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Journal of Clinical Investigation Vol. 45, No. 1, 1966
Patterns of Nephron Perfusion in^ Acute^ and^ Chronic
Hydronephrosis *
WADI SUKI, GARABED EKNOYAN,^ FLOYD^ C.^ RECTOR,^ JR.,^ AND^ DONALD^ WV. SELDIN^ t
(From the^ Department^ of^ Internal^ Medicine,^ The^ University^ of^ Texas^ Southwestern^ Medical School, Dallas, Texas)
Partial urinary tract obstruction is^ known^ to produce, in addition to a nonspecific depression in renal function, certain characteristic derangements, especially profound polyuria (1-5); release of^ the obstruction may result in a transient salt-wasting state (6,^ 7).^ Three^ hypotheses^ may^ be^ advanced to explain the^ altered^ function^ of^ the^ hydro- nephrotic kidney.^ It^ is^ possible^ that^ with^ the^ ele- vation of^ intrapelvic^ pressure^ a^ significant^ frac-
tion of the nephron^ mass^ stops^ functioning, due
either to^ mechanical^ damage^ or^ cessation^ of^ filtra- tion, whereas^ the^ remaining^ nephrons^ continue^ to function with decreased^ tubular^ flow.^ This^ de- creased rate of tubular flow^ could^ be^ due^ to^ re- duced filtration per nephron^ or^ increased^ proximal fractional reabsorption, or^ both.^ This^ hypothesis would imply a reduced delivery^ of^ filtrate^ to^ the loop of Henle and the distal convoluted^ tubule^ and
would, therefore, result in a pattern of^ nephron
underperfusion (8). An alternative possibility^ is that the initially elevated intrapelvic pressure^ re- sults in a reduction in nephron mass; the subse- quent return of intrapelvic pressure towards nor-
mal might produce a compensatory increase in^ the
rate of tubular flow in the residual nephrons^ (9). The increased rate of tubular flow could result from increased filtration per nephron or^ diminished
proximal fractional reabsorption, or both. The
increased tubular flow per nephron increases the
- (^) Submitted for publication August 19, 1965; accepted October 13, 1965. Supported in^ part^ by^ grants^ I-SOI-FR^5426 and^ 5TI HE-5469 from the National Institutes^ of^ Health,^ U.^ S. Public Health Service. Presented in part at the National Meeting of^ the American Society for Clinical Investigation on^ May 2, 1965; a preliminary report appeared in^ J.^ clin.^ Invest. 1965, 44, 1103. t Address^ requests^ for^ reprints^ to^ Dr.^ Donald^ W. Seldin, Dept. of^ Internal^ Medicine,^ The^ University^ of Texas Southwestern Medical School, Dallas, Texas
delivery of filtrate to the distal nephron resulting in overperfusion of that portion. Finally, varying
degrees of^ nephron^ damage^ might^ be^ superimposed
on either of^ the two^ patterns^ of^ nephron^ perfusion.
No studies are^ available^ to^ determine^ which^ of
these theoretical considerations^ best^ fits^ the^ ob-
served disorders of^ renal function.
This study^ was^ undertaken,^ therefore,^ to^ clarify
the pattern of renal^ function^ in^ hydronephrosis.
