Individual nephron function in experimental bilateral pyelonephritis. II. Distal tubular sodium and water reabsorption and the concentrating defect.

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Abstract The renal concentrating defect in rats with nonobstructive bilateral pyelonephritis was studied by combined clearance and micropuncture methods. Control groups consisted of normal rats and those in which approximately 65 to 70 per cent of renal mass had been ablated by bilateral subtotal nephrectomy. The residual functioning renal mass and solute load per nephron were estimated to be of about the same order of magnitude in the pyelonephritic and partially nephrectomized animals. It was found, however, that both U max and t c h 2 o were diminished to a greater extent in the rats with intrinsic renal disease. Measurements of osmolality, sodium, and inulin concentrations in the distal tubular fluid of surviving cortical nephrons failed to reveal any specific defect in sodium transport by the thick ascending limb of Henle's loop, or any change in the permeability characteristics which could account for the severity of the concentrating defect in the pyelonephritic animals. The data suggest, rather, that at comparable rates of total solute excretion in the urine, individual surviving loops of Henle in the pyelonephritic rats were actually transporting more sodium into the medullary interstitium than were the loops in the normal controls. The concentrating defect in the pyelonephritic animals thus could not be accounted for by the reduction in renal mass, by the adaptational increases in glomerular filtration rate per surviving nephron, or by any detectable defect in salt or water transfer in individual cortical nephrons. The observations localize the disturbance to the renal medulla. It is suggested that disruption of the architecture of the renal medulla may be an important factor contributing to the concentrating defect.