Observations on the Concentrating and Diluting Mechanisms of the Diseased Kidney*

Abstract

The concentrating and diluting mechanisms of the normal kidney contribute in an impressive manner to the defense of water economy. In health, a given amount of solute may be excreted in a widely varying volume of water which is determined under most circumstances by the water needs of the organism. This ability to regulate the osmolality of the urine accounts for a range of urine concentrations which extends from marked hypotonicity to marked hypertonicity.1 In the course of advancing renal disease, the total amount of solute excretion per 24 hours may remain comparable to values achieved in health. It is a clinical observation of long standing, however, that the patient's ability to vary the volume of water in which this solute is contained becomes progressively limited. Hence, the range over which urine tonicity may be extended becomes more and more restricted. Typically, this restriction is manifested initially by a decrease in the maximum attainable urine osmolality, followed somewhat later by a progressive inability to decrease the tonicity of the urine. Ultimately, urine tonicity deviates little in either direction from the concurrent plasma osmolality, and the stage of so-called "permanent isosthenuria" or "fixed specific gravity" supervenes.The intrarenal mechanisms responsible for the impaired ability to concentrate and dilute the urine in chronic renal disease have never been adequately explained.

The Influence of Glomerular Filtration Rate, Solute Excretion and Hydration on the Concentrating Mechanism of the Experimentally Diseased Kidney in the Dog *

“…The foregoing sequence of events should re- The present observations, in concert with studies previously reported (1) provide evidence that the concentrating ability of the experimentally diseased kidney in the dog is not markedly impaired when the contralateral kidney is intact and the internal environment remains essentially normal. Comparison of the concentrating ability of the diseased kidney with that of the normal kidney, however, did reveal certain differences.…”

“…Each of the latter drained urine from one kidney and permitted the simultanous study of the separate kidneys. The details of this preparation have been previously described (1,4). When bilateral disease was produced, the urethra was ligated and divided and a permanent polyethylene cystotomy tube, similar to those used in the hemibladders, was employed.…”

“…Recent studies from this laboratory indicate that the concentrating ability of the diseased kidney in the dog is not markedly impaired when the contralateral kidney is intact and the internal environment remains essentially normal ( 1 ). These data suggested that the direct effects of the pathological processes on the structural integrity of the functioning nephrons did not render the concentrating mechanism impotent.…”

“…Further details of the experimental procedures employed have been described (1,4). Creatinine was determined according to the method of Bonsnes and Taussky (5); para-aminohippurate (PAH) was determined according to the method of Smith and associates (6) ; osmolalities were measured using a Fiske osmometer; sodium and potassium were analyzed with an internally compensated Baird flame photometer, and urea was determined manometrically according to the method of Van Slyke and Kugel (7).…”

A Case for Water in the Treatment of Polycystic Kidney Disease

“…As CKD progresses, the compensatory process accelerates the flow of filtered solutes within surviving nephron units to the point that tubule solute reabsorptive transport mechanisms are eventually exceeded. When this point is reached, the osmolality of the final urine is clamped close to that of the plasma because of the osmotic effect of the increased solute excretion per nephron (isosthenuria) (41,42).…”