: 187+/-25 vs. 100+/-17%, p< 0.05; beta: 155+/-8 vs. 100+/-15%, p< 0.05; gamma: 168+/-16 vs. 100+/-9%, p< 0.05) and outer medulla (alpha: 171+/-27 vs. 100+/-17%, p< 0.05; beta: 986+/-91 vs. 100+/-33%, p< 0.01; gamma: 242+/-24 vs. 100+/-22%, p< 0.01). Consistent with these results, ENaC beta-subuint immunohistochemistry showed a remarkable increase in immunoreactivity in the principal cells of collecting ducts with furosemide treatment. CONCLUSION: These increases in the abundance of ENaC protein may account for the generation of diuretic tolerance.
Absorption ; Aldosterone ; Animals ; Body Weight ; Creatinine ; Drinking Water ; Epithelial Sodium Channels ; Extremities ; Furosemide* ; Immunoblotting ; Immunohistochemistry ; Kidney* ; Nephrons ; Rats* ; Rats, Sprague-Dawley ; Sodium*

OBJECTIVE: Cardiovascular disease is the most frequent cause of death in rheumatoid arthritis(RA) patients and hyperhomocysteinemia is an independent risk factor for cardiovascular disease. We evaluated the status of homocysteine, vitamin B12 and folate in RA patients and the influence of the drugs used in RA on homocysteine and vitamin levels. METHODS: Fifty-six RA patients and 22 controls were studied. Plasma total homocysteine was measured by HPLC method and serum folate and vitamin B12 were measured by chemiluminescence immunoassay. In RA patients, age, sex, disease duration, medications and laboratory findings were analyzed. RESULTS: Serum vitamin B12 level was significantly lower in RA patients compared to controls(p=0.033). No significant difference in serum folate level was found between RA patients and controls but plasma total homocysteine level was significantly higher in RA patients. There was no difference in plasma total homocysteine level between patients taking MTX with folate and controls, but plasma total homocysteine level was significantly higher in patients not taking MTX compared with controls(p=0.028). In RA patients taking only hydroxychloroquine(HCQ) as a DMARD, there was significantly lower serum folate level(p=0.033) and higher plasma total homocysteine level(p=0.043) compared with controls. There was a significant negative correlation between plasma total homocysteine level and serum folate level in RA patients(r=-0.319, p=0.017). CONCLUSION: Plasma total homocysteine level was increased in RA patients but not in patients taking MTX and folate. These findings suggested that folate supplementation may be effective to prevent hyperhomocysteinemia in RA patients.
Antirheumatic Agents ; Arthritis, Rheumatoid* ; Cardiovascular Diseases ; Cause of Death ; Chromatography, High Pressure Liquid ; Folic Acid* ; Homocysteine* ; Humans ; Hyperhomocysteinemia ; Immunoassay ; Luminescence ; Plasma* ; Risk Factors ; Vitamin B 12* ; Vitamins*

BACKGROUND: Sodium retention occurs in some patients taking NSAIDs (nonsteroidal anti-inflammatory drugs). Although the renal effects of NSAIDs are predominantly mediated through the inhibition of prostaglandins synthesized by cyclooxygenase-2 (COX-2), the mechanisms of sodium retention are not clear at the sodium transporter levels in the kidney. Previous studies have shown that compensatory upregulation of COX-2 is induced in renal medulla by high salt intake and that NSAID-induced sodium retention may be transitory. METHODS: To investigate whether renal sodium transporter abundances are altered by NSAID administration and whether renal sodium transporter abundances are affected by high salt intake or chronic NSAID administration, we performed an acute study treated with a single injection of diclofenac and another chronic study treated with 7 days' administration of DFU, a selective COX-2 inhibitor, using semiquantitative immunobotting from rat kidneys. Male Sprague-Dawley rats were divided into three groups in each study: controls, NSAID treatment, and high-salt intake plus NSAID treatment. The control diet contained sodium 1 mmol/200 g BW/day, and the high-salt diet 10 mmol/200 g BW/day. RESULTS: The acute study using diclofenac (100 mg/kg BW) increased the abundances of NKCC2 (by 73%) and ENaC-alpha (by 60%) in cortex and of NKCC2 (by 165%) and ENaC-alpha (by 91%) in outer medulla, in association with a significant decrease in urinary sodium excretion. The increased ENaC-alpha abundance was reversed by addition of high salt intake in both cortex and outer medulla. The chronic study using DFU (40 mg/kg/d for 7 days) showed no significant changes in distal renal sodium transporters except a decreased abundance of Na-K- ATPase alpha1-subunit (by 24%) in outer medulla. The addition of high salt intake decreased the abundances of ENaC-alpha (by 35%) and ENaC-beta (by 47 %) in outer medulla. CONCLUSION: The abundances of thick ascending limb NKCC2 and collecting duct ENaC are altered in response to NSAID administration. It is suggested that NKCC2 & ENaC are contributory to NSAID- induced sodium retention and also have a compensatory role in high salt intake and chronic NSAID administration.
Adenosine Triphosphatases ; Animals ; Anti-Inflammatory Agents, Non-Steroidal ; Cyclooxygenase 2 ; Diclofenac ; Diet ; Extremities ; Humans ; Kidney ; Male ; Prostaglandins ; Rats ; Rats, Sprague-Dawley ; Sodium* ; Up-Regulation

Hemodynamic factors play an important role in the development and/or progression of diabetic nephropathy. We hypothesized that renal sodium transporter dysregulation might contribute to the hemodynamic alterations in diabetic nephropathy. Otsuka Long Evans Tokushima Fatty (OLETF) rats were used as an animal model for type 2 diabetes. Long Evans Tokushima (LETO) rats were used as controls. Renal sodium transporter regulation was investigated by semiquantitative immunoblotting and immunohistochemistry of the kidneys of 40-week-old animals. The mean serum glucose level in OLETF rats was increased to 235+/-25 mg/dL at 25 weeks, and the hyperglycemia continued up to the end of 40 weeks. Urine protein/ creatinine ratios were 10 times higher in OLETF rats than in LETO rats. At 40th week, the abundance of the epithelial sodium channel (ENaC) beta-subunit was increased in OLETF rats, but the abundance of the ENaC gamma-subunit was decreased. No significant differences were observed in the ENaC alpha-subunit or other major sodium transporters. Immunohistochemistry for the ENaC beta-subunit showed increased immunoreactivity in OLETF rats, whereas the ENaC gamma-subunit showed reduced immunoreactivity in these rats. In OLETF rats, ENaC beta-subunit upregulation and ENaC gamma-subunit downregulation after the development of diabetic nephropathy may reflect an abnormal sodium balance.
Animals ; Blood Glucose/analysis ; Diabetes Mellitus, Type 2/*metabolism ; *Disease Models, Animal ; Epithelial Sodium Channel/*analysis ; Hypertension/complications ; Immunoblotting ; Immunohistochemistry ; Kidney/*metabolism ; Male ; Rats ; Sodium/*metabolism ; Sodium-Hydrogen Antiporter/genetics ; Sodium-Potassium-Chloride Symporters/genetics