The effect of calcium chloride infusion on the renal handling of magnesium was evaluated in thyroparathyroidectomized dogs during normal and acute reduction in glomerular filtration rate. The results show that calcium infusion increased urinary magnesium even when the filtered load of magnesium was markedly reduced. The augmented magnesium excretion was associated with an absolute increase in calcium reabsorption. These observations indicate that calcium infusion reduces the tubular reabsorption of magnesium and is consistent with the concept that these two ions share and compete for a common reabsorptive pathway in the nephron. Sodium excretion also increased during chloride infusion but a comparison of the clearances of magnesium (C_Mg), sodium (C_Na) and calcium (C_Ca) indicates that C_Mg was more closely related to C_Ca than C_Na when calcium chloride was infused alone. With the addition of saline infusion, C_Mg became more dependent on C_Na

A case of isolated hypoaldosteronism associated with chronic renal failure is reported. Potassium retention and hyperkalemia, sodium wasting, and inability to acidify the urine were all corrected by mineralocorticoid administration. Aldosterone secretion was 86.0 µg/day on a high sodium intake, 30.1 µg/day on a low sodium intake, and 36.2 µg/day after an angiotensin infusion. An important physiologic role is postulated for the hypersecretion of aldosterone usually seen in patients with chronic renal failure.

A technique has been developed for the quantitative estimation of perfusible glomeruli in the normal and diseased kidney. This technique is a modification of that originally described by Cook and Pickering (5). It entails the perfusion of the intact or excised kidney under standardized conditions with magnetic oxide of iron, which specifically localizes in the glomerular capillaries. The kidney is then emulsified and ground through a 100-mesh copper wire sieve and passed through an electromagnetic field. The magnetized glomeruli adhere to the glass under the influence of the magnetic field, the rest of the suspension passing through. The suspension is run through the electromagnetic field four or five times with the recovery of at least 90% of the glomeruli. The glomeruli are suspended in 30% aqueous solution of PVP and counted under microscopic vision on a scored glass microscope slide. The perfusible glomeruli and creatinine clearance of rats, ages 1 to 18 months and rabbits, ages 1 week to six months, have been determined and indicate that in the rat there is no increase in glomerular counts with maturation (mean 3.78 × 10⁴); GFR per glomerulus reaches the adult level by four weeks. In the rabbit the number of perfusible glomeruli increased from 5.5 × 10⁴ at one week to the adult level of 19.3 × 10⁴ at 1 month. There is a progressive increase in GFR per glomerulus from one week through six months, thus indicating the pattern of structural and functional maturation of the glomerulus in rat and rabbit. The collagen and non-collagen nitrogen in these animals was also studied. The techniques appear applicable to the study of the diseased kidney.

The sodium-conserving ability of 46 patients with renal disease of varying etiology was observed during rigid sodium restriction and mineralocorticoid administration. Glomerular filtration rate (inulin clearance) was used to estimate the number of residual nephrons. The patients were divided into two groups: (1) predominantly glomerular disease (glomerulonephritis, amyloidosis, diabetic nephropathy, lupus nephritis), (2) predominantly tubular disease (pyelonephritis, gouty nephropathy, polycystic disease, renal tubular acidosis, nephrocalcinosis, multiple myeloma). With few exceptions, patients with glomerular lesions showed sodium wasting only when the glomerular filtration rate was severely reduced (less than one-fifth normal). On the other hand, a higher proportion of the patients with tubular lesions showed sodium wasting with minimal to moderate reductions in glomerular filtration rate. Thus, the sodium-wasting abnormality in the first group appeared to be related principally to the increased osmotic load per residual nephron, whereas an additional tubular defect in the reabsorption of sodium may have played a significant role in certain patients within the second group.

The effect of calcium infusion on serum levels of calcium and phosphorus and on the fractional excretion of phosphorus (Cp/C_cr) was studied in eight normal subjects and in 35 patients with varying degrees of renal failure. The increment in serum calcium in patients with advanced renal failure and radiographic evidence of osteitis fibrosa was significantly less than that observed in patients with a comparable renal function but without evidence for such bone disease. The increase in serum phosphorus usually observed after calcium infusion in normal subjects was also seen in patients with chronic renal disease but was less marked as renal failure worsened. In patients with advanced renal failure and osteitis fibrosa serum phosphorus fell after calcium infusion. The fall in Cp/C_cr following calcium infusion in patients with mild renal failure was similar to that observed in normal subjects (50 to 90%), but was diminished in patients with advanced renal failure; in the latter group the maximal decrements in Cp/C_cr were less than 25% in most patients irrespective of the presence or absence of osteitis fibrosa and overt secondary hyperparathyroidism. The results indicate that in patients with advanced renal failure: (1) the usefulness of changes in Cp/C_cr following calcium infusion as a diagnostic or prognostic guide is questionable ; and (2) the difference in the changes in serum calcium and phosphorus after calcium infusion may prove to be helpful in differentiating between uremic patients with and without marked osteitis fibrosa.