Time-Course for Recovery of Renal Function After Unilateral (Single-Tract) Percutaneous Access in the Pig

2010 ◽  
Vol 24 (2) ◽  
pp. 283-288 ◽  
Author(s):  
Rajash K. Handa ◽  
Lynn R. Willis ◽  
Bret A. Connors ◽  
Sujuan Gao ◽  
Andrew P. Evan ◽  
...  
Hypertension ◽  
2012 ◽  
Vol 60 (suppl_1) ◽  
Author(s):  
Xuexiang Wang ◽  
Ashley Johnson ◽  
Jonathan Lee ◽  
Leah Solberg-Woods ◽  
Michael R Garrett

A relatively common abnormality of the urogenital tract in humans is the development of only a single kidney (1:500 to 1:1000). Clinical studies suggest that patients born with a single kidney can develop proteinuria, hypertension, and even renal failure later in life. In contrast, studies in children who undergo nephrectomy or adults who serve as kidney donors appear to exhibit little difference in renal function compared to two-kidney subjects. Invasive techniques such as nephrectomy or renal ablation have been used to generate animal models to recapitulate this human congenital disorder. The progression of injury in these models is attributed to hyperfiltration which refers to changes in hemodynamics that cause glomerular damage leading to hypertension. Recently, our lab developed a new genetic animal model [heterogeneous stock derived model of unilateral renal agenesis, (HSRA)] that develops with a single kidney in 50-75% of offspring. The model is characterized by reduced nephron number, kidney hypertrophy, and renal injury that leads to a decline in renal function. Time course evaluation of blood pressure, renal hemodynamics, and renal injury was performed in 4 groups; (1) HSRA-S (1-kidney), (2) HSRA-C (2-kidney littermates), (3) HSRA-UNX3 (uninephrectomy-week 3) and (4) HSRA-UNX8 (uninephrectomy-week 8). Nephrectomized animals demonstrated hyperfiltration, whereas single kidney animals (HSRA-S) did not. This suggests a different pathophysiological mechanism of injury between congenital and nephrectomized rats. At later time points, proteinuria for HSRA-UNX3 (82±22.9 mg/24h) and HSRA-UNX8 (46±18.1) were significantly higher than HSRA-C (11±6.4), while HSRA-S (109±15.7) demonstrated the highest proteinuria. GFR was lowest in HSRA-S (656±123.9 ul/min/gKW), followed by HSRA-UNX3 (1151±112.4), HSRA-UNX8 (1309±98.3) and HSRA-C (1544±111.7). Microarray studies have identified several developmental genes ( Hox5b , Smoc2 and c- Kit ) that may be linked to reduced nephron number and other structural changes that could predispose the HSRA-S to kidney injury later in life. These results demonstrate that rats born with a single kidney are more prone to renal injury than nephrectomized rats and the mechanism is likely different.


2016 ◽  
Vol 196 (1) ◽  
pp. 131-136 ◽  
Author(s):  
Ilya Gorbachinsky ◽  
Kyle Wood ◽  
Marc Colaco ◽  
Sij Hemal ◽  
Jayadev Mettu ◽  
...  

1982 ◽  
Vol 53 (6) ◽  
pp. 1449-1454 ◽  
Author(s):  
H. Tazawa

First, preliminary experiments were designed in the 16-day-old individual chick embryo to elucidate the effect of electrolyte infusion and blood samplings on hemodilution, which might influence the acid-base balance. Three kinds of hemodilution were observed: 1) hemodilution caused by four repetitive samplings, which had no influence on acid-base balance; 2) hypervolumic hemodilution caused by infusion of solution whose volume equaled about 5–6% of total blood volume, which induced dilution acidosis; and 3) hypertonic hemodilution caused by hypertonic electrolyte infusion, which also induced dilution acidosis. The embryo recovered from the hypertonic dilution acidosis in 6 h after infusion, but it did not recover from hypervolumic acidosis. Second, the time course of changes in metabolic and respiratory acid-base disturbances was studied in the individual embryo. Metabolic acid-base disturbances made by hypertonic NaHCO3 infusion were restored to control state in 6 h. Respiratory acid-base disturbances were also regulated in terms of changes in plasma[HCO-3] and pH. The renal function and redistribution of HCO-3 may in part be responsible for the regulation.


