Journal of nephrology
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Metabolic alkalosis is a primary pathophysiologic event characterized by the gain of bicarbonate or the loss of nonvolatile acid from extracellular fluid. The kidney preserves normal acid-base balance by two mechanisms: bicarbonate reclamation mainly in the proximal tubule and bicarbonate generation predominantly in the distal nephron. Bicarbonate reclamation is mediated mainly by a Na-H antiporter and to a smaller extent by the H-ATPase. ⋯ The effects of metabolic alkalosis on the body are varied and include effects on the central nervous system, myocardium, skeletal muscle, and the liver. Treatment of this disorder is simple, once the pathophysiology of the cause is delineated. Therapy consists of reversing the contributory factors promoting alkalosis and in severe cases, administration of carbonic anhydrase inhibitors, acid infusion, and low bicarbonate dialysis.
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Journal of nephrology · Mar 2006
Case ReportsThe pathology of jaundice-related renal insufficiency: cholemic nephrosis revisited.
The spectrum of jaundice-related nephropathy can range from limited proximal tubulopathy to renal failure. The latter condition was known as cholemic nephrosis in the early literature on this subject. Elevated plasma concentrations of bile salts and bilirubin conjugated or not, putatively mediate the nephrotoxicity. ⋯ Both bilirubin and bile salts are potential nephrotoxins in animal models, but their precise role in the pathogenesis of jaundice-related nephropathy is not known. Patients with bilirubin plasma concentrations >20 mg/dL, a low serum albumin concentration or endo-toxemia, could be more prone to develop renal failure due to jaundice-related tubulopathy. In conclusion, jaundice-related nephropathy is essentially a tubulopathy, but the exact nature of the Pathogenesis is still uncertain.
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Journal of nephrology · Mar 2006
ReviewMetabolic acidosis: pathophysiology, diagnosis and management.
Derangements in the intermediate metabolism of nutrients can lead to organic acid acidoses, which in turn can have severe clinical consequences that include even the patient's death. Lactic acidosis and ketoacidosis represent the most relevant clinical forms of this type of metabolic acidosis. Assessment and proper management of the organic acid acidoses require the intervention of a skillful clinician that balances the potential benefits and risks of the prescribed measures to the specific needs of the individual patient. To this aim, knowledge of the pathophysiology, diagnosis, and therapy of the various forms of acidoses including alkali administration, represent essential requirements.
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Journal of nephrology · Sep 2005
Serum cystatin C and urinary enzymes as screening markers of renal dysfunction in diabetic patients.
In clinical practice, the assessment and follow-up of early renal dysfunction is important in diabetic nephropathy. Therefore, this study was designed to determine whether the serum cystatin C (Cys C) and activities of some tubular enzymes could be used as screening markers for renal dysfunction in diabetic patients. ⋯ This study demonstrated that measuring serum Cys C levels and urinary NAG, ALP and LDH activities could be useful as screening markers to follow-up glomerular and tubular dysfunction in diabetic patients.
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Journal of nephrology · May 2005
Randomized Controlled Trial Clinical TrialSodium bicarbonate versus THAM in ICU patients with mild metabolic acidosis.
Sodium bicarbonate is despite its side effects, considered the standard alkali therapy in metabolic acidosis. THAM is an alternative alkalizing agent; however, there are limited data on the use of THAM in metabolic acidosis. The aim of this study was to compare the efficacy and adverse effects of a single dose of sodium bicarbonate and THAM in intensive care unit (ICU) patients with mild metabolic acidosis. ⋯ Sodium bicarbonate and THAM had a similar alkalinizing effect in patients with mild metabolic acidosis; however, the effect of sodium bicarbonate was longer lasting. Sodium bicarbonate did decrease serum potassium, and THAM did not; THAM is therefore not recommended in patient with hyperkalemia. As sodium bicarbonate leads to an increase of serum sodium and THAM to a decrease, THAM may be the alkalinizing agent of choice in patients with hypernatremia. Similarly, because sodium bicarbonate increases PaCO2 and THAM may even decrease PaCO2, sodium bicarbonate is contraindicated and THAM preferred in patients with mixed acidosis with high PaCO2 levels.