The excretion of^ salt^ and^ water^ during^ water^ and
hypotonic saline^ diuresis^ was^ examined^ in^ dogs
with either acute^ or^ chronic^ unilateral^ hydrone-
phrosis; the^ contralateral^ kidney^ served^ as^ an^ in-
ternal control. The^ results^ from^ these^ two^ models
of hydronephrosis were^ compared^ to^ those^ from
an experimental model^ known^ to^ result^ in^ nephron
underperfusion, namely, renal^ arterial^ constriction
Methods The effects of acute and^ chronic^ hydronephrosis and of renal arterial constriction were^ studied^ in^14 female mongrel dogs weighing 8 to^15 kg and^ fed^ commercial diets. A total of 22 studies was^ performed during water diuresis followed by hypotonic saline^ diuresis. Water diuresis^ was^ induced^ by^ the^ administration^ of 50 ml^ of^ water^ per^ kg^ body^ wt^ via^ a^ gastric^ tube^ and maintained by the intravenous infusion^ of^ 2.5% solution of dextrose^ in^ distilled^ water^ at^ a^ rate^ of^10 ml^ per^ min- ute. When^ the^ water^ diuresis^ was^ well^ established,^ two or three^ urine^ and^ blood^ collections^ were^ made.^ Hy- potonic saline^ solution^ (0.45^ to^ 0.58%)^ was^ then^ started at a rate of 20 ml per minute, and^30 to^45 minutes^ later two or three more urine^ and^ blood^ collections^ were made. After the termination^ of^ the^ urine^ collections^ dur- ing hypotonic saline^ diuresis, the^ maximal^ tubular^ trans-
port rate for p-aminohippurate (TmPAH) was^ measured
in four experiments during^ acute^ hydronephrosis^ and
four experiments during chronic^ hydronephrosis^ by^ the
infusion of loading and^ maintenance^ doses^ of^ PAH^ suffi- cient to produce a plasma level^ of^11 to^30 mg per 100 ml. This insured a^ load^ to^ Tm^ ratio^ of^ at^ least^2 to^ 3,^ even in the presence of marked^ reductions^ in^ renal^ blood^ flow (10). 122
RENAL FUNCTION IN ACUTE AND CHRONIC HYDRONEPHROSIS
Acute hydronephrosis was induced in seven dogs by the elevation to variable levels (60 to 80 cm H20) of a poly- ethylene tube inserted in the left ureter. The animals were first (^) anesthetized with 30 mg per kg pentobarbital int-venously, and then through a midline abdominal in- cisiun each ureter was cannulated with a polyethylene tube reaching into the renal pelvis. The renal artery was constricted in four anesthetized animals. Through a left flank incision, a silk tie was placed around the left renal artery, which was constricted sufficiently to reduce blood pressure distal to the con- striction by 50%. The blood pressure was monitored by a small needle in the renal artery distal to the point of constriction, connected to a Statham strain gauge and a Sanborn recorder. Both ureters were cannulated with polyethylene tubing. In six dogs a bladder-splitting operation was first per- formed to permit the collection of urine from each kidney separately (11). Nine to 12 days later a control study was performed to ascertain whether glomerular filtration rate (GFR), sodium excretion, and free water clearance (CH20) were equal on the two sides. Through a para- median abdominal incision the left ureter was then ex- posed and a silk tie placed around it, partially occluding it in^ the region of the ureteropelvic junction. In one dog the induction of chronic hydronephrosis was preceded by the cannulation of the left ureter and a study of acute hydronephrosis. These chronically hydronephrotic ani- mals were (^) then studied 7 to 124 days after the constric- tion of the ureter. The (^) GFR was measured by the (^) clearance of inulin. Inulin, (^) PAH, sodium, potassium, and urinary solute concentrations were^ measured by previously published methods (8). The data were analyzed by a (^) nonparametric median test (12).
Results Figure 1, constructed from^ our previously pub-
lished data (8), depicts the effects of acute renal
arterial -constriction. During water diuresis GFR,
urinary flow, and urinary sodium concentration
(UNa) were always lower, and total solute concen-
tration (Uosm) always higher, on the constricted
than on the control side. During hypotonic saline
diuresis, two striking changes were seen: first, UNa
on the control side rose sharply, but little or no
change was noted on^ the constricted side; second,
UOsm on^ the constricted side, which was above the
control side during water diuresis, fell to a value
below that of (^) the control side. A typical experiment during acute hydronephro-
sis is shown in Figure 2. The results of this study
disclose a pattern similar to that of renal arterial
constriction. During water diuresis GFR, urinary
flow, and UNa were lower, whereas Uosm was
higher, on the hydronephrotic than on the control
0 FIG. 1. THE EFFECTS OF RENAL^ ARTERIAL^ CONSTRICTION ON WATER AND ELECTROLYTE EXCRETION DURING WATER AND HYPOTONIC SALINE DIURESIS. GFR =^ glomerular filtration rate.
side. During hypotonic saline diuresis UNa on
the normal side rose with little or no change on the
hydronephrotic side, and Uosm fell from a value
above that of the normal side during water diure-
sis to below the normal side during hypotonic
saline diuresis. A representative experiment on an animal with
chronic hydronephrosis is shown in Figure 3. In
contrast to acute hydronephrosis, UNa was mark-
edly higher on the hydronephrotic than the con-
trol side during both water and hypotonic saline
diuresis. The failure of the U..m on the hydro-
nephrotic side to fall from a value above that of the
control side during water diuresis to below the
control side during hypotonic saline diuresis also
is in^ marked^ contrast to^ the pattern seen^ in^ both
renal arterial constriction and acute hydro-
nephrosis.
