Richard E. Rieselbach

Hypertrophy of the Normal Human Kidney Following Contralateral Nephrectomy

Intravenous pyelograms were performed on 22 kidney donors, both before and from 2 weeks to 4 years after nephrectomy. A significant increase in kidney size was demonstrated by four different measureme

Intrinsic Renal Disease Leading to Abnormal Urate Excretion

Since approximately two thirds of daily urate production is normally excreted by the kidney, intrinsic renal disease resulting in abnormalities of urate excretion may have a profound effect upon urate homeostasis. Alterations in the pattern of urate excretion encountered in chronic renal failure are reviewed in depth, with a description of adaptive mechanisms for urate excretion which develop in residual nephrons, as exemplified by the remaining normal kidney of transplant donors. In addition, abnormalities in urate excretion in the presence of a normal complement of nephrons are described. Diminished urate excretion per nephron appears to be responsible for hyperuricemia in some patients with gout, while a variety of tubular defects resulting in excessive renal urate excretion have been documented as the basis for some cases of hypouricemia.

Comparison of urinary phosphate, urate and magnesium excretion following parathyroid hormone administration to normal man

Abstract A phosphaturic dose of parathyroid hormone (PTH) administered intravenously to 14 normal volunteers significantly decreased magnesium excretion and did not significantly alter urate excretion. Elevated plasma levels of endogenous PTH appear to mediate the increased excretion of phosphate per nephron observed in progressive chronic renal disease. In this setting, a similar pattern of urate and magnesium excretion is seen. Results of this study fail to support the concept that PTH might play a role in the enhanced urate and magnesium excretion per nephron of subjects with chronic renal failure.

Renal Handling of Uric Acid

The pathogenesis of gout has intrigued physicians for centuries. A pathogenetic role for the kidney was first suggested by Garrod more than 125 years ago (1). During the ensuing century, many studies were performed attempting to measure urate excretion in patients with gout. However, the role of the normal kidney in maintaining urate homeostasis was not clearly defined. The first comprehensive study designed to investigate the mechanism of urate handling by the normal kidney, employing contemporary principles of renal physiology, was carried out by Berliner and colleagues in 1950 (2). They concluded that “the difference between the clearance of urate and the clearance of inulin must be due to either non-filterability of a large fraction of the plasma urate, to tubular reabsorption of a major fraction of the filtered urate, or to some combination of these two”. It is remarkable that in the same year, Praetorius and Kirk described a patient with marked hypouricemia, who had a urate to inulin clearance ratio of 1.46 (3). These authors concluded that urate was either secreted or synthesized in the kidney.

Renal Urate Excretion in Normal Man

The development of our knowledge of the intrarenal process involved in the control of urate excretion in normal man is summarized. Although there are many gaps in our current knowledge, and different interpretations may be given to the available data, current evidence seems to favor the existence of extensive tubular reabsorption of urate following its glomerular filtration. Subsequently, tubular secretion of urate and the reabsorption of an unknown amount of the secreted urate probably take place. For reasons discussed, it seems most likely that the regulation and control of urate excretion are accomplished through modulations in tubular secretion, post-secretory reabsorption, or both.

The Effect of Glucose upon Reabsorptive Transport of Urate by the Kidney

The mechanism of the increase in urinary excretion of urate following hyperglycemia has been variously interpreted by different workers (1,2,3,4,5). Hyperglycemia and/or its consequences, in all probability inhibit the tubular reabsorption of urate. This inhibitory effect may be the result of: 1) the elevation of blood sugar per se, 2) an increase in filtered load of glucose with an associated acceleration of reabsorptive transport in that segment of the proximal tubule where glucose is primarily reabsorbed, or 3) the presence of glucose in tubular fluid in a distal segment of the proximal tubule in a concentration substantially greater than that usually present.

The Feasibility of Consortia for Internal Medicine Graduate Medical Education: Perspectives from a Survey of Residency Directors.

PURPOSE: To assess the perspectives of internal medicine (IM) residency directors on issues that might determine the feasibility of consortia for IM graduate medical education (GME). METHOD: A self-administered questionnaire was mailed to all 413 U.S. IM program directors in June 1994. Of the 413 IM programs, 215 were located in community hospitals; 123 in university hospitals; and 75 in municipal, Veterans Administration, or military hospitals, or hospitals associated with multispecialty clinics (“other”). The questionnaire elicited responses concerning (1) perspectives on the quality of academic affiliations, (2) experience with formal institutional collaboration on GME issues and projection of consortium success, and (3) possible barriers to the success of consortia. Data were analyzed by comparing responses from the three program categories. RESULTS: In all, 330 (80%) program directors responded. Two-thirds reported ongoing academic affiliations. A larger percentage of university program directors considered these ties to be strong and advantageous than did their colleagues in community or other hospitals, who also considered their affiliations to be less equitable and less mutually trusting. Only 31% of community and university programs and 40% of other programs reported any prior experience with institutional collaboration on GME issues. A high percentage of those respondents considered these collaborative experiences to be successful and were optimistic about the projected success of consortia. Of seven possible barriers to consortium success, competition, governance, bureaucracy, and mistrust were most often perceived as major barriers. CONCLUSION: The data appear to indicate some optimism for the prospects of GME consortia, thereby supporting their feasibility for IM GME. Although many respondents perceived barriers to success, such perceptions were less common among program directors who had had direct experience with previous collaborative efforts. Nevertheless, these barriers may require attention if consortia are to succeed in achieving their many possible advantages.

The Effect of Furosemide on Residual Nephrons of the Chronically Diseased Kidney in Man

Clearance studies were performed in 50 patients with varying degrees of stable chronic renal disease and 13 normal subjects in order to determine the effect of intravenous furosemide on residual nephr

Renin Output by Diseased and Contralateral Normal Dog Kidneys Following Extracellular Fluid Volume Expansion and Furosemide

In order to assess the ability of the diseased kidney (DK) to modulate renin output in response to extracellular fluid (ECF) volume expansion and intravenous furosemide administration, we studied eigh