1995 ◽  
Vol 73 (1) ◽  
pp. 107-112 ◽  
Author(s):  
Francine G. Smith ◽  
Jessica Abraham

Despite the widespread use of furosemide in the treatment of various fluid and electrolyte disorders in the preterm and term human infant and child, the physiological effects of this potent diuretic agent on renal function and renin release during postnatal maturation are poorly understood. To test the hypothesis that the renal and renin responses to furosemide are altered during postnatal maturation, experiments were carried out in conscious chronically instrumented newborn lambs (11 ± 3 days, n = 7) and older lambs (28 ± 3 days, n = 6), at least 5 days after surgery under halothane anesthesia for placement of catheters. Renal function and plasma renin activity (PRA) were measured for 1 h before and 2 h after intravenous injection of furosemide (2 mg/kg; 0.2 mL/kg) or vehicle (0.2 mL/kg). Glomerular filtration rate (GFR) decreased after furosemide administration to both groups of lambs. However, the time course of this decrease in GFR was different, occurring sooner in older lambs (30 min) than in newborns (90 min). GFR remained significantly decreased after 150 min in both age-groups. The natriuretic and diuretic responses to furosemide were similar in newborns and older iambs, peak diuretic and natriuretic responses occurring within 30 min. PRA increased dramatically in both age-groups after furosemide; the response was accentuated in newborns. After 2 h, PRA was still elevated in newborns but returned towards control levels in older lambs. These data demonstrate that both the GFR and renin responses to furosemide are altered during ontogeny.Key words: renal function, diuretic, blood volume, renin–angiotensin system, renal nerves, neonate, baroreflex.


1999 ◽  
Vol 89 (3) ◽  
pp. 786 ◽  
Author(s):  
Dennis M. Fisher ◽  
Kellie Schoolar Reynolds ◽  
Virginia D. Schmith ◽  
James Hsu ◽  
Martin D. Sokoll ◽  
...  

2007 ◽  
Vol 30 (3) ◽  
pp. 322-334 ◽  
Author(s):  
Michael R. Garrett ◽  
William T. Gunning ◽  
Tracy Radecki ◽  
Arti Richard

Previously, we conducted a genome scan on a population derived from the Dahl salt-sensitive hypertensive (S) and the spontaneously hypertensive rat (SHR) using urinary albumin excretion (UAE) as our primary measure of renal function. We identified 10 quantitative trait loci (QTL) linked to several renal and/or cardiovascular traits. In particular, linkage and subsequent congenic strain analysis demonstrated that the loci on chromosome 2 had a large and significant effect on UAE compared with the S rat. The present work sought to characterize the chromosome 2 congenic strain [S.SHR( 2 )] by conducting a time-course analysis ( week 4–20), including evaluating additional renal parameters, histology, electron microscopy, and gene expression/ pathway analysis. Throughout the time course the congenic strain consistently maintained a threefold reduction in UAE compared with S rats and was supported by the histological findings of significantly reduced glomerular, tubular and interstitial changes. Gene expression/pathway analysis performed at week 4, 12, and 20 revealed that pathways involved in cellular assembly and organization, cellular movement, and immune response were controlled differently between the S and congenic. When all the data are considered, the chromosome 2 congenic appears to attenuate renal damage primarily through an altered fibrotic response. Recombinant progeny testing was employed to reduce the QTL to ∼1.5 cM containing several interesting candidate genes. The concordance of this rat QTL with renal disease loci on human chromosome 1q21 demonstrate that elucidating the causative gene and mechanism of the rat QTL may be of particular importance for understanding kidney disease in humans.


Sign in / Sign up

Export Citation Format

Share Document