The effects of all three experimental models on
the process of urinary dilution are shown in Fig-
ure 4 and the results expressed as the ratio of the
experimental to the control side. Renal^ arterial
123
RENAL FUNCTION IN ACUTE AND CHRONIC HYDRONEPHROSIS
(Figure 4, middle panel) and the fractional excre- tion of free water (^) [CHoG per 100 ml GFR (Figure
4, panel on the right)] were always lower on the
side with renal arterial constriction or acute hy- dronephrosis than on the control side. In chronic hydronephrosis, by contrast, although the absolute CH20 was^ lower^ on^ the^ experimental^ than^ on^ the
control side (Figure 4, middle panel), CHO per
100 ml GFR was greater on the hydronephrotic
than on the control side (Figure 4, panel on the right) in 8 of 10 studies during water diuresis (p < 0.01) and 7 of 10 studies during hypotonic
saline diuresis (p.< 0.05).
The effects of renal arterial constriction and acute and chronic hydronephrosis on urinary so- dium are shown in Figure 5. Urinary sodium concentration was always lower on the side with renal arterial constriction than on the control side
during both water and hypotonic saline diuresis.
In acute hydronephrosis a pattern similar to that of renal arterial constriction was^ seen^ in^ all^ ex-
periments. In contrast, in chronic hydronephrosis
the urinary sodium concentration was^ always greater on the hydronephrotic side than on^ the
control side^ (p^ <^ 0.05^ during^ water^ diuresis^ and
< 0.005 during hypotonic saline diuresis).
The absolute rate of sodium excretion (UNaV)
and the^ fractional^ rate^ of^ sodium^ excretion^ [^ (CNa/
inulin clearance) X^ 100] were^ always^ lower^ on^ the
side with renal^ arterial^ constriction^ than^ on^ the
control side^ (Figure 5). A^ similar^ effect^ on^ the
absolute and^ fractional^ rates^ of^ sodium^ excretion
was obtained in^ the^ experiments with^ acute^ hydro-
nephrosis. Chronic hydronephrosis, on^ the^ other
hand, resulted in^ higher absolute^ rates^ of^ sodium
excretion in^9 of 10 experiments during water^ diu-
resis (p < 0.01) and^6 of^10 experiments during
hypotonic saline^ diuresis^ (p <^ 0.005);^ the^ frac-
tional rate of sodium^ excretion^ was^ uniformly
greater on^ the^ side- with^ chronic^ hydronephrosis
than on the^ control side^ (p <^ 0.01^ during^ water
diuresis and <^ 0.005^ during hypotonic saline
diuresis).
The effect of acute and^ chronic^ hydronephrosis
on the relationship between nephron perfusion and
tubular mass was also examined.^ The^ GFR^ on
the experimental, as compared with^ the^ control,
side was reduced 24 to 42%o in^ renal^ arterial^ con-
WWATER RAC A H ==^ ACUTERENAL^ ARTERYHYDRONEPHROSIS^ CONSTRICTION (7 (^) EXPS)^ (4^ EXPS) HYPOTONIC SALINE C H = CHRONIC HYDRONEPHROSIS (II EXPS) RAC AH CH RAC^ AH^ CH^ RAC^ AH^ CH
10 8 6 4
2
uIll¶Y -t,
.8 F
(UNaV) EXP (UNOV) CONT
FIG. 5. THE EFFECTS OF RENAL ARTERIAL CONSTRICTION AND ACUTE AND CHRONIC HYDRONEPHROSIS ON URINARY SO- DIUM CONCENTRATION (UN), AND ABSOLUTE (UN.V) AND FRACTIONAL (CNx X^ 100/INULIN CLEARANCE) RATES^ OF^ SO- DIUM EXCRETION. The vertical bars represent the mean of the ratios of the^ experimental to^ the^ control^ side^ ±^ stand- ard error.
[UN,] EXP [UN,] CONT
125
.
.
.
