scholarly journals RENAL FUNCTION DURING CHRONIC ANEMIA IN MAN

Blood ◽  
1947 ◽  
Vol 2 (2) ◽  
pp. 192-202 ◽  
Author(s):  
STANLEY E. BRADLEY ◽  
GERALDINE P. BRADLEY

Abstract 1. Renal function has been studied quantitatively in 15 patients with chronic anemia, 8 of whom were proved to have pernicious anemia. In 7 the anemia was secondary to chronic blood loss, iron deficiency, paroxysmal nocturnal hemoglobinuria, and leukemia. The effective renal plasma flow and glomerular filtration rate were measured by clearance technics; and tubular function, by saturation methods (diodrast Tm and glucose Tm). 2. The effective renal plasma flow, the glomerular filtration rate, and the filtration fraction (percentage of plasma filtered at the glomerulus) were reduced slightly below the normal values in most subjects. The effective renal whole blood flow was always greatly reduced, by 46 per cent on the average in males and by 31.8 per cent in females. 3. Since arterial pressure was not significantly depressed it was concluded that renal vasoconstriction occurs in chronic anemia, possibly as a homeostatic device for the diversion of blood to tissues more sensitive to oxygen lack. The relatively small reduction of filtration fraction implies afferent and efferent arteriolar vasoconstriction with dominance by the afferent arterioles. These changes were shown to be reversible, a return to normal values paralleling the return of the blood picture to normal. 4. Diodrast Tm was reduced significantly in 9 of 10 patients while the values of glucose Tm were normal in 6 of 7 patients. The normal values for glucose Tm indicated continued operation of all glomeruli and implied the absence of shunting or of cessation of blood flow in any significant portion of the kidney. The fall in diodrast Tm, which appeared to be reversible in 2 of 4 individuals, was interpreted as evidence of intracellular dysfunction rather than destruction or inactivation of nephrons.

1965 ◽  
Vol 20 (5) ◽  
pp. 1026-1027 ◽  
Author(s):  
Rodolfo Lozano ◽  
Carlos Monge C.

When compared with sea-level residents, the healthy natives living at an altitude of 4,540 m show a 12% reduction in the glomerular filtration rate, a 37% reduction in effective renal plasma flow, a 12% reduction in effective renal blood flow, and an increase of 39% in the filtration fraction. The corresponding values in patients with chronic mountain sickness living at 4,300 m above sea level are: glomerular filtration rate, 32% reduction; effective renal plasma flow, 57% reduction; effective renal blood flow, 9% increase; and filtration fraction, 56% increase. The mean hematocrit values of the healthy and sick natives investigated were 59 and 79%, respectively. The possible relationships between cardiac output, hematocrit values, and renal hemodynamics are discussed. altitude stress; blood flow, kidney; glomerular filtration Submitted on October 5, 1964


1971 ◽  
Vol 10 (01) ◽  
pp. 16-24
Author(s):  
J. Fog Pedersen ◽  
M. Fog Pedersen ◽  
Paul Madsen

SummaryAn accurate catheter-free technique for clinical determination simultaneouslyof glomerular filtration rate and effective renal plasma flow by means of radioisotopes has been developed. The renal function is estimated by the amount of radioisotopes necessary to maintain a constant concentration in the patient’s blood. The infusion pumps are steered by a feedback system, the pumps being automatically turned on when the radiation measured over the patient’s head falls below a certain preset level and turned off when this level is again readied. 131I-iodopyracet was used for the estimation of effective renal plasma flow and125I-iothalamate estimation of the glomerular filtration rate. These clearances were compared to the conventional bladder clearances and good correlation was found between these two clearance methods (correlation coefficients 0.97 and.90 respectively). The advantages and disadvantages of this new clearance technique are discussed.


2010 ◽  
Vol 299 (5) ◽  
pp. F954-F962 ◽  
Author(s):  
Torrance Green ◽  
Jorge Rodriguez ◽  
L. Gabriel Navar

