SUMMARY1. Daily changes in water and electrolyte balance during pregnancy were investigated in rats housed in metabolism cages.2. Fluid intake was significantly elevated above control values from day 13 of pregnancy, with urine output failing to be raised to the same extent. This would result in an extensive fluid retention if extrarenal fluid losses were not substantially altered.3. Electrolyte intake increased from as early as the third day after mating with an accompanying increase in renal ionic excretion. A net retention of Na, Cl and K did not occur until the final week of pregnancy when the urinary output of these ions was reduced.4. In a parallel study, changes in plasma volume and composition throughout pregnancy were investigated. 5. A significant increase in plasma volume occurred from day 6 of pregnancy at a time well before fluid intake or urine output were altered. This indicates either an altered extrarenal output or. a shift of fluid between body fluid compartments.6. Maternal plasma sodium and total osmolality were reduced during the last week of pregnancy despite the salt retention, suggesting an increased fetal usage.7. Such findings are related to the known renal and endocrine changes of rat pregnancy.

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SUMMARY1. In rats receiving 200 gl. min-sodium chloride, glomerular filtration rate, single nephron glomerular filtration rate, and fractional reabsorption were measured at various points along the nephron, and ionic concentrations measured in early distal tubular fluid in virgin and 6, 12 and 19 day pregnant rats.2. Glomerular filtration increased progressively until the twelfth day ofpregnancy. At 19 days of pregnancy the glomerular filtration rate, while still above virgin levels, was reduced below 12 day pregnant levels.3. Single nephron glomerular filtration rates measured in proximal and distal tubules were different at both 12 and 19 days of pregnancy, indicating an alteration of tubuloglomerular feed-back. 4. A change in the ratio ofglomerular filtration rate: distal single nephron filtration rate indicated a redistribution of glomerular filtrate to juxtamedullary nephrons by the sixth day of pregnancy.5. Fluid reabsorption is similar up to the early distal tubule but it is not possible to say whether reabsorption is the same in proximal tubules. More fluid is reabsorbed by late distal tubules and collecting ducts in 12 and 19 day pregnant animals than in the virgin and 6 day pregnant animals.6. Changes in ion reabsorption by the loop of Henle occurred during pregnancy; sodium reabsorption was increased by the sixth day of pregnancy and potassium reabsorption by the twelfth day.

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Abstract. Metabolic and renal clearance techniques were used to examine kidney function in conscious and anesthetised streptozotocin diabetic rats. All diabetics showed an enhanced calcium and magnesium excretion compared to controls. However, the renal handling of these ions in relation to other electrolytes varied with different experiments. In non-infused conscious rats, the excretion of all ions was higher in diabetics, but the increased output of Ca2+ and Mg2+ was far greater than that of other electrolytes. In infused anesthetised diabetics only the outputs of Ca2+ and Mg2+ were significantly raised. This resulted from a significant reduction in the tubular reabsorption of both ions (% Ca2+ reabsorption: Controls 97.0±0.5; Diabetics 86.1±2.1; p<0.001). Insulin treatment reversed these changes. Major differences therefore exist in the renal handling of Ca2+ and Mg2+ in control and diabetic kidneys. Such differences do not simply parallel changes in the handling of other ions, and thus represent specific Ca2+ and Mg2+ lesions. Anesthetised infused diabetic rats also showed a reduced glomerular filtration rate and urine output compared to controls. Such differences may relate to an altered fluid balance in the two groups, different responses to surgery and anesthesia, or the degree of hyperglycemia in diabetic animals.

Pregnant rats became significantly heavier than non-pregnant controls 2 days after conception. Just prior to term, they exhibited a gross 52% increase over their non-pregnant body weight. Dry kidney weight had increased by 13% in 7-day-pregnant animals, which also showed a 20% increase in proximal renal tubule lengths. At term, the former was not maintained as compared with controls; whereas the latter is maintained throughout pregnancy, and may, at least partially, account for the enhanced renal reabsorption of salt and water found in these animals.

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1 Standard renal clearance techniques were used to assess the dose-response relationship between acute gentamicin infusion and the magnitude of hypercalciuria and hypermagnesiuria in the anaesthetized Sprague-Dawley rat. Also investigated were whether these e ects occurred independently of renal tubular cell injury. 2 Acute gentamicin infusion was associated with a signi®cant hypercalciuria and hypermagnesiuria evident within 30 min of drug infusion. The magnitude of these responses was related to the dose of drug infused (0.14 ± 1.12 mg kg 71 min 71 ). Increased urinary electrolyte losses resulted from a decreased tubular reabsorption of calcium and magnesium. 3 A rapid dose-related increase in urinary N-acetyl-b-D-glucosaminidase (NAG) excretion was also observed in response to gentamicin infusion. However, there was no evidence of renal tubular cell injury and no myeloid bodies were observed within the lysosomes of the proximal tubular cells. Gentamicin may thus interfere with the mechanisms for cellular uptake and intracellular processing of NAG causing increased NAG release into the tubular lumen. 4 The absence of changes in renal cellular morphology indicates that the excessive renal losses of calcium and magnesium were an e ect of gentamicin per se and not the result of underlying renal tubular injury. The renal e ects described in this paper were apparent after administration of relatively low total drug doses, and with plasma concentrations calculated to be within the clinical range. These ®ndings suggest that disturbances of plasma electrolyte homeostasis could occur in the absence of overt renal injury in patients receiving aminoglycoside antibiotics.