SUKI, EKNOYAN, RECTOR, AND^ SELDIN
striction, 14 to 77% in acute hydronephrosis, and 5 to (^) 92%o in chronic hydronephrosis. The (^) TmPAHE on the experimental side was reduced below that of the control side in both acute and chronic hy- dronephrosis. The^ relative^ effects^ of^ acute^ hydro- nephrosis and^ of^ chronic^ hydronephrosis^ on^ the
GFR and TmPAH expressed as a ratio are^ shown
in Table I. It is apparent that^ in^ acute^ hydro-
nephrosis the ratio^ of^ the^ GFR^ to^ TmPAH was
consistently reduced on the hydronephrotic side as compared to the control side; the ratio on the experimental side was 9 to 37% lower than on the control side, indicating that there was a dispro-
portionate fall of GFR compared to TmPAH.
These findings in acute hydronephrosis are similar
to those of Thompson, Barrett, and Pitts in ani- mals where renal underperfusion was induced by the inflation of a balloon in the aorta (13). In chronic (^) hydronephrosis a different pattern was evi-
dent; the ratio of GFR to TmPAH was 18 to 76%o
higher on the hydronephrotic side than on the control side.
Discussion The terms^ nephron^ overperfusion^ and^ nephron underperfusion are^ usually^ taken^ to^ mean^ in- creased or^ decreased GFR per nephron. For^ pur- poses of the present study, however,^ where^ the
diluting capacity of the kidney is used as an index
of perfusion, it is more useful to redefine these
terms in a -more restrictive sense as the amount of fluid delivered to the diluting segment, without
specifying the mechanism that might be responsible
for alterations in delivery rate. This requires that a standard be available in terms of which de- livery rate to the diluting segment can be assessed; the contralateral control kidney serves this pur-
pose. Thus redefined, underperfusion and over-
perfusion mean, respectively, reduced or in-
creased tubular flow through individual distal
nephrons,2 as compared to the flow of the contra-
lateral control kidney. (^2) For purposes of this discussion the distal nephron is defined as that portion of the nephron that is imperme- able to water during maximal suppression of antidiuretic hormone (ADH). This presumably includes the as- cending limb of Henle's loop, the^ distal^ convoluted^ tu- bule, and the collecting duct.^ The^ proximal nephron in- cludes those segments proximal to^ the^ water-impermeable segment and consists of^ the^ proximal convoluted^ tubule, pars recta, and the^ descending limb^ of^ Henle's^ loop.
Constriction of the renal artery in the present experiments reduced the glomerular filtration rate by 24 to 42%. Although it has been demonstrated
that glomerulotubular balance is maintained under
such circumstances so that the percentage of fil- trate reabsorbed in the proximal tubule remains
constant (14-16), the absolute delivery of filtrate
to the distal nephron is sharply reduced. Con- striction of the renal artery, therefore, furnishes an excellent model to examine the pattern of uri-
nary formation during underperfusion of the distal
nephron.
Two consequences result from diminished de-
livery of filtrate to the distal nephron. First, so-
dium reabsorption is more complete and therefore
the formation of solute-free water per unit volume
of tubular fluid is enhanced. Second, back-diffu-
sion of^ free^ water^ in^ the^ collecting^ duct^ per^ unit
volume of^ tubular^ fluid^ is^ augmented,^ thereby^ in-
creasing free^ water^ loss.^ Which^ of^ these^ processes
will predominate during slowed^ flow^ depends^ prin-
cipally on^ whether^ sodium^ reabsorption^ in^ the^ di-
luting segment is^ already^ functioning^ near^ its
limiting concentration^ gradient.^ During^ water
diuresis the^ concentration^ gradient^ of^ sodium
across the distal nephron is near a^ maximal^ value.
Slowed flow^ will^ augment sodium^ reabsorption
slightly; this^ will^ increase^ free^ water^ formation
per unit volume^ only minimally,^ but^ will^ markedly
lower UNa. The^ absolute^ volume^ of^ free^ water
formed is diminished^ due^ to^ the^ reduction^ of^ the
volume of^ fluid^ delivered^ to^ the^ diluting^ segment.
