A decrease in the ability of the kidneys to excrete a highly concentrated urine is one of the earliest hallmarks of potassium depletion in animals and in humans (1). According to present views of the mechanism of the renal concentrating process (2), this might be the result of a) impairment of the countercurrent multiplier system by which a high concentration of sodium (and urea) is created and maintained in the interstitial space of the renal papilla, and/or b) decreased permeability of the walls of the collecting ducts and distal tubules to the back-diffusion of water. If the first alternative were correct, analysis of the renal papilla from potassium-deficient animals excreting a maximally concentrated urine should reveal a lower concentration of sodium than that present in the papilla of normal animals. Should the second mechanism be operative, the fall in maximum urinary osmolality observed in potassium deficiency might be entirely unassociated with a decrease in papillary sodium, or else would be out of proportion to it.In the present experiments samples of maximally concentrated urine and renal papilla, medulla and cortex from potassium-depleted rats and dogs were analyzed. By placing all animals on a sodium-free diet prior to sacrifice, difficulties in the interpretation of tissue analyses consequent to high concentrations of sodium in the urine were avoided. The results indicate that the * Aided by grants from the American Heart Association, the National Heart Institute, the Lawrence M. Gelb Foundation, and a contract (MD-116) with the Office of the Surgeon General, Department of the Army. concentration of sodium and total solutes in the renal papilla is indeed decreased by potassium depletion, though the decrease is not as great as the fall in maximum urinary osmolality. METHODS I. RatsWhite male Sprague-Dawley rats initially weighing 150 to 200 g were divided into the following groups. The composition of the diets is given in Table I.Group IE. Twenty-four animals were fed a low potassium diet for 29 days, followed by 5 days of a low sodium, low potassium diet before sacrifice.Group IC. Twenty-two rats received a normal diet for 23 days, followed by 5 days of a low sodium diet.Group IIE. Twenty-eight rats received a high sodium, low potassium diet for 6 days. Desoxycorticosterone acetate (DCA), 0.2 mg per rat, was injected subcutaneously daily for 5 days. Following this, a low sodium, low potassium diet was given for 9 days.Group IIC. Twenty-four animals received a high sodium diet for 6 days and a low sodium diet for 5 days.In order to obtain enough papillary tissue for accurate analysis, 3 or 4 animals were kept in a cage and analyses of urine, plasma and tissue were performed on pooled material.Twenty-four hours before sacrifice food and water were withheld. Twelve hours later 50 mU of vasopressin in oil was injected subcutaneously and micturition was induced. The rats were then placed in metabolism cages with screens so placed as to deflect feces, and urine was collected under oil for 12 hours. Alt...

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A decrease in the ability of the kidneys to concentrate the urine is characteristic of many varieties of experimental and clinical hypercalcemia, hypercalciuria and nephrocalcinosis (1). Vitamin D intoxication in rats (2) and large doses of parathyroid extract in dogs (3, 4), in addition to producing hyposthenuria, have been shown to cause morphological changes which are most marked in the epithelial cells lining the collecting ducts but are also present in the distal convoluted tubules and the loops of Henle. Such lesions might impair renal concentrating capacity by interfering with the accumulation and concentration of sodium in the interstitial fluids of the medulla and papilla, or by impairing the back-diffusion of water from the lumen of the collecting duct into a hypertonic interstitium (5).In the present studies the composition of renal cortex, medulla and papilla was compared with that of plasma and urine in hydropenic rats in which hypercalcemia had been induced by large doses of vitamin D. The results indicate that the hyposthenuria observed in such animals results at least in part from a diminished concentration of sodium in renal medulla and papilla. MATERIALS AND METHODSWhite male Sprague-Dawley rats weighing 150 to 200 g were fed a synthetic diet containing liberal amounts of sodium and potassium (6).

Pediatric condition falsification may masquerade as chronic and serious digestive disease, including chronic intestinal pseudo-obstruction. The purpose of this study was to define clinical criteria to discriminate between these two conditions. We compared medical records of 8 pediatric condition falsification victims to those of 14 children with chronic intestinal pseudo-obstruction. Clinical features suggesting pediatric condition falsification in toddlers presenting with chronic and severe digestive complaints included (a) daily abdominal pain, (b) illness involving three or more organ systems, (c) an accelerating disease trajectory, (d) a reported history of preterm birth, (e) absence of dilated bowel on x-ray, (f) normal antroduodenal manometry, and (g) no urinary neuromuscular disease. These results suggest that a diagnosis of pediatric condition falsification may be suspected in toddlers presenting with a phenotype for enteric neuromuscular disorders by features in the clinical history, symptoms, and signs.