Since day to day sodium and water intake is more or less constant, the output by urinary sodium excretion is the key to maintain extracellular fluid volume within physiologic ranges. To achieve this goal, the kidneys ensure that most of the large quantities of filtered sodium are reabsorbed, a function that takes place in the proximal tubule, the loop of Henle and the distal tubule, and then the kidneys adjust the small amount of sodium that is excreted in urine in such a way that sodium balance is maintained. This adjustment occurs in the collecting duct. Three groups of diuretic-sensitive sodium transport mechanisms have been identified in the apical membranes of the distal nephron based on their different sensitivities to diuretics and requirements for chloride and potassium: 1) the sulfamoylbenzoic (or bumetanide)-sensitive Na+:K+:2CI- and Na+:CI- symporters in the thick ascending loop of Henle; 2) the benzothiadiazine (or thiazide)-sensitive Na+:CI- cotransporter in the distal tubule; and 3) the amiloride-sensitive Na+ channel in the collecting tubule. The inhibition of any one of these proteins by diuretics results in increased sodium urinary excretion. Recently, the use of molecular biology techniques, specially the functional expression cloning in Xenopus laevis oocytes, has led to the identification of cDNA's encoding members of the three groups of diuretic-sensitive transport proteins. The present paper reviews the primary structure and some aspects of the relationship between structure and function of these transporters as well as the new protein families emerging from these sequences. It also discusses the future implications of these discoveries on the physiology and pathophysiology of kidney disease and sodium retaining states.

Amino Acid Sequence↗

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Ultrasonographic images of spontaneous intramural hematomas of the intestinal wall in two patients with congenital bleeding tendency.

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Appendicitis↗

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Low serum albumin and the increased risk of amikacin nephrotoxicity.

AIM: The purpose of the present study was to know the incidence and risk factors associated with amikacin nephrotoxicity in a cohort of patients form a general medial center. STUDY DESIGN: Prospective follow-up of a cohort of 104 patients treated with intravenous amikacin for at least 36 hours. We assessed serum creatinine every other day and amikacin plasma levels at 48 and 96 hours after treatment was begun. Patients with other risk factors to develop acute renal failure were excluded. The study was conducted at the Hospital de Especialidades, Centro Médico de Occidente, Instituto Mexicano del Seguro Social. RESULTS: Ten patients developed nephrotoxicity (9.6%). According to the logistic regression model, the most powerful predictor of high nephrotoxicity probability was the serum albumin concentration. The lower the serum albumin concentration, the higher the risk of toxicity. The mean serum albumin in the group of patients with nephrotoxicity was 2.6 +/- 0.55 g/dL, while in the group of patients without toxicity it was 3.5 +/- 0.55 g/dL. No differences were observed in the age, sex, diagnosis, renal function and amikacin doses between both groups. Furthermore, low serum albumin concentration was also associated with amikacin accumulation in plasma. The group of patients with hypoalbuminemia (< or = 3.0 g/dL) had a significantly higher trough amikacin plasma level (assessed at 48 and 96 hours of the initiation of treatment) than those with normal serum albumin, with no differences among the age, sex, baseline renal function and received amikacin doses. CONCLUSIONS: We conclude that serum albumin concentration is the most powerful predictor of amikacin nephrotoxicity. The risk factors observed in the present study are similar to those previously observed by us at the Instituto Nacional de la Nutrición Salvador Zubirán.

Adult↗

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