An additional effect^ of^ slowed^ flow^ during^ water
diuresis will^ be^ seen^ in^ the^ collecting duct^ where
the loss of^ the^ same, or^ even^ reduced, absolute
amounts of^ free^ water^ from^ a^ markedly diminished
volume of fluid will result in a sharp reduction
in CH2O per unit volume^ of^ tubular^ fluid^ and^ a^ rise
in Uosm.
During water^ diuresis,^ therefore,^ the^ side^ with
renal arterial^ constriction^ will^ display a^ reduced
rate of CH20 because reduced delivery of^ filtrate
to the diluting segment diminishes free^ water^ for-
mation; a lower UNa, because the^ magnitude of
reabsorption during slowed flow, though small^ in
absolute amount, is proportionately greater than
the rate of back-diffusion of^ free^ water; and^ a
higher Uosm because free water back-diffusion
concentrates nonsodium solutes, principally urea,
126
SUKI, EKNOYAN, RECTOR, AND SELDIN
TABLE I The ratio of glomerular filtration^ rate^ (GFR)^ to^ maximal tubular transport^ rate^ for^ p-aminohippurate^ (TmPAH) in acute and chronic^ hydronephrosis
GFR/TmPAH Experimental Experi- model mental Control Exp./Cont. Acute 6.3 8.3^ 0. hydronephrosis 4.8^ 7.7^ 0. 7.1 9.9 0. 9.5 10.5 0. Mean ±SD 6.941.7 9.141.1^ 0.7540. Chronic 10.7 8.3^ 1. hydronephrosis 12.5^ 7.1^ 1. 13.0 8.8 1. 5.4 4.6 1. Mean -SD^ 10.4^ 43.0^ 7.2^ ::1.6^ 1.4540. *p (^) <0.01.
segment, could result in the^ high^ UNa,^ high^ Uo.m,
and low CH2o characteristic^ of^ chronic^ hydro-
nephrosis. To examine the functional^ integrity^ of^ the^ di-
luting segment, we plotted Cia2o per^100 ml^ GFR
against urinary flow .(V) per 100 ml GFR^ (Fig-
ure 6). CH20 was plotted against V^ rather^ than
solute clearance (Co.m) because the rate of urinary
flow in water diuresis is a closer approximation of the rate of delivery of filtrate to the loop of Henle than is Cosm.3 If free water formation were
significantly impaired, less CH20 should be found
on the hydronephrotic than on the normal side at any given rate of urinary flow. This is, how- ever, not the case. It is apparent from Figure 6 that, at comparable rates of delivery, the normal and chronically hydronephrotic kidneys generate
the same CH20. Therefore, there is no apparent
defect in CH20 in chronic hydronephrosis.
Since CH20 represents- a^ balance^ between^ free
water formation and free water^ back-diffusion,^ it might be^ argued^ that^ a^ defect^ in^ formation^ could be masked by a commensurate reduction^ in^ back- diffusion. The shrinkage^ and^ scarring^ of^ the medulla so characteristic of chronic hydronephro- sis (^) undoubtedly prevents the establishment of (^3) During water diuresis the distal convoluted tubule and the collecting duct are relatively impermeable to^ water. The rate of urinary flow, therefore, is^ the^ best^ index^ of the rate of (^) delivery of tubular fluid to the distal nephron. Urinary flow, however, does^ not^ equal the^ rate^ of^ de- livery since some^ back-diffusion^ of^ water^ from^ the^ col- lecting duct^ is known^ to^ occur^ even^ in^ the^ absence^ of ADH (8, 11, 17, 18).
medullary hypertonicity and impairs diffusion^ of
water out of the collecting duct. However, re-
duction in free water loss would contribute equally
to urinary flow and CH20. Consequently, although
a reduction in free water back-diffusion would in-
crease CH2o, it would not correct the low CH20 to
a normal value when C1120 is compared to urinary
flow. Since the relations between CH20 and urinary
flow in the normal and hydronephrotic kidney are superimposable, this would constitute evidence against the hypothesis that the pattern of urinary formation in chronic hydronephrosis is attributable
to a combination of underperfusion of nephrons,
tubular damage, and reduced free water back-dif-
fusion. None of these arguments excludes the pos-
sibility that^ some^ degree^ of^ tubular^ damage^ might
exist, and that free water back-diffusion might be
reduced. Indeed,^ the^ profound^ destruction^ of^ the
medulla almost certainly means^ that^ the^ normal
back-diffusion of free^ water is^ drastically^ curtailed.