Nonsteroidal anti-inflammatory drug usage has long revealed renoprotective prostaglandin actions on the renal microvasculature during increased pressor hormone influence, but whether increased cyclooxygenase (COX)-2 expression supports prostaglandin vasodilatory influence by interfering with the actions of ANG II remains unresolved. Therefore, we tested the hypothesis that COX-2 inhibition causes hemodynamic and excretory effects that are increased in proportion to ANG II activity. In anesthetized Sprague-Dawley rats having augmented cortical COX-2 expression but different ANG II activity, we conducted renal clearance experiments during acute inhibition of COX-2 with nimesulide (NMSLD) and inhibition of COX-1 with SC-560. In one series of experiments, acute captopril [acute angiotensin-converting enzyme (ACE) inhibitor (aACEi)] was administered alone ( n = 13) or in combination with chronic captopril [chronic ACEi (cACEi)] pretreatment ( n = 19). In another series of experiments, rats were fed a normal-sodium [0.4% (NS), n = 12] or a low-sodium [0.03% (LS), n = 18] diet. NMSLD did not alter mean arterial blood pressure in any group but, in the LS and cACEi groups, decreased renal plasma flow (from 3.99 ± 0.33 to 2.85 ± 0.26 and from 4.30 ± 0.19 to 3.22 ± 0.21 ml·min−1·g−1), cortical blood flow (−12 ± 8% and −13 ± 4%), and glomerular filtration rate (from 0.88 ± 0.04 to 0.65 ± 0.05 and from 0.95 ± 0.07 to 0.70 ± 0.05 ml·min−1·g−1). In contrast, medullary blood flow (MBF) was significantly decreased by COX-2 inhibition in NS (−24 ± 5%), LS (−27 ± 8%), aACEi (−16 ± 3.8%), and cACEi (−24 ± 4.2%) groups. Absolute and fractional sodium excretion rates were unchanged by NMSLD, except in the LS group (0.75 ± 0.05 μeq/min and 0.43 ± 0.15% and 0.51 ± 0.06 μeq/min and 0.26 ± 0.10%). SC-560 did not augment the effects of NMSLD. These results demonstrate an augmented COX-2-mediated vasodilation that is not contingent on ANG II, in contrast to COX-2-mediated augmented sodium excretion, where ANG II activity is requisite. Furthermore, the COX-2 effects on MBF are not contingent on ANG II or changes in cortical microvascular responses. These results reflect COX-2 continual regulation of MBF and adaptive opposition to ANG II prohypertensinogenic effects on renal plasma flow, cortical blood flow, glomerular filtration rate, and absolute and fractional sodium excretion.


2014 ◽  
Vol 307 (4) ◽  
pp. F445-F452 ◽  
Author(s):  
Anne D. Thuesen ◽  
Henrik Andersen ◽  
Majken Cardel ◽  
Anja Toft ◽  
Steen Walter ◽  
...  

Voltage-gated Ca2+ (Cav) channels play an essential role in the regulation of renal blood flow and glomerular filtration rate (GFR). Because T-type Cav channels are differentially expressed in pre- and postglomerular vessels, it was hypothesized that they impact renal blood flow and GFR differentially. The question was addressed with the use of two T-type Cav knockout (Cav3.1−/− and Cav3.2−/−) mouse strains. Continuous recordings of blood pressure and heart rate, para-aminohippurate clearance (renal plasma flow), and inulin clearance (GFR) were performed in conscious, chronically catheterized, wild-type (WT) and Cav3.1−/− and Cav3.2−/− mice. The contractility of afferent and efferent arterioles was determined in isolated perfused blood vessels. Efferent arterioles from Cav3.2−/− mice constricted significantly more in response to a depolarization compared with WT mice. GFR was increased in Cav3.2−/− mice with no significant changes in renal plasma flow, heart rate, and blood pressure. Cav3.1−/− mice had a higher renal plasma flow compared with WT mice, whereas GFR was indistinguishable from WT mice. No difference in the concentration response to K+ was observed in isolated afferent and efferent arterioles from Cav3.1−/− mice compared with WT mice. Heart rate was significantly lower in Cav3.1−/− mice compared with WT mice with no difference in blood pressure. T-type antagonists significantly inhibited the constriction of human intrarenal arteries in response to a small depolarization. In conclusion, Cav3.2 channels support dilatation of efferent arterioles and affect GFR, whereas Cav3.1 channels in vivo contribute to renal vascular resistance. It is suggested that endothelial and nerve localization of Cav3.2 and Cav3.1, respectively, may account for the observed effects.


1967 ◽  
Vol 38 (2) ◽  
pp. 107-114 ◽  
Author(s):  
J. W. BAUMAN

SUMMARY Glomerular filtration rate (GFR), renal plasma flow (RPF) and solute-free water reabsorption (TcH2O) were measured in anaesthetized intact and hypophysectomized rats and in hypophysectomized rats treated with corticotrophin (ACTH). GFR and RPF were measured by [14C]inulin and [3H]p-aminohippuric acid clearances. In agreement with previous reports, these two functions were found to be reduced by hypophysectomy. Infusion of vasopressin increased TcH2O in the intact rat but failed to produce a significant change in the hypophysectomized rat. Treatment of hypophysectomized rats with ACTH restored the effects of vasopressin on TcH2O. ACTH also increased the RPF of hypophysectomized rats to normal values, but only partially restored GFR.


2020 ◽  
Vol 2 (5) ◽  
pp. 670-672
Author(s):  
Jesse C. Seegmiller ◽  
Brian J. Wolfe ◽  
Nansy Albtoush ◽  
Isabella Melena ◽  
Susan P. Gross ◽  
...  

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