We merely wish to emphasize that^ the^ combina-
tion of tubular damage and^ reduced^ free^ water
back-diffusion cannot readily explain the^ striking
increase in sodium excretion^ in^ the^ face^ of^ normal CH120 in^ the^ setting of^ distal^ nephron under-
perfusion.
The changes in sodium and^ water^ excretion^ in
chronic hydronephrosis can be^ more^ easily ex-
plained on the basis of reduced nephron mass^ with
overperfusion of residual nephrons. It^ is^ not^ un-
reasonable to assume that the GFR per nephron in
chronic hydronephrosis is elevated. Although in-
trapelvic pressure rises sharply with^ acute^ obstruc-
tion of the ureter, it has been shown that^ with^ the
persistence of obstruction the intrapelvic pressure
falls gradually towards normal^ values^ (9). De-
spite the fall in intrapelvic pressure some^ nephrons
never regain function and the^ functional^ renal^ mass
is reduced. When the intrapelvic pressure falls,
however, the remaining nephrons of^ the^ hydro-
nephrotic kidney may respond in^ a^ similar^ man-
ner to those of a kidney damaged from^ any other
cause by a compensatory increase^ in^ the^ rate^ of
filtration per nephron (19).
Furthermore, the^ data^ relating^ the^ GFR^ to^ re-
nal tubular mass (TmPAH) are consistent with^ the
presence of^ increased^ GFR^ per^ nephron^ in^ chronic,
as distinct from acute, hydronephrosis (Table I).
In renal underperfusion due to inflation of^ a^ bal-
loon in the aorta a fall in maximal tubular trans-
128
RENAL FUNCTION IN ACUTE AND CHRONIC HYDRONEPHROSIS
port of glucose (^) (TmgiucO,,,) (13) has been re- ported. Acute elevation of ureteral pressure has also been reported to result in a reduction in Tmglu,08e (10) and^ TmpAH [(10) and^ present study]. In both experimental procedures the fall
in GFR almost always exceeded the fall in the
tubular maximum, thus suggesting a reduced fil- tration rate per nephron. In chronic hydronephro-
sis, however, the fall of TmPAH was always in ex-
cess of the fall in GFR. The increased GFR per
TmPAH may be interpreted as an increased filtra-
tion rate per nephron. It is likely, therefore, that the combination of an elevated GFR per nephron and diminished frac- tional reabsorption of filtrate in the proximal nephron results in marked overperfusion of the distal nephron. The larger volume of fluid de- livered to each distal nephron results not only in
greater CH2o per 100 ml GFR, but also in a higher
rate of sodium excretion and a higher Uosm in wa-
ter diuresis. The low absolute rates of CH20 must
be due to a diminution in the total number of
nephrons.
The striking difference in^ the pattern of water
excretion between acute and chronic hydronephro-
sis is displayed in^ Figure 7, where the fraction of the glomerular filtrate excreted into the urine (V/GFR) on the experimental side is compared to that of the contralateral control kidney during both water and hypotonic saline diuresis. It is evident that at any given level of fractional volume excretion on the control side, fractional excretion
is lower on the side with renal arterial constriction
or acute hydronephrosis and higher on the side with chronic hydronephrosis. The proportion of the GFR that is excreted into the urine during maximal suppression of antidiuretic hormone rep- resents the difference between fractional delivery to, and fractional water loss from, the distal nephron. The low fractional volume excretion during acute hydronephrosis and renal arterial constriction is probably the consequence of dimin-
ished delivery of filtrate to the diluting segment in
the face of a well-maintained absolute rate of free water back-diffusion out of the (^) collecting duct. The well-maintained absolute rate of free water
back-diffusion will result in an increased fractional
'loss of^ water^ and^ a^ diminished^ fractional^ volume
excretion. The^ demonstration^ by Levinsky, David- son, and Berliner^ (20) that during antidiuresis
WATER DIUR ES/S
£ a (^0 ) so (^) a (^) °a 0
, l o0a
HIYPOTONIC SALINE D/IRES/S .
0 5 10 /5 20 0 5 /0 /5 20 25 30 35 V Cornzrol Xidnry GFiv^ X^100 FIG. 7. FRACTION OF GFR (V/GFR X 100) DELIVERED TO THE DILUTING SEGMENT IN RENAL ARTERIAL CONSTRICTION AND ACUTE AND CHRONIC HYDRO- NEPHROSIS, COMPARED TO THE CONTROL SIDE. Graph to the left represents data obtained during water diuresis, graph to the right during hypotonic saline diuresis. Lines drawn are the theoretic lines of equal fractional delivery.
F
' (^40) o X. 0 35
b 25 '.. (^20)
'
0
145
129
p
RENAL FUNCTION IN ACUTE AND CHRONIC HYDRONEPHROSIS
dium salts (^) following decompression of the urinary bladder. J. Urol. (Baltimore) 1951, 66, 805.
- Bricker, N. S., (^) E. L. Shwayri, J. B. Rearden, D. Kellog, J. P. Merrill, and J. H. Holmes. An ab- normality in renal function resulting from urinary tract obstruction. Amer. J. Med. 1957, 23, 554.
- Van Giesen, G., M. (^) Reese, F. Kiil, F. C. Rector, Jr., and D. W. Seldin. The characteristics of renal hypoperfusion in dogs with acute and chronic re- ductions in glomerular filtration rate as disclosed by the^ pattern of water and solute excretion after hypotonic saline infusions. J. (^) clin. Invest. 1964, 43, 416.
- Kiil, F. The Function of the Ureter and Renal Pel- vis. (^) Philadelphia, Saunders, 1957.
- Malvin, R. L., H. Kutchai, and F. Ostermann. De- creased nephron (^) population resulting from in- creased ureteral pressure. Amer. J. Physiol. 1964, 207, 835.
- Berliner, R. W., and D. G. Davidson. Production of hypertonic urine in the absence of pituitary anti- diuretic hormone. (^) J. clin. Invest. 1957, 36, 1416.
- Ostle, B. Statistics in Research. Ames, Iowa, Iowa State University Press, 1963.
- Thompson, D. D., M. J. Barrett, and R. F. Pitts. Significance of glomerular perfusion in relation to variability of filtration rate. Amer. (^) J. Physiol. 1951, 167, 546.
- Dirks, J. H., W. J. Cirksena, and R. W. Berliner. The effect of saline infusion on sodium reabsorp- tion by the proximal tubule of the dog. J. clin. In- vest. (^) 1965, 44, 1160.
- Glabman, S., H. S. Aynedjian, and N. Bank. Micro- puncture study of the effect of acute reductions in
glomerular filtration rate on sodium and (^) water re- absorption by the proximal tubules of the rat. J. clin. Invest. 1965, 44, 1410.
- Brunner, F. P., F. C. Rector, Jr., and D. W. Seldin. Unpublished observations.
- Kiil, F., and K. Aukland. Renal tubular localization of water and sodium reabsorption in antidiuresis and water diuresis. Scand. J. clin. Lab. Invest. 1960, 12, 277.
- Gottschalk, C. W. Micropuncture studies of tubu- lar function in the mammalian kidney. Physiologist 1961, 4, 35.
- Bricker, N. S., P. A. F. Morrin, and S. W. Kime, Jr. The pathologic physiology of chronic Bright's disease. An exposition of the "intact nephron hy- pothesis." Amer. J. Med. 1960, 28, 77.
- Levinsky, N. G., D. G. Davidson, and R. W. Berliner. Effects of reduced glomerular filtration on urine concentration in the presence of antidiuretic hor- mone. J. clin. Invest. 1959, 38, 730.
- Earley, L. E., and R. M. Friedler. Observations on the mechanism of decreased tubular reabsorption of sodium and water during saline loading. J. clin. Invest. 1964, 43, 1928.
- Carone, F. A., and F. H. Epstein. Nephrogenic dia- betes insipidus caused by amyloid disease. Evidence in man of the role of the collecting ducts in con- centrating urine. Amer. J. Med. 1960, 29, 539.
- Kleeman, C. R., and F. H. Epstein. An illustrative case of chronic pyelonephritis with persistently hy- potonic urine. Amer. J. Med. 1957, 23, 488.
- Kleeman, C. R., W. L. Hewitt, and L. B. Guze. Pyelonephritis. Medicine^ (Baltimore) 1960, 39, 3.
